INTRODUCTION
1. SHOULDER INSTABILITY: DEFINITIONS AND CLASSIFICATION
• Definitions
• Classification of Shoulder Instability
• Table I : Clinical Classification of Shoulder Instability
2. PATHOANATOMY AND BIMECHANICS OF ANTERIOR INSTABILITY
• Glenoid labrum lesions • Capsular lesions
• Superior labrum lesions and Biceps detachment • Rotator interval lesions.
• Humeral bone defects • Glenoid bone defects • Rotator cuff lesions
3. REPORTED RESULTS OF ARTHROSCOPIC STABILISATIONS
• Metal staples
• Transglenoid sutures Techniques (Morgan vs Caspari) • Cannulated bioabsorbable tacks
• Suture-anchor techniques
• Arthroscopic versus open Bankart repairs
• Arthroscopy in first time anterior shoulder dislocations
4. FACTORS ASSOCIATED WITH RECURRENCES AFTER ARTHROSCOPIC STABILIZATION
• Age of the patient
• Athletes and type of sport • Absence of initial trauma • Degree of instability
• Number of instability episodes • Associated hyperlaxity
• Capsular pathology • Glenoid bone defects • Humeral bone defects • Absence of immobilization
• Arthroscopic technique and surgeon’s experience
5. PATIENT SELECTION
ANTERIOR SHOULDER INSTABILITY
CURRENT CONCEPTS in ARTHROSCOPIC MANAGEMENT
Pascal Boileau*, Margareta Berg**, Matias Villalba
ABSTRACT max 300 words (249)
Purpose
To review the published results of arthroscopic shoulder stabilisation, and to compare those with the results of open stabilizing procedures.
Type of Study
A review.
Materials and Methods
The literature on open and arthroscopic shoulder stabilisation between 1987 and 2003 was reviewed, comparing different surgical techniques.
Results
Arthroscopic treatment of chronic shoulder instability has evolved during the last fifteen years. Our review of the literature shows different arthroscopic techniques to have different recurrence rates, with an over all reduction over time: Metal staples 25%, Morgan transglenoid sutures 39,5%, Caspari transglenoid sutures 21%, Bioresorbable tacks (Suretac) 17.5%, and Anchors with sutures 13%. These recurrence rates approaches the ones of open Bankart procedures by time, but are still higher than those.
The review also indicates some contra-indications of arthroscopic stabilisation: 1) absence of a classical Bankart lesion, 2) a distended or torn capsule, 3) a capsular detachment on the humeral side or 4) bony or cartilage defects or impression fractures including more than 25% of the glenoid or the humeral head. In these cases open surgical technique is still recommended.
Conclusions
We conclude that arthroscopic shoulder stabilisation should neither be condemned nor abandoned, but that attention must be paid to the surgical indication and to further improvements of the surgical technique. The selection of patients, the systematic addition of a capsular tightening, and the
treatment of associated pathologies have shown promising results. However, prospective, controlled, randomized studies comparing conventional and arthroscopic shoulder stabilisation are still lacking in the literature.
1. INTRODUCTION
Arthroscopic anterior shoulder stabilization has slowly evolved in Europe, in contrast to the United States where arthroscopic techniques have gone forward and have become rapidly popular, despite initial reports showing higher failure rates than conventional open techniques. The rationale for this enthusiasm is based on the theoretical advantages of arthroscopic stabilization: more accurate assessment of the intraarticular structures involved in instability, ability to manage concomitant pathology (i.e. SLAP lesions), less postoperative pain, better cosmesis, better postoperative range of motion, possibility of out-patient surgery and decrease hospital charges. Conversely, arthroscopic procedures are technically demanding, time-consuming, and need a long learning curve. Furthermore, only few scientifically valid studies (randomized, prospective, blinded independent review) authorize us to evaluate success rates compared to conventional techniques.
As our understanding of the pathology associated with anterior shoulder instability increases, and the clinical experience accumulates, indications for arthroscopic stabilization are better defined. Patient selection criteria, operative techniques, fixation devices and rehabilitation programs continue to evolve in order to improve clinical outcomes.
2. SHOULDER INSTABILITY: DEFINITIONS AND CLASSIFICATION
Laxity and instability are terms often applied to the shoulder, yet they should be clearly characterize and separated from each other.
Shoulder laxity is defined as the asymptomatic and physiological translation of the humeral head (HH) in the glenoid fossa, necessary for the normal function of the joint. Laxity is a an individual trait of body constitution and varies very much between different individuals, although is of greater amplitude in young patients (1, 2). Hyperlaxity is a term commonly used but poorly defined. Same patients will fit the classic description of this disorder and demonstrate generalized “hiperextensibility” of their joints (elbows, metacarpophalangeal joints, thumbs, patellas) caused by collagen tissue abnormalities. However, these patients are rarely seen in clinical practice. The larger subset of patients will have normal body ligamentous laxity but have developed shoulder hyperlaxity owing to capsular strain and plastic deformation. Shoulder hyperlaxity is difficult to evaluate clinically (3, 4). For instance, Neer and Foster(5) originally described the sulcus sign as the clinical hallmark of multidirectional instability (MDI). However, the sulcus sign, or the ability to inferiorly subluxate the HH while the arm is at the patient’s side, only indicates “inferior hyperlaxity”. When positive on physical examination, it is always bilateral and one or both shoulders may be asymptomatic. Increase HH translation while stressing the shoulder inferiorly, with the arm abducted 90° (Gagey’s hyperabduction test)(6), is another indicator of inferior hyperlaxity. Although both signs denote inferior hyperlaxity, a large sulcus (inferior drawer >1-2cm) in external rotation (ER) suggests possible rotator interval pathology, while a positive Gagey’s test (>20° of differential abduction) assess elongation of the IGHL complex.(6,7,8) Shoulder
hyperlaxity may also have an anterior component. External rotation greater than 85° with the arm at the side defines this “anterior hyperlaxity” (9). These findings should be contemplated in the context of the athlete’s sport demands, many overhead athletes will demonstrate increase ER as compared with the opposite shoulder without functional complains. However, being hiperlax may be a risk factor for having shoulder pain and instability develop.
Shoulder instability is defined as a non-physiological excessive translation of the humeral head out of the glenoid socket, resulting in clinical symptoms as dislocation, subluxation or pain. It is essential to make a distinction between instability and laxity and to be aware of they may be present alone or simultaneously.
Classification of shoulder instability
Instability can be classified according to five major criteria: degree, direction, etiology, frequency, and presence of associated hyperlaxity (Table I).
Degree of instability is illustrated by dislocation, subluxation, or pain. Dislocation is defined as a total and lasting loss of congruency between joint surfaces requiring a reducing maneuver by the patient or, most likely, another person. Subluxation is a partial and temporary loss of congruency between joint surfaces followed by spontaneous reduction (9). Pain can be the only complain in a small percentage of patients with instability. These patients may describe a sudden sharp or paralyzing pain when performing activities with the arm in external rotation, abduction and extension. The limb is weak or
“goes dead” and the patient is no longer able to throw, serve in tennis, or work with the arm above shoulder level. Patte and Bernegeau (10) named this phenomenon “épaule douloureuse et instable” (painful and unstable shoulder), Rowe and Zarins (11) referred to it as “dead arm syndrome”. This syndrome, due to subtle subluxations of the shoulder, has led in many times to misdiagnosis because patients are not conscious of any abnormal displacement of the HH. Conversely typical radiological findings such as Hill-Sachs lesions or anterior glenoid rim defects, and an apprehension test positive on physical examination, should lead the physician identify a veiled instability.
Shoulder instability can be classify by the direction (anterior, inferior, posterior) of the most important humeral translation. Neer(5), in 1980, introduced the concept of MDI to describe shoulder joints presenting abnormal HH translation in more than one direction due to an excessively wide joint capsule. The dominant finding of Neer’s MDI was inferior laxity (positive sulcus sign). However, by means of using the sulcus sign almost as a synonymous of MDI, confusion has emerged amongst the orthopaedic community. Provocative maneuvers (anterior and posterior drawer test, apprehension and relocation test, posterior stress test, Gagey test) should be used to determine the direction of
instability. But these tests must always be performed on and compared with the contralateral shoulder, and the findings taken in the context of reproduction of the patient’s symptoms and complains. For instance, anterior instability, the most frequent form of recurrent shoulder instability, is rarely only anterior but anterior-inferior. Patients have a positive apprehension-relocation test and show severe apprehension if we attempt to perform an hyperabduction test. However, hyperlaxity signs may not be present. On the other hand, professional baseball players may have more than 85° of ER in their dominant arm without any symptoms or signs of shoulder instability.
Shoulder instability is generally post-traumatic. Integrity of the capsuloligamentous complex can be destroy by a significant single trauma, such as a fall with the arm in extreme abduction and ER. Likewise, repetitive loading of the glenohumeral ligaments at increasing levels of subfailure strain (micro-trauma) has shown to produce plastic deformation, capsular stretching and subsequent instability. Infrequently, atraumatic, congenital or neuromuscular backgrounds can be established. This classification can seem a little simplistic. However, it has been useful in defining surgical indications, and has allowed us to evaluate results by comparing homogeneous groups of patients.
3. PATHOANATOMY and BIOMECHANICS OF ANTERIOR INSTABILITY
The shoulder is the most mobile joint of the body. In the glenohumeral joint, stability has been resigned at the expense of vast ranges of multi-planar motions. Normal motion is largely
non-constrained ball-and-socket kinematics, though some translation during active range of motion (ROM) is normal. However, several different mechanism involving the articular geometry, dynamic (muscular) stabilizers, static (cartilaginous, capsular and ligamentous structures) stabilizers, and intraarticular forces (negative intraarticular pressure, surface forces of adhesion and cohesion) interact to restrict excessive translation and maintain the humeral head in the glenoid fossa. Some authors prefer the terms active/passive stabilizers since all structures are actually shifting during shoulder joint
movement. At mid-ROM, the capsular ligaments are relatively lax and stability is maintained mostly by the configuration of the articular surfaces, labrum and muscle forces of the rotator cuff, which
compress the humeral head into the glenoid. At extreme ROM, the capsuloligamentous stabilizers are taut and assume more importance in providing stability for the joint.(12) Surgeons should be familiar with normal anatomy and its inherent variability, and must be prepared to address any of the multiple pathological entities commonly encountered in shoulder instability, whether acting alone or in
combination.
Glenoid labrum lesions
Perthes (13) and Bankart (14) were the first authors to describe the detachment of the capsulo-labral complex from the edge of the glenoid and the scapular neck. For long time this lesion was regarded as the "essential lesion" responsible for the chronic character of anterior instability (15, 16). In the classic “Bankart lesion” the anterior-inferior portion of the labrum is detached “below the equator” of the glenoid, destroying the anchorage point of the inferior and middle glenohumeral ligaments (IGHL and MGHL)(14-18), (Figure 1). A Bankart lesion damages the "embankment effect" resisting humeral head (HH) translation out of the glenoid, decreases the concavity depth of the gleno-labral cavity by 50%, and impairs the rotator cuff “concavity-compression” mechanism (19,20). Lippitt et al. (20)
showed that a resection of the labrum reduces HH translation resistance by 20%. Lazarus et al. (21) showed a 65% reduction in joint stability by experimentally produced chondro-labral defects.
Arthroscopies made in first time traumatic dislocations reveal Bankart lesions in 95 % of the cases (9, 22-25). In chronic instabilities we may see the typical persistent labral detachment, but occasionally a fibrous scarring has taken place, giving the false impression of gleno-labral integrity. Therefore the importance of probe testing the labrum during arthroscopy. A fibrous healing of the labrum can also take place medially onto the scapular neck, Nevasier(26) named this “mal-union” anterior labral periosteal sleeve avulsion (ALPSA) lesion. The possibility of fibrous healing could explain the lower incidence (50% to 90%) of Bankart lesions reported in chronic instabilities(9, 27, 28). Bankart lesions should be considered important instability lesions to be consequently repaired (Figure 2).
Capsular lesions
Bankart lesions are not solely responsible for anterior instability. Speer et al. (29,30) demonstrated in cadaveric studies that an isolated Bankart lesion produces only a small increase in anterior translation of the HH, not sufficient to subluxate or dislocate the glenohumeral joint. Capsular injury to the
glenohumeral ligaments occur after instability events. Turkel et al(31) were the first to show that the anterior band of the IGHL is the primary anterior stabilizer of the shoulder when the arm in 90° abduction with external rotation (Figure 3).
Other studies (32-34) have confirmed these results. Thus, to restore stability to an unstable shoulder, the competency of the IGHL complex must be re-establish.
Bigliani (35) experimentally determined three failure sites for the IGHL: the glenoid insertion (40 %), ligament mid-substance (35 %) and the humeral insertion (25 %). Above all, he founded
capsuloligamentous stretching before breakage, present despite the site of rupture, and even without insertion site failure. It is now common knowledge that recurrent episodes of instability are associated to permanent capsular elongation(35-38), capsular ruptures (39-41) and/or humeral avulsion of the glenohumeral ligaments(42-47).
Capsular elongation is not easy to assess during arthroscopy, as it corresponds to invisible, ultra-structural microscopic lesions. The ability to “drive-through” the joint from superior to inferior, with the arthroscope in the center of the glenohumeral joint, results from capsular redundancy. In a normal joint, this should be difficult, if not impossible to perform. Underestimation of capsule plastic deformation could account for the substantial failure rates reported in some series of arthroscopic stabilization (48-51). On the other hand, higher success rates of open Bankart procedures could be explained by associated capsular retention and fibrous scarring (created by the surgical approach), both accountable for capsular volume reduction.
Rodeo et al. (38) observed morphological and biochemical modifications of collagen fibers (greater diameter, more "cross-links" and increased content of cysteine and elastine) in capsular tissue biopsies from patients with anterior instability. These modifications may be an attempt to reinforce the capsule, making it more resistant to plastic deformation.
Capsular ruptures have been described in acute and chronic instabilities. Johnson (39) observed glenohumeral ligament tears in 54% of arthroscopies performed in patients with anterior instability. Symenoides (40) reported 15% of capsular tears, associated to labral detachment, in patients treated for recurrent anterior dislocation.
Humeral avulsion of the glenohumeral ligaments (HAGL) lesion was described by Wolf (42). In a prospective study he founded HAGL lesions in 9.3 % of patients (Figure 4). Bokor (43) reported an incidence of 39% after traumatic dislocations in patients playing contact sports.
Last of all, it is important to draw attention to the fact that some reports fail to demonstrate primary Bankart lesion in 4 % of patients with acute anterior dislocations, and in 6% of documented recurrent instabilities (52-54). This highlights the need to identify and repair capsular injuries in the course of anterior arthroscopic stabilization.
Lesion of the superior labrum and Biceps detachment
Superior labral anterior-posterior (SLAP) lesions(55) can contribute to glenohumeral instability. Pagnani(56) and Rodosky (57) showed in biomechanical cadaveric studies SLAP lesions can lead to significant multidirectional increase in HH translation, particularly in the first degrees of abduction.
They also demonstrated that superior labral defects decrease torsional rigidity and increase IGHL strain.
There is a frequent association between SLAP lesions and anterior instability. Molé and Coudane (28) reported 33% of SLAP lesions in acute instabilities, and our own series(54) found incidence to be at 26 % in chronic instabilities. Maffet (58) called SLAP type V the combination of SLAP type II and the classic Bankart lesion. Two useful conclusions should be drawn: (1) SLAP lesions should not be regarded as an isolated diagnosis, and other signs of instability must be seek if discovered during arthroscopy. (2) All labral lesions should be repaired throughout arthroscopic stabilization. Negligence of this rule could result in a residual instability.
Rotator interval lesions
The rotator interval is a capsular space, triangular in shape, extending from the foot of the coracoid process, medially, to the bicipital groove, laterally. It is limited by the anterior border of the
supraspinatus tendon and the superior border of the subscapularis tendon. The rotator interval is normally closed by a fine capsule reinforced by two structures: the superior glenohumeral ligament (SGHL) as the inner layer, and the coracohumeral ligament (CHL)as the outer layer (59).
In cases of anterior-inferior instability, and particularly in hyperlax shoulders, rotator interval defects have been described, and traumatic or dysplasic etiologies have been proposed (59-63). There is indirect proof that the rotator interval contributes to limit glenohumeral laxity: adhesions in this area are often found in cases of shoulder stiffness or so called "capsulitis" (5). Harryman(61) (in vitro) and Gartsman(64) (in vivo) showed that closing of the rotator interval decreases inferior and posterior translation of the HH. Field (60) and Gartsman (64, 65) suggested rotator interval closing could be an important factor in avoiding recurrences of instability. Wolf (66) claimed that the rotator interval closing could be justified in cases of associated hyperlaxity, although no significant clinical data support these theories. We advocate prudence in patients older than 30-40 years, without hyperlaxity, as rotator interval closing can result in post-operative stiffness and inferior functional outcomes.
Humeral bone defects
Malgaigne(67) in 1855 and Hill and Sachs(68) in 1940 described a compression fracture of the
posterior aspect of the HH ensuing anterior shoulder dislocations. This fracture is caused by impaction of the HH against the anterior glenoid edge. The literature reported incidence varies from 40% to 100% in both acute and recurrent instabilities (9, 23, 25, 27, 69,70). They are easily noticed during arthroscopic examination(Figure 5), and graded according to Calandra(69) as: (I) only cartilaginous lesion, (II) lesion including subchondral bone, and (III) large subchondral defect. Depending on the size and orientation, these lesions may “engage” the anterior corner of the glenoid as the shoulder goes into a functional position of abduction and external rotation, causing symptoms similar to subluxation. Burkhart(71,72) called this an articular arc deficit. When the impression fracture involves more than 25 % of the articular surface, it is well known to contribute to instability recurrences, even after a satisfactory Bankart repair (16, 72, 73). Unfortunately, there is no mode to measure,
preoperatively, the size of the defect in an accurate and reproducible way. A humeral fracture of importance could therefore be a contraindication to arthroscopic treatment. In those cases, the surgeon can choose between an open capsular shift procedure(5) to restrict external rotation and prevent lesion engagement, or an osteochondral allograft(74) to fill the defect and lengthen the articular arc of the humerus. Coracoid transpositions(75) have also been suggested.
Glenoid bone defects
Anterior-inferior glenoid defects may present as real fractures (avulsion fractures) or erosions
(compression fractures) (Figure 6). The reported incidence varies from 10 % to 80 % in different series (9, 70), although erosions are probably underestimated. Glenoid bone loss can create serious
containment problem for the shoulder. Gerber’s (2) biomechanical studies showed that lesions involving loss of the normal anterior-inferior glenoid rim of more than half of the maximal AP diameter of the glenoid (in Lamy glenoid profile view) lead to a loss of dislocation resistance of more than 30%. This may not be compensated for by soft tissue repair alone. Walch(75) has proposed the Bernageau glenoid profile view to assess glenoid rim defects. Nonetheless, this technique must be performed under fluoroscopic control, requires a contralateral comparison view and should be examined by an experienced observer. Recently, Sugaya(76) described a reproducible method to evaluate glenoid rim morphology and quantify the size of the defect as percentage of glenoid fossa using 3-D reconstructed computed tomography. Arthroscopy is less successful than radiography to identify glenoid bone
lesions, and especially to estimate their importance (28). Significant deficiencies were define by Burkhart(72) as a glenoid with an “inverted pear” shape ( inferior glenoid that is narrower than the superior glenoid on arthroscopic visualization).
In avulsion fractures, also named “bony Bankart lesions”, the capsule and labrum usually remain attached to the bone fragment. Pavlov (70) reported a higher incidence of avulsion fractures in subluxations, compared to dislocations (50 % versus 15 %). Small bone fragments are repositioned during capsulo-labral repair. Larger fragments can be treated with open reduction and internal fixation. Arthroscopically assisted fixation techniques using cannulated screws through the subscapularis muscle(77) or standard suture-anchor techniques have also been proposed.
In glenoid erosions, sometimes called “impression Bankart lesions”, there are no bone fragments to fix. These defects represent a loss of bone from the anterior glenoid rim and usually indicate a chronic recurrent instability. In our opinion, glenoid erosions are more difficult to treat than avulsion fractures and may contraindicate arthroscopic repair, especially if the defect comprises 25% or more of the glenoid articular surface. In these cases, open reconstructive surgery must be carry out to recreate the glenoid cavity by means of a coracoid transfer (Latarjet procedure) (51, 72, 75) or an iliac crest bone graft (74).
Rotator cuff lesions
Symeonides (40) stated that the subscapularis muscle suffered between 1 and 1.5cm. of elongation in the unstable shoulder. He observed midsubstance muscular lesions and muscle detachments from the sub-scapular fossa. He concluded that treatment of anterior instability should include shortening of the subscapularis tendon, to restrain external rotation and prevent contact between humeral bone defect and the glenoid rim.
Partial tears of the supraspinatus tendon are relatively frequent in acute dislocations, even in young patients. Baker(24) found 12 % and Molé(28) 23 % of deep partial tears during arthroscopic
examination of unstable shoulders. In chronic instabilities incidence is at 6% (54). Complete supraspinatus tears are more rare, about 5 % according to Walch (9,75). Older patients, persisting pain and/or functional disability more than 3 weeks after an anterior dislocation should raise suspicion about rotator cuff tears(78). Citing Gilles Walch: "any shoulder dislocation in a patients over the age of 40 has an associated rotator cuff tear until proved otherwise" (75).
5. REPORTED RESULTS OF ARTHROSCOPIC STABILIZATIONS
As stated before, critical analysis of the literature shows no studies of sound level of evidence (randomized, prospective, blinded independent review) reporting clinical outcome results of arthroscopic shoulder stabilization. Most of the data presented is the result of retrospective cohort studies, case series or expert opinion. Common methodological flaws include: unclear patient selection criteria, different operative techniques and insufficient follow-up (less than 2yrs.) (49,79). In addition, methods of evaluation and definition of failure have varied among series. In our opinion, at least four criteria must be considered when reporting outcomes: 1) recurrence rate: dislocations, subluxations or persistent apprehensions, 2) revision rate: results of subsequent operative procedures, 3) loss of ROM, and 4) athlete’s level of performance after surgery. Few papers have compared arthroscopic and open repairs. Reported failure rates after open techniques are inferior or equal to 10 % (16,70-83). Recurrence ratesfor all arthroscopic repairs have been higher (4 to 50%) in most cases.
Stapling, transglenoid suture techniques, biodegradable tacks and suture-anchor techniques have been used in arthroscopic anterior shoulder stabilization. (Figure 9)
Metal staples
The first arthroscopic shoulder stabilization was performed by Lany Johnson (39) in 1982. He used metal staples, reproducing Dutoit open procedure under arthroscopic control. No published study has a follow-up longer than two years, and only five have a follow-up longer than one year (27, 49, 84-86). Global recurrence rate is 25% (range 19 to 32 %)(Table II), although this probably an underestimation due to short follow-up.
Stapling technique uses single-point-fixation to re-attach the capsuloligamentous complex on the scapular neck. Medialization of the labrum, unsatisfactory recreation of the glenoid cavity and inability
to address capsular laxity account for the poor results of this technique, whether performed arthoscopically or open.(87)
Complications rate ranged 5 % to 26 %.. Hardware removal was often necessary due to rupture, intra-articular penetrations, migration, infection or persistent pain secondary to conflicts between the staples and subscapularis or coracoid process.(39,49, 88-92). Coughlin et al.(27) reported 25% loss of ER in half of the patients, and 50% loss in other 25% of the serie.
Because of the high failure rate, associated complications, and hardware problems, stapling techniques were abandoned.
Transglenoid sutures techniques (Morgan vs. Caspari)
In 1987 Morgan (93, 94) proposed to repair Bankart lesion by mattress sutures that capture the labrum, passed through the scapular neck and were tied over the posterior infraspinatus fascia. In 1988 Caspari (95, 96) described a similar technique, but using multiple (6 to 10) PDS sutures. Sutures were passed, by means of a special forceps (Caspari's forceps), through the capsulo-labral complex, and then through the scapula. Although the two techniques repair the labrum by transglenoid sutures, they are in fact different: Caspari’s technique theoretically allows some capsular shift and retention, while Morgan’s technique does not. Therefore, the results of both techniques should be analyzed separately.
Among seven series reporting the results of Morgan’s transglenoid suture technique (Table III), 88 failures in 214 patients are reported, given a recurrence rate of 39,5 % (range 5 to 49%). Loss of ER greater than 10° was found in 5 % of cases.(48, 97)
Table IV shows results of Caspari’s technique. One hundred nineteen recurrences were found between 549 patients, setting recurrence rate at 22 % (range 16 to 30%).
Loss of external rotation greater than 10° was reported by Hayashida et al. (98) in 10 out of 89 patients (12%).
Besides the high recurrence rate, tying sutures over the posterior fascia may injure the suprascapular nerve (reported incidence 1.5 % - 6 %), and suture tightness is loss due to infraspinatus muscle atrophy. Therefore these techniques were gradually abandoned.
Cannulated bioabsorbable tacks
Warren et al.(99,100), in 1990, advocated the use of the Suretac device (Acufex, Norwood, MY, USA), to treat shoulder anterior instability. In series with follow-up longer than 2 years, the reported
recurrence rate 17.5 % (range 13 to 24%)(Table V).
Theoretical advantages of using the Suretac device, such as its technical simplicity and avoidance of knot tying, are weighed down by the fact it allows only single-point-fixation of the capsulo-labral complex. As a result, cannulated tacks can not quite manage capsule elongation, and therefore failures closely match those of metal staples.
Absorbable tacks are molded from polyglyconate (PGA), which is degraded by hydrolysis quite rapidly. Barber (101) demonstrated a 50% loss of strength at 2 weeks and 100% loss at 4 weeks. Other possible complication is “foreign-body reaction” to the device, described in 4 to 6% of patients as an intra-articular inflammatory response associated to fever and general fatigue (75, 102, 103). This synovitis has be treated with arthroscopic debridement and intra-articular injections of steroids (104, 105).
Suture-anchor techniques
This method was described by Wolf in 1993 (106) when he reported using a metal anchor and tying knots with absorbable sutures. Snyder(107, 108) proposed the use of non-absorbable sutures on screwed anchors. The technique authorizes for knots to be tied in the joint arthroscopically, avoiding a posterior incision. Individual knot tying allows proper tension of the IGHL complex to be reestablished by means of superior shifting and east-to-west plication of the labrum and capsule. However, the ability to tie secure knots arthroscopically remains a demanding technical step for this stabilization procedure (109, 110). The cost of anchors can be considered as a supplementary inconvenience (111).
The reported failure rate is at 13 % (range 4% to 30%), (Table VI).
Other complications include anchor mal-position, anchor pull-out and intra-articular migration causing severe chondral damage, suture ruptures, and insufficient capsular retension (112-119).
Bioabsorbable anchors constitute a technological progress. They are radio-transparent, less aggressive for the passing sutures than metal anchors and allow easier gliding during knot tying (110,114).
At present time, suture-anchor techniques seems to be the most predictable method of arthroscopic stabilization with the least amount of associated morbidity.
Arthroscopic versus open Bankart repairs
There have been few articles addressing the comparative results of arthroscopic and open Bankart repairs in pure anterior traumatic instability (Table VII). Results of arthroscopic shoulder stabilizations are still less satisfactory than open techniques, especially regarding recurrences rates.
Green et al. (120) compared morbidity and complications of both techniques. Arthroscopic stabilization was associated with increased operating time (1.8 times), but blood loss was diminished by 10 times and postoperative anesthetics by 2.5 times. Barber et al. (111) affirmed that "arthroscopic Bankart" was faster and less expensive than conventional techniques. Finally, several studies show that ER loss is less important after arthroscopic repairs (121-124).
Karlsson’s (122) study is particularly interesting as it is a non-randomized prospective study, with a single surgeon performing all procedures and a follow-up longer than 2 years. He shows results of arthroscopic techniques approaching those of open surgery: 15 % versus 10% recurrence rate. Further studies of this type, with an acceptable methodology (and randomisation), are needed to further evaluate and compare outcomes. Reasonably, in trained hands, the results of both techniques should come near 10% of recurrences (125). On the other hand, Latarjet’s technique of coracoid transfer still has less than 5% failures.(9, 75)
Arthroscopy in first time anterior shoulder dislocations
The first surgeons who reported on arthroscopic repair for acute initial dislocations were those treating young cadets at West-Point military academy in the United States (23, 126). The decision making was based on the known natural history of non-operated anterior instabilities. Hovelius(127) followed patients for more than 15 years, and these long-term results are in this sense fundamental. He demonstrated that: 1) recurrence rate is at 52 % in the general population, and 2) only 23 % will eventually need surgical treatment within 10 years after the primary dislocation. Hovelius thought
preventive arthroscopic stabilization was not justified after a primary dislocation, even in young patients(128).
Conversely, in young patients, under the age of 25, recurrence rates have range from 60% to 94% after conservative treatment.(27, 126-135). Failure rates after arthroscopic stabilization in first time dislocators are at 15% (range 4% to 27%), and no complications have been reported.(Table VIII). Two prospective randomized studies by Sandy Kirkley (132, 134), with 2 and 5-years follow up, showed results after surgical or conservative treatment may deteriorate with time. Recurrence rate increase from 16 % to 27 % in the arthroscopy group and from 45% to 60 % after functional treatment.
Finally, Wintzell (136) proved that simple arthroscopic lavage decrease recurrence risk. His hypothesis was that capsule and labrum would heal in better position if capsular distension derived from traumatic bleeding could be reduced.
Thus, although natural history after conservative treatment is favorable in the majority of patients, there seems to be a place for immediate arthroscopic repair in a selected population of young athletes practicing sports at risk, such as throwing or contact sports. In acute instability, the state of the tissues might promote better healing than in chronic cases with more severe capsular plastic deformation. (79, 135) The evolution in this sense is not very different from that in knee surgery, where ACL tears in high level athletes are repaired rapidly, before multiple episodes of instability occur.
6. FACTORS ASSOCIATED WITH RECURRENCES AFTER ARTHROSCOPIC STABILIZATION Age of the patient
More than any other factor, age has been reported to impair results of arthroscopic shoulder stabilization. Several series (9, 79, 137, 138,143) showed significantly inferior results in very young patients. In the series of Torchia (79) the recurrence rate was at 4 % for patients older than 25 years, whereas 29 % for younger patients (p=0.0003). In the same series, 6 out of 10 patients aged under 16 years, with a verified Bankart lesion, had re-dislocate at final follow- up. Different age “cut-lines” have been proposed: 25 yrs for Lafosse (139), 21yrs for Gartsman (65) and Kandziora (140), and 18 yrs for Bacilla (137). Less predictable results in young people, either treated conservatively or surgically, are certainly multifactorial: 1) the soft tissue is more lax in young patients (141), hyperlax patients are often younger, with a mean age of 21 years compared to 28 years for not hyperlax patients (142), 2) young patients are less compliant with post-operative immobilization and rehabilitation protocols, and 3) young patients are more often involved in sports-at-risk.
Athletes and type of sport
Several series have found more recurrences in patients involved in athletic activities, compared to non-active patients (144, 145). In addition, patients participating in contact sports, have less favorable prognosis (23, 39, 78, 94, 139, 145-147). However, it seems that the risk factor is not the sport itself but in fact the bone lesion often associated with instability. Burkhart and De Beer(72) showed that rugby players without bony lesions, treated arthroscopically, had comparable success rates than other patients. On the other hand, certain investigators have showed that throwing/overhead athletes have better chances to return to high level function with arthroscopic repair(78, 138, 148), probably due to less important loss of ER.
Absence of initial trauma
The absence of initial trauma, in primary anterior instability, is unfavorable to all types of surgery and particularly to arthroscopic procedures (2,75, 149). Unfortunately, an atraumatic not invalidating instability also may sustain acute trauma and turn out to be unacceptably symptomatic. Voluntary instability, due to selective contraction of the periscapular muscles, is a clear contraindication to arthroscopic and open stabilization.
Degree of instability
Pagnani (147) and Mologne (150, 151) found equal failure rates between dislocations and
subluxations. In contrast, Coughlin(27) and Lafosse (139) found better clinical results and less failures in the dislocation group compared to the subluxation group. Patients with subluxations often have many more episodes of instability before being diagnosed and treated, thus anatomic lesions are of greater importance. Lastly, painful shoulders due to a veiled instability show results comparables to
those of conventional techniques (152). This subset of patients constitutes an indication of choice for arthroscopic stabilization.
Number of instability episodes
The number of dislocations or subluxations showed to influence results in certain studies (140, 153-155) but not in others (51, 156). Kandziora (140) and Koss (154) consider a history of more than 5 dislocations to be a risk factor, while Hoffmann (155) set the limit at 10.
Associated hyperlaxity
In the multicentric study of the French SOFCOT (139, 142),in 1999, it seemed clear that anterior hyperlaxity (ER > 85°) was a negative prognostic factor. Recurrence rate decreased from 25 % to 13 % when hyperlax patients were excluded from the analysis of failures.
Inferior hyperlaxity (sulcus sign > 1-2 cm) is not necessarily a negative prognostic factor, provided some type of capsular re-tension is performed (78, 156). Other series also showed hyperlaxity to impair results (51, 146).
Capsular pathology
Numerous studies warned against arthroscopic treatment in cases of deficient capsular tissue (Detrisac’s III or IV), mid-substance tears or HAGL lesions (42,51,88, 140, 153, 158, 159). Capsular distension seems to be a constant finding in chronic instability. The real problem is to estimate the importance of this elongation. A recent biomechanical study by MacMahon (160) found 5 to 8 % incidence of irreversible capsular distension, even in a single trauma scenario. (Figure 10) Absence of classic Bankart lesions have been considered unfavorable to arthroscopic stabilization (147).
Glenoid bone defects
Walch et al. (51) reported a failure rate of 70 % in patients with visible fractures on plain x-rays and of 42 % in cases of glenoid erosion. Burkhart and De Beer (72) found 61% of recurrences in patients with “inverted pear” shape glenoids. Kim(112) stated that recurrences in his series were related to an osseous defect >30% of the entire glenoid circumference.
Humeral bone defects
The influence of Malgaigne's fracture on the recurrence rate has been a subject of discussion (51, 74, 144, 161, 162). Burkhart and De Beer (72) defined “engaging” Hill-Sachs lesion as one that presents the long axis of its defect parallel to the anterior glenoid with the shoulder in a functional position of abduction and ER, so that the Hill-Sachs lesion engages the corner of the glenoid. Patients presenting with this lesion had a 100% recurrence rate.
Postoperative immobilization
In a series with 148 patients, Detrisac(88) found 30% of recurrences in patients immobilized for less than 3 weeks compared to 4 % in those immobilized for 3 weeks or more. Grana (159), showed recurrences in 8 of 10 patients who removed the splint after one week. Hawkins (85), Mologne (150, 151) and Green (153) also found absence of immobilization to be a negative prognostic factor. However, the ideal immobilization time is not clear, varying from 3 to 6 weeks in the literature.
Arthroscopic technique and surgeon’s experience
Disagreement exist in the literature. In certain series, results of arthroscopic stabilization were clearly influenced, as in all surgical procedures, by surgeon’s experience and training (9, 49, 140, 153). On the contrary, others have found no differences (51, 159, 163).
Improvements in arthroscopic techniques and fixation devices allow re-attachment of loose structures in a more anatomical fashion. Studies that have showed the best short- and mid-term results are those using suture-anchor stabilization. The temporary outside traction suture (TOTS) (166) and the use of the posterior accessory portal are technical progresses that permit surgeons to perform a re-tension of the previously inaccessible axillary pouch.
7. PATIENT SELECTION
Arthroscopic techniques should still be regarded as rather new, relative and absolute contraindications are actually the subject of a constant modification.
History, clinical examination (either preoperatively or under anesthesia) and standard radiology are usually enough to select patients for arthroscopic stabilization (165). In some cases, CT or MRI arthrograms could be useful in better defining bone lesions, or if there is a suspected rotator cuff tear. However, only arthroscopic examination itself allows the precise diagnosis of intraarticular pathology, and sometimes the scheduled arthroscopic procedure must be abandoned for a conventional open technique. Table IX summarize the decision tree we use to assess negative prognostic factors for arthroscopic repair.
8. CONCLUSIONS
Shoulder arthroscopy has permitted the recognition of a variety of lesions responsible for anterior instability. Better understanding of the pathology and improved surgical techniques have raise the success rate of arthroscopic techniques closer to that of open Bankart repairs, but still far from coracoid transfer techniques (Latarjet-Bristow).
In the light of our experience, and as reported in the literature, we believe that arthroscopic anterior shoulder stabilization has a place in our therapeutic arsenal under three conditions: 1) selecting
patients, by reserving this technique for patients without hyperlaxity, older than 20 years and not
practicing sports "at risk" , 2) selecting lesions, by reserving the arthroscopic technique for cases where the glenohumeral ligaments are sound. The entire problem is to appreciate the severity of capsular distension, which is not easy. It can be estimated clinically, in patients with many episodes of instability and a positive hyperabduction test. However, only arthroscopic examination will provide an accurate assessment of tissue quality. And 3) improving arthroscopic techniques by systematically associating a medial plication and a proximal capsular shift.
Anyway, arthroscopic repairs are not going to disappear in the years to come, but will further develop under the pressure from the patients (who expect less aggressive interventions) and public health authorities (who expect less expensive outpatient care). Participation in courses and scientific meetings will permit surgeons to acquire specialized training, on plastic models and cadaveric shoulders, essential to initiate their clinical practice. In addition, patients must be informed that the arthroscopic techniques are still in evolution, and have inferior results than conventional techniques. Finally, arthroscopic stabilization of the shoulder will not be completely accepted before its
effectiveness has been demonstrated in major prospective randomized studies with long follow-up time, allowing a comparison of results between conventional and arthroscopic surgical techniques.
---
We express our gratitude to the French Society for Arthroscopy for the support, and Dr
Jonathan Hobby for the help with the preparation of this manuscript.
REFERENCES
1. Emery RJH, Muladji AB. Glenohumeral instability in normal adolescent : incidence and
significance. J Bone Joint Surg 1991 ; 73B : 406-408.
2. Gerber C. Les instabilités de l’épaule. In : Cahiers d’Enseignement de la SOFCOT n° 33.
Paris : Expansion Scientifique Publications ; 1988. p. 51.
3. Harryman DT, Sidles JA, Scott LH, Matsen FA. Laxity of the glenohumeral joint:a quantitative
in vivo assessment. J Shoulder Elbow Surg 1992 ; 1 : 66-76.
4. Tilander B, Norlin R. Intraoperative measurement of shoulder translation. J Shoulder Elbow
Surg 2001 ; 10(4) : 358-364.
5. Neer CS, Foster C. Inferior capsular shift for involuntary inferior and multidirectional
instability of the shoulder. J Bone Joint Surg Am 1976 ; 58 : 252-256.
6. Gagey J, Gagey M: The hyperabduction tesy. An assessment of the laxity of the inferior
glenohumeral ligament. JBJS 2001;83-B(1):69-74.
7. Gerber C, Ganz R. Clinical assessment of of instability of the shoulder, with special reference to
anterior and posterior drawer tests. J Bone Joint Surg 1984 ; 66b : 551.
8. Coste JS, Trojani C, Boileau P. Le test d’hyperabduction compraratif. Rev Chir Orthop 2000
9. Coudane H, Walch G. L’instabilité antérieure chronique de l’épaule chez l’adulte. Symposium
de la SOFCOT, Paris Nov 1999. Rev Chir Orthop 2000 ; Suppl. I : 86 : 91-150.
10. Patte D, Bernegeau J, Rodineau J, Gardes JC. Epaules douleureuses et instables. Rev Chir
Orthop 1980 ;66 :157-65.
11. Rowe CR, Zarins B. Recurrent transient subluxation of the shoulder. JBJS 1981;63-A(6): 863
–871.
12. Warner JJP, Boardman DN. Anatomy, Biomechanics and Physiopathology of glenohumeral
instability. In : The unstable shoulder. Warren RF, Craig EV, Altcheck DW, Ed.
Lippincott-Raven Publishers ; 1999.
13. Perthes G. Uber operationen bei habitualer schulter luxationen. Deutsch Z Chir 1906 ; 85 :
199-207.
14. Bankart A. The pathology and treatment of recurrent dislocation of the shoulder joint. Br J
Surg 1938 ; 26 : 23-29.
15. Rowe C, Sakellarides H. Factors related to recurrences of anterior dislocations of the shoulder.
Clin Orthop 1961 ; 20 : 40-48.
16. Rowe C, Patel D, Southmayd W. The Bankart procedure : a long-term end result study. J Bone
Joint Surg 1978 ; 60A : 1-16.
17. Cooper DE, Arnoczky SP, O’Brien SJ, Warren RF, DiCarlo E, Allen AA. Anatomy, histology,
and vascularity of the glenoid labrum. J Bone Joint Surg (Am) 1992 ; 74A :46-52.
18. Eberly VC, McMahon PJ, Lee QT. Variation in the glenoid origin of the Ighl anterior band :
implications for repair of the Bankart lesion. The Pittsburg Orthopaedic Journal 2000 ;
154-158.
19. Howell SM, Galinat BJ. The glenoid labral socket : a constrained articular surface. Clin Orthop
1989 ; 233 :122-126.
20. Lippitt S, Vanderhooft J, Harris S, et al. Glenohumeral stability frorn concavity compression:
A quantitative analysis. J Shoulder Elbow Surg 1993 ; 2 : 27-35.
21. Lazarus M, Sidles J, Harryman DI, et al. Effect of a chondral-labral defect on glenoid
concavity and glenohumeral stability. J Bone Joint Surg Am 1996 ; 78 : 94-102.
acute, initial anterior dislocation of the shoulder. Am J Sports Med 1994 ; 22 : 589-594.
23. Arciero R, Taylor D, Snyder R, Uhorchak J. Arthroscopic Bioabsorbable Tack Stabilisation of
Initial Anterior Shoulder Dislocations: A Preliminary Report, Arthroscopy 1995 ; 11(4) Aug:
410-417.
24. Baker C, Uribe J, Whitman C. Arthroscopic evaluation of acute initial anterior shoulder
dislocations. Am J Sports Med 1990 ; 18 : 25-28.
25. Taylor D, Arciero R. Pathologic changes associated with shoulder dislocations. Am J Sports
Med 1997 ; 25 : 306-311.
26. Neviaser TJ. The ALPSA lesion, a cause of anterior instability of the shoulder. Arthroscopy
1993 ; 9 : 17-21.
27. Coughlin L, Rubinovich M, Johansson J, et al. Arthroscopic staple capsulorrhaphy for anterior
shoulder instability. Am J Sports Med 1992 ; 20 : 253-256.
28. Molé D, Coudane H. Traitement arthroscopique de l’instabilité antérieure de l’épaule.
Symposium de la Société Française d’Arthroscopie, Nancy 1993. Rev Chir Orthop 1994 ; 80
: 560-5.
29. Speer KP, Deng X, Borrero S et al. Biomechanical Evaluation of a Simulated Bankart Lesion.
J Bone Joint Surg 1994 ; 76-A(12) : 1819-1826.
30. Speer KP, Deng X, Torzilli PA, Altcheck DA, Warren RF. Strategy for an anterior capsular
shift of the shoulder : A Biomechanical Comparison. Am J Sports Med 1995 ; 23 : 264-269.
31. Turkel SJ, Pannios MW, Marshall JL, Girgis FG. Stabilizing mechaniums preventing anterior
dislocation of the glenohumeral joint. J Bone Joint Surg 1981 ; 63A :1208-17.
32. Blasier RB, Guldberg RE, Rothmann ED. Anterior shoulder stability : contribution of rotator
cuff forces and capsular ligaments in a cadaver model. J Shoulder Elbow Surg 1992 ; 1 :140.
33. O’ Brien SJ, Neves MC, Arnoczky SP, Rozbruck SR, DiCarlo EF, et al. The anatomy and
histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med
1990 ; 18 : 449-56.
34. O' Brien S, Schwartz R, Warren R, et al: Capsular restraints to anterior-posterior motion of the
abducted shoulder: A biomechanical study. J Shoulder Elbow Surg 1995 ; 4 : 298-308.
35. Bigliani LU, Pollock RG, Soslowsky LJ, Flatow EL, Pawluk RJ, Mow VC. Tensile properties
of the inferior glenohumeral ligament. J Orthop Res 1992 ; 10 :187-97.
36. Gohlke F, Eulert J. Structure de la capsule de l’articulation glénohumérale : orientation des
faisceaux de fibres collagènes et applications à la biomécanique de l’instabilité. In :
Instabilité chronique de l’Epaule, sous la direction de M. Mansat. Cahier d’Enseignement de
la SOFCOT n° 49. Paris : Elsevier , p. 15-26.
37. Ticker J, Bigliani L, Soslowsky L, et al. Inferior glenohumeral ligament: Geometric and
strain-rate dependent properties. J Shoulder Elbow Surg 1996 ; 5 : 269-279.
38. Rodeo S, Suzuki K, Hannafin J. Analysis of collagen and elastic fibers in shoulder capsule in
patients with shoulder instability. Am J Sports Med 1998 ; 26 : 624-643.
39. Johnson L. Diagnostic and Surgical Arthroscopy of the Shoulder. In : Mosby-Year Book 1993.
St. Louis : Mosby ; 1993. p. 276-364.
40. Symeonides P. The significance of the subscapularis muscle in the pathogenesis of recurrent
anterior dislocation of the shoulder. J Bone Joint Surg Br 1972 ; 54 : 476-483.
41. Bach B, Warren R, Fronek J. Disruption of the lateral capsule of the shoulder: A cause of
recurrent dislocation. J Bone Joint Surg Br 1988 ;70 : 274-276.
42. Wolf E, Cheng J, Dickson K. Humeral avulsion of glenohumeral ligaments as a cause of
anterior shoulder instability. Arthroscopy 1995 ; 11 : 600-607.
avulsion of the gleno humeral ligament. A review of 41 cases. J Bone Joint Surg 1999 ; 81(1)
: 93-96.
44. Field LD, Bokor DJ, Savoie FH. Humeral and glenoid detachmentof the anterior inferior
glenohumeral ligament : a cause of shoulder instability. J Shoulder Elbow Surg 1997 ; 6:1 :
6-10.
45. Oberlander MA, Morgan BE, Visotsky JL. The BHAGL lesion : a new variant of anterior
shoulder instability. Arthroscopy 1996 ; 12:5 : 627-633.
56. Schippinger G, Vasiu PS, Frankhauser F, Clement HG. HAGL lesion occuring after successful
Bankart repair. Arthroscopy 2001 ; 17(2) : 206-208.
47. Warner JJP, Beim G. Combined Bankart and HAGL lesion associated with anterior shoulder
instability. Arthroscopy 1997 ; 13 : 749-752.
48. Cole B, L'Insalata J, Irrgang J, Warner J. Comparison of arthroscopic and open anterior
shoulder stabilisation. J Bone Joint Surg. 2000 ; 82A :1008-1114.
49. Lane J, Sachs R, Riehl B. Arthroscopic staple capsulorrhaphy: A long-term follow-up.
Arthroscopy 1993 ;9 :190-194.
50. Speer KP, Warren RF, Pagnani M, Warner J. An arthroscopic technique for anterior shoulder
stabilisation of the shoulder with a bio-absorbable tack. J Bone Joint Surgery Am 1996 ;
78(12) :1801-1807.
51. Walch G, Boileau P, Levigne C, Mandrino A, Neyret P, Donell S. Arthroscopic stabilisation
for recurrent anterior shoulder dislocation: results of 59 cases. Arthroscopy 1995 ; 11(2)
:173-9.
52. Larrain MV, Botto GJ et al. Arthroscopic Repair of Acute Traumatic Anterior Shoulder
Dislocation in Young Athletes. Arthroscopy 2001 ; 17(4) : 373-377.
53. Salmon J, Bell S. Arthroscopic Stabilisation of the Shoulder for Acute Primary Dislocations
Using a Transglenoid Suture technique. Arthroscopy 1998 ; 14(2) :143-147.
54. Boileau P, Lafosse L. Evaluation arthroscopique et prospective des lésions d’instabilité
antérieure chronique de l’épaule. In : Perspectives en Arthroscopie. SpringerVerlag ; 2002. p.
194-196.
55. Snyder SJ, Karzel RP, Delpizzo W, Ferkel RD, Friedman MJ. SLAP lesions of the shoulder.
Arthroscopy 1990 ; 6 : 274.
56. Pagnani M, Xiang-Hua D, Warren R, et al. Effect of lesions of the superior portion of the
glenoid labrum on glenohumeral translation. J Bone Joint Surg Am 1995 ; 77 : 1003-1010.
57. Rodowsky MW, Harner CD, Fu FH. The role of the long head of the biceps muscle and
superior glenoid labrum in anterior stability of the shoulder. Am J Sports Med 1994 ; 22 :
121-130.
58. Maffet MW, Garstman GM. Moseley B. Superior labrum-biceps tendon complex lesions of
the shoulder. Am J Sports Med 1995 ; 23 : 93-98.
59. Cole B, Rodeo S, O’Brien S, et al. The anatomy and histology of the rotator interval of the
capsule. Clin Orthop 2001 ; 390 : 129-137.
60. Field LD, Warren RF, OBrien. SJ et al. Isolated closure of rotator interval defects for shoulder
instability. Am J Sports Med 1995 ; 23 : 557-563.
61. Harryman DT, Sidles JA, Harris SL, et al. The role of the rotator interval capsule in passive
motion and stability of the shoulder. J Bone Joint Surg Am 1992 ; 74 : 53-66.
62. Nobuhara K, Ikeda H. Rotator interval lesion. Clin Orthop 1987 ; 223 : 44-50.
63. Ikeda H. Rotator interval lesion: Clinical study. J Jpn Orthop Assoc 1986 ; 60 :1261-1274.
64. Gartsman G, Taverna E, Hammerman S. Arthroscopic rotator interval repair in glenohumeral
instability: Description of an operative approach. Arthroscopy 1999 ; 15 : 330-332.
65. Gartsman G, Roddey T, Hammerman S. Arthroscopic treatment of anterior-inferior
glenohumeral instability. J Bone Joint Surgery 2000 ; 82A (7) : 991-1003.
66. Wolf E, Eakin CL. Arthroscopic Plication for posterior shoulder instability. Arthroscopy 1998
; 14(2) :153-163.
67. Malgaigne JF. Traité des fractures et des luxations. Paris :JB Baillière, 1855.
68. Hill SA, Sachs MD. The grooved defect of the humeral head : a frequently unrecognized
complication of dislocation of the shoulder. Radiology 1940 ; 35 : 690-700.
69. Calandra JJ, Baker CL, Uribe J. The incidence of Hill-Sachs lesions in initial anterior shoulder
dislocations. Arthroscopy 1989 ; 5 : 254-7.
70. Pavlov H, Warren R, Weiss C, et al. The roentgenographic evaluation of certain surgical
conditions. Clin Orthop 1985 ; 184 : 317-321.
71. Burkhart SS, Danaceau M. Articular arc length mismatch as a cause of failed Bankarrt repair.
Arthroscopy 2000 ; 16 : 7 : 740-744.
72. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to
failure of arthroscopic Bankart repairs : Significance of the inverted-pear glenoid and the
engaging Hill-Sachs lesion. Arthroscopy 2000 ; 16 : 7 : 677-694
73. Rowe C, Zarins B, Ciullo J: Recurrent anterior dislocation of the shoulder after surgical repair.
J. Bone Joint Surg 1984 ; 66A : 159-168.
74. Gerber C, Lambert S. Allograft reconstruction of segmental defects of the humeral head for the
treatment of chronic locked posterior dislocation of the shoulder. J Bone joint Surg 1996 ;
78A : 376-382
75. Walch G. La luxation récidivante antérieure de l’épaule. Table Ronde. Journées de printemps
de la SOFCOT, 1990 Estoril. Rev Chir Orthop 1991 ; 77:Suppl 1 : 77-148.
76. Sugaya H, Moriishi J, Dohi M et al. Glenoid rim morphology in recurrent anterior
glenohumeral instability. JBJS 2003;85-A(5):878-84.
77. Resch H, Povacz P, Wambacher M, et al. Arthroscopic extra-articular Bankart repair for the
treatment of recurrent anterior shoulder dislocation. Arthroscopy 1997 ; 13 :188-200.
78. Neviaser RJ, Neviaser TJ, Neviaser JS. Concurrent rupture of the rotator cuff and anterior
dislocation of the shoulder in the older patient. J Bone Joint Surg 1988 ; 70A : 1308.
79. Torchia M, Caspari R, Asselmeier M, Beach W, Gayari M. Arthroscopic transglenoid multiple
susutre repair: 2 to 8 year results in 150 shoulders. Arthroscopy 1997 ; 13(5) : 609-619.
80. Bigliani L, Kurzweil P, Schwartzbach C, et al. Inferior capsular shift procedure for
anterior-inferior shoulder instability in athletes. Am J Sports Med 1994 ; 22 : 578-584.
81. Gill TJ, Micheli LJ, Gebhard F et col. Bankart repair for anterior instabilty of the shoulder.
Long term outcome. J Bone Joint Surg 1997 ; 79A(6) : 850-857.
82. Wirth M, Blatter G, Rockwood C. The capsular imbrication procedure for recurrent anterior
instability of the shoulder. J Bone Joint Surg Am 1996 ; 78 : 246-259.
83. Chapnikoff D, Besson A, Chantelot C, et al. Operation de Bankart. Etude clinique et
radiographique a dix ans de recul minimum. RCO 2000;86: 558-65.
84. Gross R. Arthroscopic shoulder capsulorrhaphy: Does it work? Am J Sports Med 1989 ; 17 :
495-500.
85. Hawkins R. Arthroscopic stapling repair for shoulder instability: A retrospective study of 50
cases. Arthroscopy 1989 ; 5 :122-128.
86. Mathews L, Vetter W, Oweida S, et al. Arthroscopic staple capsulorrhaphy for recurrent
anterior shoulder instability. Arthroscopy 1988 ; 4 : 106-111.
87. O’Driscoll SW, Evans DC. Long-term results of staple capsulorraphy for anterior instability of
the shoulder. J Bone Joint Surg. 1993 ; 75A : 249-258.
88. Detrisac DA. Athroscopic shoulder staple capsulorrhaphy for traumatic anterior instability. In :
McGinty JB et al, Ed. Operative arthroscopy. New York :Raven Press ; 1991. p. 517-28.
89. Nérisson D, Kempf JF, Bonnomet F, Gastaud F. Traitement atrthroscopique de l’instabilité
antérieure chronique de l’épaule par capsulorrhaphie avec agrafage. Rev Chir Orthop 1996 ;
82: 275-287.
90. Wiley A. Arthroscopy for shoulder instability and a technique for arthroscopic repair.
Arthroscopy 1988 ; 4 : 25-30.
91. Kempf JF. Arthroscopie de l’Epaule. Cahiers d’Enseignement de la SOFCOT. Conférences
d’Enseignement 1994. Paris : Elsevier ; p. 105-119.
92. Zuckermann JD, Matsen FA. Complications about the glenohumeral joint related to the use of
screws and staples. J Bone Joint Surg 1984 ; 66A :175-80.
93. Morgan C, Bodenstab A. Arthroscopic Bankart suture repair: Technique and early results.
Arthroscopy 1987 ; 3 :111-122.
94. Morgan C . Arthroscopic transglenoid Bankart suture repair. Op Tech Orthop 1991 ;1 :
171-179.
95. Caspari R. Arthroscopic reconstruction for anterior shoulder instability. Tech Orthop 1988 ; 3 :
59-66.
96. Caspari R, Savoie F. Arthroscopic reconstruction of the shoulder: The Bankart repair. In : J
McGinty, Ed. Operative Arthroscopy. New York : Raven Press ; 1991. p. 507-516.
97. Boileau P, Walch G. Traitement arthroscopique de l’instabilité antérieure de l’épaule : à
propos d’une série de 93 cas opérés selon la technique de Morgan In : Instabilité chronique
de l’Epaule, sous la direction de M. Mansat. Cahier d’Enseignement de la SOFCOT n° 49,
1994 ; p. 57-64
98. Hayashida K, Yoneda M, Nakagawa S, Okamura K, Fukushima S. Arthroscopic Bankart
suture repair for traumatic anterior shoulder instability : analysis of the causes of a recurrence
Arthroscopy 1998 ; 14(3) : 295-301.
99. Warner JJP, Warren R. Arthroscopic Bankart repair using a cannulated absorbable fixation
device. Operative Techniques in Orthopaedics 1991 ; 1 :192-198.
100. Warner JJP, Miller M, Marks P, et al. Arthroscopic Bankart repair with the Suretac device.
Arthroscopy 1995 ; 1 : 2-13.
101. Barber F, Herbert M. The ultimate strength of Sutures anchors. Arthroscopy 1999 ; 11 :1 :
21-28.
102. Cole B, Warner J. Arthroscopic versus open Bankart repair for traumatic anterior shoulder
Instability. In :Clinics in Sports Medicine, Warner J JP Ed. 2000 : 19-48.
103. Karlsson J, Kartus J, Ejerhed L, Gunnarsson AC, Lundin O, Sward L. Bioabsorbable tacks
for arthroscopic treatment of recurrent anterior shoulder dislocation. Scand J Med Sci Sports
1998 ; 8(6) : 411-5.
104. Edwards D, Howy G, Saies A et al. Adverse reactions to an absorbable shoulder fixation
device. J Shoulder Elbow Surg 1994 ; 3 : 230-233.
105. Fealy S, Drakos M, Answorth A, Warren R. Arthroscopic Bankart repair: experience with an
absorbable, transfixing implant. Clin Orthop 2001 ; 390 : 31-41.
106. Wolf E. Arthroscopic capsulolabral repair using suture anchors. Orthop Clin North Am 1993
; 24 : 59-69.
107. Belzer J, Snyder J. Arthroscopic capsulorrhaphy for traumatic anterior shoulder instability
using suture anchors and nonabsorbable suture. Arthroscopy 1995;11:359.
108. Snyder S, Strafford B. Arthroscopic management of instability of the shoulder. Orthopedics
1993 ; 16 : 993.
109. McEleney ET, Donavan MJ, Shea KP, Nowak MD. Initial failure strength of open and
arthroscopic Bankart repairs. Athroscopy 1995 ;11 : 426-31.
110. Noojin F, Savoie F, Field L. Arthroscopic Bankart repair using long term absorbable anchors
and sutures. Techn in Shoulder and Elbow Surg 2000 ; 1(4) : 262 - 267.
111. Barber F, Click S, Weidmeman C. Arthroscopic or open Bankart procedures: What are the
costs? Arthroscopy 1998 ; 14 : 671-674.
112. Kim SH, Ha KI, Cho YB, et al. Arthroscopic anterior stabilization of the shoulder : two to
six-year follow-up. JBJS 2003; 85-A (8):1511-18.
113. Boileau P, Lafosse L. Traitement arthroscopique de l’instabilite antérieure de l’épaule :
résultats d’une étude multicentrique, rétrospective de la Société Française d’arthroscopie. In :
Perspectives en Arthroscopie. Springer Verlag ; 2002. p. 180-183.
114. Cole B, Romeo A: Arthroscopic shoulder stabilisation with suture anchors: technique,
technology, and pitfalls. Clin Orthop 2001 ; 390 : 17-31.
115. Ekelund A. Cartilage injuries in the shoulder joint caused by migration of suture anchors or
mini screw. J Shoulder Elbow Surg 1998 ;7 : 537-539.
116. Kaar TK, Schenk RC, Wirth MA, Rockwood CA. Complications of metallic suture anchors
in shoulder surgery : a report of 8 cases. Arhroscopy 2001 ; 17 :1 : 31-37.
117. Levine W, Richmond J, Danaldson W. Use of the suture anchor in open Bankart
reconstruction: A follow-up report. Am J Sports Med 1994 ; 22 : 723-726.
118. Silver MD, Daigneault JP. Symptomatic intra-articular migration of glenoid sutures anchors.
Arthroscopy 2000 ; 16(1) : 102-105.
119. Ticker J, Lippe R, Barkin D, et al. Infected suture anchors in the shoulder. Arthroscopy 1996
; 12 : 613-615.
120. Green M, Christensen K. Arthroscopic versus open Bankart procedures: A comparison of
early morbidity and complications. Arthroscopy 1993 ; 9 : 371-374.
121. Kailes SB, Richmond JC. Arthroscopic vs. open Bankart reconstruction: a comparison using
expected value decision analysis. Knee Surg Sports Traumatol Arthrosc 2001 ; 9 : 379-385.
122. Karlsson J, Magnusson L, Ejerhed L, Hultenheim I, Lundin O, Kartus J. Comparison of Open
and Arthroscopic Stabilisation for Recurrent Shoulder Dislocation in Patients with a Bankart
Lesion. Am J Sports Med 2001 ; (29)5 : 538-542.
123. Kartus J, Ejerhed L, Funck E, Kohler K, Sernert N, Karlsson J. Arthroscopic and open
shoulder stabilisation using absorbable implants. A clinical and radiographic comparison of
two methods. Knee Surg Sports Traumatol Arthrosc 1998 ; 6(3) :181-8.
124. Sperber A, Hamberg P, Karlsson J, Swärd L, Wredmark T. Comparison of an arthroscopic
and an open procedure for postraumatic instabilityof the shoulder : A prospective
randomized multicenter study. J Shoulder Elbow Surg 2001 ; 10(2) : 105-1068.
125. Kim SH, Ha KI, Kim SH. Bankart repair in traumatic anterior shoulder instability: open
versus arthroscopic technique. Arthroscopy 2002; 18(7): 755-63.
126. Wheeler J, Ryan J, Arciero R, et al. Arthroscopic versus nonoperative treatment of acute
shoulder dislocation. Arthroscopy 1989 ; 5 : 213-217.
127. Hovelius L, Augustini G, Fredin O, Johansen O, Norlin R, Thorling J. Primary anterior
dislocation of the shoulder in young patients : A ten years prospective study. J Bone Joint
Surg 1996 ; 78A :78 :11 : 1677-1684.
128. Hovelius L. Anterior dislocation of the shoulder in teenagers and young adults. J Bone Joint
Surg 1987 ; 69A:3 : 393-399.
129. Arciero R. Acute arthroscopic Bankart repair? Letter to the Editor of Knee Surg Sports
Trauma Arthrosc 2000 ; 8 :127-128.
130. Aronen JG, Regan K. Decreasng the incidence of recurrence of first time anterior shoulder
dislocations with rehabilitation. Am J Sports Med 1984 ; 12 : 4 : 283-291.
131. Hattrup SJ, Cofield RH, Weaver AL. Anterior shoulder reconstruction: Prognostic variables.
J. Shoulder Elbow Surg. 2001 ; 10(6) : 508-513.
132. Kirkley A, Werstin R, Ratjek A Griffin S. Prospective randomized clinical trial comparing
the effectivness of immmediate arthroscopic stabilzationversus immobilization and
rehabilitation in first anterior dislocation of the shoulder : Evaluation of longterm qualitry of
life. Arthroscopy 2002 (in press)
133. Yoneda M, Welsh RP, Macintosh DL. Conservative treatment of shoulder dislocations in
young males. J Bone Joint Surg 1982 ; 64B : 245-255.
134. Kirkley A, Griffin S, Richards C et al. Prospective randomized clinical trial comparing the
effectivness of immmediate arthroscopic stabilzation versus immobilization and
rehabilitation in first anterior dislocation of the shoulder. Arthroscopy 1999 ; 15 : 507-514.
135. Uribe JW, Hechtman KS. Arthroscopically assisted repair of acute Bankart lesion.
Orthopedics 1993 ; 16(9) : 1019-1023
136. Wintzell G, Hovelius L et al. Arthroscopic lavage speeds reduction in effusion in the
glenohumeral joint after primary anterior shoulder dislocation: a controlled randomized
ultrasound study. Knee Surg Sports Traum Arthrosc 2000 ; 8 : 56-60.
138. Savoie F, Miller C, Field L. Arthroscopic reconstruction of traumatic anterior instability of
the shoulder: The Caspari technique. Arthroscopy 1997 ; 13 : 201-209.
139. Lafosse L, Iserin A, Kempf JF, Hardy Ph. Traitement arthroscopique de l’instabilité antérieur
chronique de l’épaule. Instabilité antérieure chronique de l’épaule chez l’adulte. Symposium
de la SOFCOT, Paris Nov 1999. Rev Chir Orthop 2000 ; Suppl. I :86 : 106-109.
137. Bacilla P, Field LD, Savoie FH, 3rd. Arthroscopic Bankart repair in a high demand patient
population. Arthroscopy 1997 ; 13(1) : 51-60.
140. Kandziora F, Jäger A, Bischof F et al. Arthroscopic Labrum Refixation for Post-traumatic
Anterior Shoulder Instability: Suture Anchor Versus Transglenoid Fixation Technique.
Arthroscopy 2000 ; 16(4) : 359-66.
141. Uhthoff HK, Piscopo M. Anterior redundancy of the shoulder : congenital or traumatic. J
Bone Joint Surg 1985 ; 363-366.
142. Kempf JF, Lacaze F, Hila A. Instabilité antérieur et hyperlaxité de l’épaule. Instabilité
antérieure chronique de l’épaule chez l’adulte. Symposium de la SOFCOT, Paris Nov 1999.
Rev Chir Orthop 2000 ; Suppl. I :86 : 132-137.
143. Simonet W, Cofield R. Prognosis in anterior shoulder dislocation. Am J of Sports Med 1984 ;
12(1) :19-23.
144. Lafosse L. Traitement arthroscopique de l’instabilité antérieure In : Perspectives en
Arthroscopie. Springer Verlag ; 2002 p. 194-196.
145. Roberts S, Taylor D, Brown J, Hayes M, Saies A. Open and Arthroscopic Techniques for the
Treatment of Traumatic Anterior Shoulder Instability in Australian Rules Football Players. J
Shoulder Elbow Surg 1999 ; 8(5) : 403-409.
146. Manta J, Organ S, Nirschl R, et al. Arthroscopic transglenoid suture capsulolabral repair. Am
J Sports Med 1997 ; 25 : 614-618.
147. Pagnani M, Warren R, Altcheck D, Wieckiewicz T, Anderson A. Arthroscopic shoulder
stabilisation using transglenoid suture. Am J Sports Medicine 1996 ; 24(4) : 459-467.
148. Weber SC. Arthroscopic suture anchor repair versus open Bankart repair in the management
of traumatic anterior glenohumeral instability. Arthroscopy 1996 ; 12 : 382.
149. Matsen F, Lippitt S, Iserin A. Mécanisme patho-anatomique de l’instabilité gléno-humérale.
In : Instabilité chronique de l’Epaule, sous la direction de M. Mansat. Cahier d’Enseignement
de la SOFCOT n° 49. Paris : Elsevier ; p. 7-14.
150. Mologne TS, McBride MT, Morin WD et al. Arthroscopic anterior labral reconstruction
using a transglenoid suture technique. Am J Sports Med 1996 ; 24 : 268-274.
151. Mologne TS, McBride MT, Lapoint JM. Assessment of failed Arthroscopic anterior labral
repair : Findings at open surgery. Am J Sports Med 1997 ; 25:6 : 813-817.
152. Boileau P. Epaules douloureuses pures par accidents d’instabilité inapparents. Instabilité
antérieure chronique de l’épaule chez l’adulte. Symposium de la SOFCOT, Paris Nov 1999.
Rev Chir Orthop 2000 ; Suppl. I 86 : 122-125.
153. Green MR, Christensen KP. Arthroscopic Bankart procedure : two- to five-year follow-up
with clinical correlation to severity of glenoid labral lesion. Am J Sports Med 1995 ; 23(3) :
276-81.
154. Koss S, Richmond J, Woodward J. Two to Five-year follow-up of arthroscopic Bankart
reconstruction using a suture anchor technique. Am J Sports Medicine 1997 ; 25(6) :
809-812.
155. Hoffmann F, Reif G. Arthroscopic shoulder stabilisation using Mitek anchors. Knee Surg
Sports Traumatol Arthrosc 1995 ; 3(1) : 50-4.
156. 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 ; 12 :144-149.
157. O’Driscoll SW, Evans DC. Controlalateral shoulder instability following anterior repair : An
epidemiological study. J Bone Joint Surg Br 1991 ; 73 : 941-946.
158. Goldberg B, Nirschl R, McConnell J, et al. Arthroscopic transglenoid suture capsulolabral
repairs: Preliminary results. Am J Sports Med 1993 ; 21 : 656-665.
159. Grana WA, Buckley PD, Yates CK. Arthroscopic Bankart suture repair. Am J Sports Med
1993 ; 21(3) : 348-53.
160. McMahon PJ, Dettling, J, Sandusky MD, Tibone JE, Lee TQ. The anterior band of the
inferior glenohumeral ligament. Assessment of its permanent deformation an
