The shoulder is a common site of injury in athletes who compete in contact sports and sports that require repetitive overhead motions. For example, collision athletes are prone to sudden macrotrauma to the stabilizing static and dynamic elements of the shoulder. This chapter provides a comprehensive overview of the pathophysiology, evaluation, and management of shoulder injuries specific to nonthrowing overhead and contact athletes.
Nonthrowing overhead athletes
The tennis serve has been likened to an overhead pitch, with similar biomechanical forces responsible for injury. As in throwing, the shoulder is driven through a highly dynamic arc of motion, often exceeding the biomechanical constraints of the joint. Within this context, the shoulder has to maintain a balance between flexibility and instability. As with pitching, optimal kinetic chain energy transfer, proper scapular movement, and rotator cuff function are prerequisites to mitigating shoulder injury. However, there are several key differences. In the tennis serve, the racquet provides an added source of kinetic energy in addition to the human kinetic chain to generate ball velocity. Instead of releasing the ball as in the pitching motion, the tennis player repetitively strikes the ball in a fashion that makes the shoulder susceptible to overuse injury. Tennis players typically have stronger internal rotator muscles than the external rotator muscles, and this imbalance can predispose to injury during arm deceleration. Furthermore, in contrast to the pitch, the forceful ball strike creates a sudden impact that the joint must absorb.
The tennis serve has five distinct phases ( Fig. 8.1 ), similar to the baseball pitch: wind-up (the knees are flexed and the trunk is rotated), early cocking, late cocking (where the shoulder is maximally abducted and externally rotated), acceleration, and follow-through.
The demands on the shoulders of competitive swimmers are immense, and the number of strokes exceeds 500,000 per arm per year. Here, the issue is not impact or extreme shoulder positions, but rather the high number of repetitions that exceeds that of any other sport. The freestyle swimming stroke has been subdivided into five distinct phases: hand entry, catch, in-sweep, finish, and recovery ( Fig. 8.2 ). Swimming strokes repetitively place the shoulder in the impingement position described by Neer and Welsh. Consequently, shoulder pain and dysfunction in swimmers have traditionally been equated with subacromial impingement and rotator cuff tendinitis. However, swimmer’s shoulder, unlike classic impingement, is caused by overuse and poor mechanics and treatment should focus on proper technique and inserting rest days in the training schedule.
Biomechanical analyses of shoulder function have found that swimmers suffer from a variety of problems common to all overhead athletes. Impressive shoulder laxity is observed in swimmers, placing them in the spectrum of multidirectional instability; this is a consequence of tremendous forces on soft tissue stabilizers and extreme motion requirements, combined with swimmers’ propensity for baseline ligamentous laxity. Associated muscle imbalances therefore can contribute to pathologic instability processes in these shoulders. As in throwing, the swimmer’s shoulder must maintain the narrow margin between having enough flexibility to generate body propulsion and developing pathologic instability. Proper strength and coordination of the dynamic scapular stabilizers (the levator scapulae, rhomboids, and trapezius) and glenohumeral stabilizers (the rotator cuff) are critical in preventing symptomatic instability.
Phases of freestyle swimming
In the initial catch, the swimmer’s hand enters the water with the shoulder in internal rotation. Swimmers are trained to completely elevate the shoulder at this time while flexing the elbow to catch the water. The hand then extends under the water as the palm turns to face down. The lift provided by the water upon hand entry generates a large force on the glenohumeral joint, particularly when the swimmer’s arm nears full extension. This force forward elevates the shoulder, placing it in the classic impingement position.
Yanai and Hay have recommended four changes in the technique to reduce impingement during this phase. The first three—streamlining hand entry, strengthening muscles that resist forcible elevation (the latissimus dorsi, pectoralis major, teres major, and biceps brachii), and bending the elbow to decrease moment arm length—all reduce the forcible moment arm. The fourth involves externally rotating the scapula on hand entry to reduce the angle subtended by the axis of the humerus and the superior border of scapula, lessening subacromial impingement. ,
The hand entry foreshadows the next phase of the stroke, called the catch. As soon as maximal arm extension in the water is reached, the pulling arm begins an S-shaped pull, which coincides with the opposite hand’s emergence from the water. The elbow flexes as the hand begins to pull the body over itself, generating the highly propulsive phase of the stroke. As the hand continues to push back, it moves in a downward and outward direction. At the mid pull-through point, the humerus is aligned perpendicular to the swimmer’s torso, with the hand still cranial to the shoulder.
During the catch phase, the shoulder is adducted and internally rotated. A common technical error during this phase is the dropped elbow. Counsilman demonstrated that the dropped-elbow stroke combines external rotation and adduction at the shoulder, whereas the correct, high-elbow technique combines internal rotation with abduction. Richardson found that the increased glenohumeral external rotation placed the muscles of propulsion (the latissimus dorsi and triceps) at a mechanical disadvantage.
The correct high-elbow technique provides a mechanical advantage, but it also increases the percentage of the stroke during which the shoulder is left in the impingement position. Swimmers might adopt the faulty dropped-elbow technique at the onset of incipient impingement in an attempt to curtail pain during the stroke (or secondary to fatigue). Accordingly, biomechanical studies have measured decreased activity in the anterior and middle deltoids when the elbow is dropped, suggesting that the faulty technique uses less energy.
As the hand reaches the deepest point, the downward motion shifts to an upward, inward, and backward motion, and the hand pushes toward the midline of the body and toward the swimmer’s chest. Problems in this phase relate to the stabilizing periscapular muscles, particularly the serratus anterior in the overhead motion. In the swimmer with a painful shoulder, the serratus anterior muscle activity drops considerably. This is likely to be secondary to fatigue due to constant splinting of the painful shoulder. The rhomboids attempt to stabilize the scapula, but because they are antagonists of the serratus anterior, normal synchronous scapular rotation is disrupted.
The finish is the culmination of the S-shaped pull. The hand turns outward and backward as it is pushed from underneath the body. The humerus must internally rotate significantly to help the hand move in this direction. The hand then flexes upward toward the water surface while still moving backward. The phase ends as the hand breaks the surface of the water. During the finish, the swimmer with impingement might excessively roll the body in an attempt to reduce the amount of internal rotation (painful in impingement) the shoulder has to produce to have the hand exit the water. This is manifested by a noticeably early hand exit.
The recovery phase begins with the hand exiting the water. As the hand exits the water, the shoulder abducts and externally rotates as it is brought forward for the next arm entry. Shoulder impingement occurs during a large part of this phase, particularly if the shoulder is kept internally rotated. Codman first described the prerequisite of externally rotating the shoulder to achieve full abduction. Otherwise, the greater tuberosity comes in contact with the acromion at approximately 90 degrees of abduction. Externally rotating as early as possible in the recovery phase reduces the amount of time that the shoulder spends in an impingement position. ,
Instability in swimmers
The biomechanics of swimming favors swimmers with higher degrees of shoulder laxity. As a result of this self-selection, elite swimmers tend to be hyperlax at baseline and are more at risk for related shoulder pathology. Fine-wire electromyography (EMG) studies have demonstrated that swimming strokes require the shoulder adductors and internal rotators to produce the majority of the propulsive force, and they minimally tax the external rotators. Therefore, like throwers, swimmers and water polo players significantly increase their internal rotator and adductor/external rotator and abductor strength ratio. , A normal shoulder might be able to compensate for these muscle imbalances, whereas a shoulder with excessive laxity might not. As a result the glenohumeral joint can have subluxation episodes, leading to other painful chronic injuries, such as labral tears, subacromial impingement, and bicipital tendinitis. ,
During the swimming stroke, the force applied to the hand by the water results in an anteriorly directed vector thrust at the shoulder. In a lax shoulder, this force can shift the humeral head excessively, injuring the labrum or the joint surface itself. The external rotators attempt to restrain the humeral head from anterior translation, becoming fatigued and prone to develop tendinitis. Some authors have cited overworked external rotators as a cause of the posterior shoulder pain commonly seen in swimmers with anterior instability. The mainstay of treatment is a rehabilitation program aimed at maintaining normal rotator cuff strength ratios and periscapular muscle strengthening; this has been effective in ameliorating pain and dysfunction. Open and arthroscopic surgical stabilization treatments for elite swimmers with symptomatic instability have not been as successful as for other athletes, with only an estimated 20% returning to their preinjury level of performance.
Swimmer adaptations to this provocative shoulder arc of motion can affect pathology and convalescence. For example, unilateral breathing increases impingement on the shoulder ipsilateral to the breathing side. Having the swimmer switch to bilateral breathing can reduce the risk of developing clinical symptoms. Maintaining a high elbow on recovery, avoiding an extended position of the arm before entry, and increasing body roll all reduce the percentage of the stroke that the shoulder is in the impingement position. Other conservative measures, such as rest (during which a kickboard can be used), ice, nonsteroidal antiinflammatory drugs, and a structured rehabilitation program, usually yield successful results. Supraspinatus tendinopathy induced by high-volume swimming should also be considered as a source of shoulder pain as its incidence in elite swimmers has been underestimated. Refractory cases might respond to subacromial decompression, although this is not conducted routinely. ,
Chronic shoulder overuse injuries can affect golfers, especially because elite-level and some recreational players perform up to 2000 swings per week. Ninety percent of shoulder problems in golfers involve the lead arm (the left arm in a right-handed golfer). , During the swing, there is a sudden deceleration of the arm as the club strikes the ball or the ground which places increased stress on the external rotator of the lead arm.
The golf swing is divided into five phases ( Fig. 8.3 ): the takeaway (from address until the club is horizontal), the backswing (from horizontal to the top of the backswing), the downswing (from the top of the backswing until the club is horizontal), acceleration (from horizontal club to impact), and follow-through (from ball contact until the end of the swing).
Each phase of the golf swing can cause specific pathology. During the backswing, the lead shoulder moves into internal rotation, forward flexion, and cross-body adduction. This position can cause subacromial impingement and acromioclavicular joint pathology. Posterior pain during the top of the backswing, with the arm fully adducted across the body, can indicate posterior glenohumeral instability. Symptoms during the follow-through, with the lead shoulder abducted and externally rotated, are consistent with anterior instability or biceps tendinitis.
Repetitive swinging of the golf club can eventually overwhelm normal shoulder restraints, especially when performed incorrectly or erratically. Fine-wire EMG studies have demonstrated that, whereas professional golfers consistently activate the same sequence of muscles with every swing, recreational golfers tend to produce different muscle-activation patterns and do not duplicate their swing with each shot. , Similarly, higher handicap players typically experience injuries that result from improper swing mechanics, whereas lower handicap and professional players are susceptible to overuse injuries. The following section presents the most typical golf injuries that affect the shoulder.
Subacromial bursitis and rotator cuff injury
The golfer’s lead shoulder is placed in extremes of shoulder motion: the top of the backswing and the end of the follow-through. Furthermore, a patient with preexisting rotator cuff disease may have a weak takeaway, which can exacerbate poor swing mechanics and worsen impingement. During the backswing, the lead shoulder can be subjected to subacromial impingement, acromioclavicular compression, and, less commonly, coracoid impingement. This can lead to bursitis and injury to the rotator cuff. During the downswing, impact, and follow-through, the trailing shoulder is subject to stress on the superior labrum, coracoid impingement, and humeral head chondral injury.
Several reports have examined impingement in golfers. Studies have found that 26% to 93% of patients with golf-related shoulder symptoms have rotator cuff or subacromial disease. Golfers may be more amenable to successful surgical treatment compared with other overhead athletes, such as throwers, because of the relatively lighter demands placed on their shoulders. Vives and colleagues found that of 29 recreational golfers with subacromial disease and rotator cuff tears, acromioplasty and mini-open repair returned all but three to playing with their previous handicaps and driving distances within 3 years. A case report has described successful arthroscopic subacromial decompression for impingement in a professional golfer that allowed him to return to competitive play. However, the mainstay of treatment in cases of bursitis and rotator cuff disease in a golfer is a focus on proper technique and adequate rest. Surgical management should be reserved for cases that are refractory to conservative measures.
Acromioclavicular joint disease
Acromioclavicular joint disease is also prevalent in golfers. Those who complain of symptoms often cite the top of the backswing as problematic, when the lead arm assumes a cross-body adduction position and compresses the acromioclavicular joint. In a study of 35 elite golfers, of whom approximately half had acromioclavicular joint arthritis, all but one returned to competitive play after treatment. Treatment consisted of physical therapy, swing modification, or, in refractory cases, distal clavicle excision.
Golfers can be susceptible to glenohumeral instability, especially because generating a powerful swing requires maximizing the shoulder turn relative to the hip turn. Posterior instability has been described as occurring in up to 12% of golfers with shoulder pain. Some authors have hypothesized that, in patients with posterior instability, the subscapularis is relatively stronger than the rest of the rotator cuff, rendering the glenohumeral joint susceptible to posterior forces, which are exacerbated by fatigue to the serratus anterior. Symptoms of pain and instability appear in the lead arm at the top of the backswing when it is placed in maximal adduction.
Physical examination findings in these patients demonstrate posterior instability on load and shift and posterior apprehension with loading in internal rotation and adduction. Small case series have described the successful treatment of posterior instability with therapy, posterior capsulorrhaphy, and subacromial decompression, if indicated. A posterior labral (reverse Bankart) lesion has been successfully treated with arthroscopic repair. Although the patient did not demonstrate signs of posterior instability, he did report pain on posterior load and shift and posterior apprehension tests. Golfers may also experience anterior instability, particularly with the lead arm in the follow-through phase of the swing, when it is in maximal abduction and external rotation. This is often successfully treated in golfers with physical therapy consisting of rotator cuff and scapular stabilizer strengthening, , with surgical treatment reserved for refractory cases.
Superior labrum and biceps disease
Superior labrum anterior and posterior (SLAP) lesions and biceps tendon disorders in golfers are infrequently reported in the literature. Patients with SLAP tears complain of pain in the lead shoulder at the end of the backswing or beginning of the downswing when the shoulder is loaded and the arm is adducted across the body. Occasionally, the golfer complains of mechanical symptoms, such as clicking or catching. Isolated biceps tendinitis causes anterior shoulder pain during the end of follow-through when the lead arm shoulder is extended, maximally abducted, and externally rotated.
Initial treatment with rest, physical therapy, and antiinflammatories is usually successful. Persistent symptoms can be addressed arthroscopically with SLAP repair or debridement as needed. Reports of treatment for SLAP tears or biceps lesions in golfers remain limited and the outcomes largely unknown. Older patients with SLAP lesions may be best treated with biceps tenodesis.
Up to 25% of golfers in the United States are 65 years or older, and thus glenohumeral arthritis is a common condition in the golfer population. Total shoulder arthroplasty has been successful in returning golfers to their sport. One study found that 23 of 24 patients were able to resume playing golf at an average of 4.5 months after surgery, the majority actually improving their scores at an average of 53 months of follow-up, without component loosening. These findings have been reproduced in the literature with return to play rates ranging from 77% to 100%, with modest improvements in both handicap and driving distance.
A typical postoperative rehabilitation program is as follows: putting may be started 6 to 8 weeks after surgery, with light chipping and pitching drills allowed at 10 to 12 weeks. At 3 months, once the subscapularis is well-healed, midiron shots may be incorporated. Long irons and woods may be used at 4 months, and a full round of golf may be played at 5 to 6 months, barring any symptoms at any point during the rehabilitation.
Evaluation of the athlete
The evaluation of an athlete requires the close integration of the history and physical examination findings. Many of the traditional examination tests of the shoulder have not been validated or critically evaluated to a significant extent and should therefore be used only as an adjunct to a wider global assessment. In addition, the precise pathophysiology of many shoulder conditions remains unknown, leaving the interpretation of some examination maneuvers uncertain.
A sport-specific approach should be used when evaluating the shoulder in an athlete. The history should include the mechanism, location of pain, any recent changes in training, associated symptoms, prior injuries, and if they have had any treatment. Furthermore, the onset and duration of the symptoms should be noted. It can be helpful to observe the athlete in a situation specific to their sport, but often this is not practical for the clinician. Alternatively, coaches and athletic trainers can provide invaluable insight into the athlete’s practice or performance-related complaints. For example, swimmers will often complain of pain during the catch or the recovery, when the shoulder is more often in the provocative impingement position. In swimmers, instability is often the principal culprit, exacerbating symptoms of bursitis.
Athletes can present with symptoms of gross instability. As traumatic and atraumatic instability are treated differently, determining the onset of the symptoms is critical. For example, an athlete who plays a contact or collision sport might report a specific incident (e.g., a dislocation) that initiated the symptoms. The history often suggests the direction of instability. For instance, symptoms elicited with the arm in adduction and internal rotation may suggest posterior instability, whereas symptoms reproduced by holding objects with the arms at the sides often indicate inferior instability and symptoms with the arm in abduction and external rotation suggest anterior instability. The location of pain or instability, its duration, and response to prior treatment should be noted for all athletes.
The physical examination mirrors that of the one described in the previous chapter, which consists of visual inspection, range-of-motion (ROM) testing, palpation, strength testing, and provocative maneuvers related to the shoulder. It is often useful to ask the athlete to demonstrate the positions in which symptoms arise.
Anterior shoulder instability in athletes
Anterior shoulder dislocations are common among contact athletes. Hovelius reported that 40% of dislocations occurred in patients 22 years of age or younger. Baker and colleagues noted that 75% of all shoulder dislocations occur in the position of external rotation and abduction during athletic activities. The pathoanatomy resulting from traumatic anterior instability varies. Rowe and colleagues found the anterior labral tears, as described by Bankart, were the essential lesion of instability in 70% of cases of traumatic instability that required surgery. Superior labral lesions have also been associated with anterior instability as well as plastic deformation of the inferior glenohumeral ligament complex. Bigliani and colleagues showed that an intrasubstance ligament injury occurs before labral avulsion. In addition, bony lesions caused by a compression fracture at the posterolateral margin of the humeral head, termed the Hill-Sachs lesions, have been reported in more than 80% of cases of traumatic instability and have been suggested as a risk factor for recurrence.
The concern over initial traumatic shoulder dislocations in athletes stems from the high reported rates of recurrence after nonoperative management. Simonet and Cofield reported that young athletes had an 82% rate of recurrence compared with 30% in nonathletes. However, this association between recurrence and being an athlete has been challenged by other authors who did not find such a correlation. , Rowe found a 100% redislocation rate in patients younger than 10 years, 94% between the ages of 10 and 20 years, and 79% between the ages of 20 and 30 years. The type of sport can also influence recurrence with nonoperative treatment. Taylor and Arciero reported a 90% rate of redislocation in athletic military cadets involved in collision sports. Athletes in collision sports, such as football, hockey, and rugby, are particularly prone to recurrence because of the high-impact nature of their sport. In 29 athletes who underwent arthroscopic stabilization, Rhee and colleagues found that 28% of the collision athletes redislocated compared with 6.7% of the noncollision athletes. Dickens and colleagues reported on 45 college athletes who sustained an in-season instability event. They found that 73% of the athletes returned to play for all or part of that season but only 27% completed the season without a subsequent instability event. In a more recent study, Dickens and colleagues reported results on collegiate contact athletes with in-season anterior shoulder instability. They found that athletes who underwent instability surgery in the off-season are more likely to return to sports without additional instability events the following season (90% vs. 40%).
Initial management of a dislocation involves shoulder reduction with a detailed neurovascular assessment before and after. The reduction can be performed on-field or in the emergency department. A recent review of the literature revealed that, although more than two dozen techniques have been described for reducing a shoulder, no one specific technique has shown superiority over the others. Factors that can increase the likelihood of a successful reduction include patient age younger than 40 years and patients with a slighter build. In the emergency department setting, intra-articular lidocaine and conscious sedation have been used as analgesic premedication with very similar good results. Some have proposed intra-articular lidocaine as preferable analgesia given the lower complication rates of intra-articular injections compared with sedation.
The overall recurrence rate following nonoperative management of traumatic anterior shoulder dislocations ranges from 33% to 67%. Despite these relatively high incidences of recurrence, nonsurgical management continues to be the initial treatment of choice for first-time dislocators. Multiple risk factors for recurrent instability have been identified, including young age, athletic activity, male sex, and the presence of an anterior bone deficiency. ,
Traditionally, immobilization in internal rotation had been implemented, but the suggested duration and position of immobilization continues to evolve. For instance, Simonet and Cofield suggested 6 weeks in internal rotation. In contrast, Buss and colleagues used no immobilization but instead initiated immediate rotator cuff and periscapular strengthening for in-season athletes; however, these authors reported an in-season recurrence rate of 41%. Bottoni and colleagues used a protocol that advocated immobilizing the shoulder for 4 weeks followed by a rehabilitation program; they found that 75% of nonoperatively treated patients experienced dislocation recurrences. McCarty and colleagues suggested that patients should meet the following six criteria before being allowed to return to their sport:
Little or no pain
Patient’s subjective impression of stability
Normal functional ability
Normal sport-specific skills
These authors also recommended that the patient should wear a brace to prevent external rotation and abduction while playing.
Itoi and colleagues performed a magnetic resonance imaging (MRI) study showing greater anatomic reduction in the anterior labrum with the humerus in external rotation rather than in the internal rotation position in which most patients are immobilized. They then compared 3 weeks of immobilization in internal rotation versus external rotation and found that the 15.5-month average follow-up recurrence rate was 30% for those in internal rotation versus zero for those in external rotation. However, these results have not been reproduced by others, and the suggested duration and position of immobilization remains an area of controversy.
Surgical treatment should be considered for patients identified as being at high risk of recurrent instability or failing nonoperative measures. In the athletic population, decision-making regarding the type of procedure and surgical timing can be challenging. In-season athletes may be managed initially nonoperatively and undergo rehabilitation with return to sport when the previously listed criteria are met and may subsequently undergo stabilization after their season is complete. Others involved in high-risk activities, such as football, white-water kayaking, and rock climbing, should be considered for early stabilization.
Both open and arthroscopic surgical procedures are commonly used in the treatment of anterior shoulder instability, and the optimal approach is the subject of considerable scrutiny. Clinical results in the literature for arthroscopic stabilization currently rival traditional open approaches to shoulder instability. Initial poor results of arthroscopic instability surgery have been attributed to inadequate techniques to correct all the necessary pathologic components of glenohumeral instability, including labral tears and capsular laxity. Arthroscopic results have improved through a combination of better understanding and recognition of these pathologic elements along with improved surgical techniques, including the use of multiple working portals, better anchor and suture-passing instrumentation, more accurate anchor placement, and more precise capsulorrhaphy. , , Suggested advantages to arthroscopic treatment include improved diagnostic capabilities to identify and treat specific pathology, less iatrogenic damage to local tissues (the subscapularis tendon), reduced postoperative pain, and improved cosmesis. , Others have argued that the open procedures have superior outcomes with lower recurrence in specific patient populations. Ultimately, the preferred surgical technique depends on a variety of patient characteristics, bony and capsulolabral pathoanatomy, and surgeon comfort level.
Some authors have suggested that a patient’s participation in a collision sport necessitates open reconstruction. For example, Rhee and colleagues found that in a study group of 48 shoulders (of 46 collision athletes) there was a 25% recurrence rate of postoperative instability in those who underwent an arthroscopic repair versus a 12.5% recurrence rate in the open group. However, these athletes had all experienced multiple (>17) preoperative episodes of dislocation. Uhorchak and colleagues found that of 66 collision or contact athletes they treated with open modified Bankart repair and anterior capsulorrhaphy, only two experienced recurrent dislocations after surgery, although 13 patients had postsurgical subluxation. Pagnani and Dome found that 55 of 58 football players achieved a good or excellent result after open anterior stabilization. However, arthroscopic techniques have improved over time, and successful stabilization in contact and collision athletes has been reported. Other indications that previously required an open approach but have now become arthroscopically manageable include an attenuated capsule, humeral avulsion of glenohumeral ligament lesions, and revision surgery cases.
Risk factors for failure of arthroscopic stabilization
In recent years, arthroscopic stabilizations have become more common, and there has been an abundance of studies reporting clinical outcomes and recurrence rates. In a prospective evaluation of arthroscopic Bankart repairs, Voos and colleagues suggested that the risk factors for failure are age less than 25, ligamentous laxity, and the presence of a Hill-Sachs lesion measuring more than 250 mm . Calvo and colleagues prospectively evaluated 61 patients treated arthroscopically for anterior instability and identified age younger than 28 years, diffuse ligamentous laxity, glenoid bone loss greater than 15%, and resumption of contact sports as independent risk factors for failure of repair. Similarly, Porcellini and colleagues retrospectively reported on 625 patients who underwent arthroscopic Bankart repair and found age at the time of the first dislocation, male sex, and the time from the first dislocation until surgery to be significant risk factors for recurrence.
Using a prospective case-control study of 131 patients, Balg and Boileau developed the instability severity index score as a simple tool for predicting the risk of failure after arthroscopic stabilization. The strongest risk factors for failure included patient age less than 20 years, involvement in competitive or contact sports or those involving forced overhead activity, shoulder hyperlaxity, a Hill-Sachs lesion on an anteroposterior radiograph, and/or loss of the sclerotic inferior glenoid contour. The recurrence rate was also significantly higher in competitive athletes (50%) than in those participating in recreational sports (14.9%).
Bone deficiencies and anterior instability.
Hill-Sachs lesions have been reported to occur in 32% to 51% of initial anterior dislocations, , and anteroinferior glenoid deficiencies (bony Bankart lesions) have been reported in 22% of primary dislocations. Concurrent glenoid and humeral head bone defects exist in nearly 100% of cases of recurrent shoulder dislocators. , In cases of bony defects, higher rates of recurrent instability have been reported after traditional Bankart repair. , , Burkhart and DeBeer compared recurrence rates after arthroscopic stabilization and found that 67% of patients with significant bone defects of either the glenoid or humeral head redislocated compared with 4% of those without such defects. For contact athletes with bony deficiencies, the dislocation recurrence rate after arthroscopic management was 89%.
Glenoid bone loss.
In collision athletes, significant glenoid bone loss, classically termed the inverted-pear glenoid , remains a relative contraindication for arthroscopic management. In normal circumstances the anteroinferior rim of the glenoid should be readily visible on both the anteroposterior and axillary radiographs, with the loss of the normal contour suggesting glenoid bone loss, especially in the setting of recurrent instability. Advanced imaging with axial computed tomography (CT) scans and three-dimensional rendering is preferred for evaluation of glenoid morphology and osseous defects ( Fig. 8.4 ). Many authors have attempted to quantify the critical amount of isolated anterior glenoid bone loss that results in anterior instability, and most agree that glenoid lesions greater than 20% to 25% of the articular surface require a bone grafting procedure ( Fig. 8.5 ). , This threshold may be lower in the setting of combined defects, such as an engaging Hill-Sachs impaction fracture, the so-called bipolar shoulder lesions. However, with improved techniques, encouraging results have been achieved with arthroscopic management in the setting of bony defects. Mologne and colleagues reported no redislocations in 11 patients with 20% to 30% bony glenoid loss and a bone fragment, who were followed up at an average of 34 months after arthroscopic stabilization. Two of 10 patients with a glenoid defect but no visible bone fragment had subluxation symptoms, and another patient experienced redislocation and required revision open surgery.
The most commonly performed bone grafting operation for anterior glenoid bone loss is the open Latarjet procedure. The native coracoid process is osteotomized from its base and transferred with the attached conjoint tendon so that its longitudinal axis is oriented parallel to the face of the glenoid. The fragment is secured with rigid screw fixation ( Fig. 8.6 A–B). The operation can also be performed arthroscopically; this can be technically challenging, requires specialized equipment, and is associated with a long learning curve. , Excellent outcomes with very low recurrence rates at long-term follow-up have been reported for the Latarjet procedure. Burkhart and colleagues noted a recurrence rate of 4.9% in 47 modified Latarjet reconstructions; similarly, Schmid and colleagues reported no recurrences in 49 consecutive patients in their series, and the best outcomes were associated with optimal graft placement. Other authors have even suggested the Latarjet as a primary stabilization procedure for contact athletes in the absence of significant anterior glenoid bone loss. Alternatively, high satisfaction and low recurrence rates have been reported with other bone grafting techniques, including autogenous tricortical iliac crest graft and distal tibial allograft. , ,
Jeon and colleagues retrospectively reviewed the outcomes between arthroscopic Bankart repair versus Latarjet in a cohort of patients with borderline glenoid bone loss that was defined as between 15% and 20% glenoid deficiency. The authors found that the Latarjet group had significantly lower recurrence rate of 6.5% compared with the Bankart repair group at 22.9%. Furthermore, the authors found that the Bankart repair resulted in a greater loss of external rotation at the side compared with the Latarjet group (13.3 degrees vs. 7.3 degrees).
Humeral head bone loss.
Previously, the presence of a large engaging Hill-Sachs lesion has been a relative contraindication for arthroscopic stabilization. An “engaging” lesion is one that engages the rim of the glenoid when the shoulder is physiologically abducted and externally rotated ( Fig. 8.7 ). When patients with these lesions are treated with arthroscopic Bankart repair alone, recurrence rates can be unacceptably high, especially in the contact athlete. Hill-Sachs lesions may represent 12.5% to 20% or more of the humeral head diameter, although preoperatively determining the extent of the lesions can be challenging ( Fig. 8.8 ). A CT scan with three-dimensional rendering can help to quantify the size and depth of the lesion, as well as identify any glenoid deficiencies ( Fig. 8.9 ).