The Shoulder in Athletes




Repetitive overhead movements and contact sports exert great stress on the shoulder, often at extreme ranges of motion. As a result, the shoulder is a common site of pathology and disability in athletes. Each athlete presents unique diagnostic and therapeutic challenges, and an understanding of sport-specific biomechanics and pathology is essential. Throwing athletes, for example, repeatedly accelerate and decelerate their shoulder over a wide arc of rotation, causing repetitive microtrauma to the static and dynamic stabilizers of the glenohumeral and scapulothoracic joints. In contrast, 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 repetitive overhead and collision athletes.


Sports-Specific Biomechanics


The Kinetic Chain


The kinetic chain of motion can be described as the sequential activation of all body areas through a link segment, progressing from the lower extremity through the trunk to the rapidly accelerating upper extremity. Overhead athletes must efficiently preserve the transmission of force from their legs and trunk to the force-delivery mechanism of their arm in a coordinated cascade of movements. The legs and trunk generate rotational and linear momentum, producing a significant proportion of the energy in the overhead motion. In tennis the legs and trunk are responsible for 50% to 55% of the total force generation required for a power serve. A variety of studies have demonstrated that poor flexibility or muscle imbalances throughout the kinetic chain are common in patients with shoulder injuries, such as shoulder impingement, rotator cuff tears, and instability. In one study that examined physical features in 64 throwers with labral tears, 46 (72%) showed infraspinatus and teres minor weakness on resisted external rotation, 31 (48%) demonstrated lower back inflexibility, 28 (44%) showed trunk and hip core musculature weakness by failing a Trendelenburg test, and 25 (39%) had asymmetrically decreased internal rotation of the nondominant hip. Injuries to the foot and ankle, tightness of the muscles crossing the hip and knee joints, weakness of hip abductors and trunk stabilizers, and conditions that alter spinal alignment can all influence kinetic chain energy transmission.


In the baseball pitcher, improper conditioning of the core and trunk can influence the positioning of the throwing arm and may result in excessive force transmission across the stabilizing structures of shoulder; this can compromise performance and predispose the athlete to injury. The “slow arm position” describes the disengaged transmission of force with compensatory increases in lumbar lordosis during the acceleration phase, which places the arm behind the body and the scapular plane. The shoulder is forced to assume a hyperabducted, externally rotated position that moves the arm out of the safe zone of glenohumeral angulation described by Jobe and colleagues. This position creates a violent acceleration out of the late cocking position, increasing compression loads and shear and traction on the rotator cuff, glenoid, and capsulolabral complex. The resultant forces can injure the posterior capsule, tear and peel the labrum off the glenoid, tear and delaminate the rotator cuff, and injure or stretch the anterior capsular restraints.




Throwing Athletes


Athletes who perform repetitive overhead motions exert abnormal stresses on the shoulder that vary in magnitude and anatomic location depending on the sport. Repetitive throwing motions can result in overuse-type injuries with the potential for acute injuries superimposed on chronic changes, a combination that can present therapeutic challenges.


Baseball Pitching


The baseball pitch has been studied extensively and is often used to extrapolate implications for other overhead sports. The predicament of the pitcher’s shoulder, the thrower’s paradox, describes the delicate balance of sufficient mobility to foster extreme rotations while maintaining adequate stability to prevent subluxation of the humeral head. In addition, the shoulder must withstand substantial repetitive forces during a pitching motion. Professional pitchers generate up to 92 N-m of humeral rotation torque, which is greater than the torsional failure limit in human cadaveric shoulders. Glenohumeral compressive loads as high as 860 N can be created with concomitant humeral angular velocities as high as 7000 degrees per second. To counteract these forces and keep the humeral head centered in the glenoid, there is significant eccentric contraction of the posterior rotator cuff (the supraspinatus, infraspinatus, and teres minor).


The six phases of the baseball pitch have been extensively examined ( Fig. 20-1 ). Most pitchers incorporate their own style into pitches, particularly during the wind-up and follow-through phases. Regardless of the appearance of the pitch during these phases, correct fundamental pitch mechanics are paramount throughout the entire motion for effective throwing and injury prevention. Improper mechanics at any stage during this energy transfer can lead to injury and affect performance. An experienced coach educated in throwing mechanics is invaluable to the young athlete in preventing and recovering from injury through detecting and correcting subtle abnormalities in form. High-speed video evaluation is a useful tool that provides pitchers and their coaches with visual feedback about technique. The following sections provide a detailed account of the correct mechanics at each pitching phase and resultant pathology associated with poor form.




FIGURE 20-1


The baseball pitch has been divided into six phases: (1) wind-up, (2) early cocking, (3) late cocking, (4) acceleration, (5) deceleration, and (6) follow-through.


Wind-up


The wind-up ( Fig. 20-2 ) sets the tone for the rest of the pitch, and poor mechanics during this phase can propagate through the remaining pitch phases. The feet are positioned parallel to one another and perpendicular to the rubber on the mound as the pitcher faces the batter. The right-handed pitcher then places the right foot parallel to the rubber stopper on the pitching mound. As the left leg is elevated, the pitcher keeps the hips level to the ground and points them toward home plate while maintaining balance. The hips then begin driving forward toward home plate and the right hand with the ball exits the left hand glove ( Fig. 20-3A ). Inexperienced throwers often have flawed form with poor trunk tilt and less hip advancement toward home plate ( Fig. 20-3B ).




FIGURE 20-2


A, Wind-up: the leading leg is elevated while the hips are kept level and pointing toward home plate. B, Early cocking: the throwing hand (not seen) must remain on top of the ball, keeping the shoulder internally rotated to minimize the anterior subluxation that can occur if the shoulder is externally rotated during this phase. C, Late cocking: a rapid arc of humeral external rotation from 45 degrees to 170 degrees occurs in the scapular plane. D, Acceleration: the propulsive force during acceleration begins in the lower extremities, and the kinetic energy is transferred through the trunk and into the shoulder, elbow, and wrist. E, Deceleration: the periscapular muscles contract eccentrically to dissipate excess kinetic energy. F, Follow-through: eccentric contraction by the scapular rotator muscles continues to decelerate the arm, and the posterior capsule experiences tension as the arm adducts. During the follow-through, the shoulder should internally rotate and horizontally adduct across the body.



FIGURE 20-3


A, The mature thrower leads with his hip toward home plate. B, The immature player fails to lead with his hip.


During the wind-up phase, the pitcher should be balanced when the leading leg reaches its highest point. If the pitcher begins to fall forward prematurely as a result of poor balance, the delivery will be rushed and pitch velocity lessened. If the hips fail to point toward home plate, the leading leg will land in an incorrect direction during subsequent pitch phases.


Early Cocking


The hand comes out of the glove while maintaining a position on top of the ball and the shoulder remains internally rotated (see Fig. 20-2B ). As the hand brings the ball back and laterally, the shoulder is elevated in the scapular plane past 90 degrees and externally rotated to approximately 45 degrees. The hips are driven toward home plate but the pelvis does not rotate. The phase ends with the left foot landing on the mound, which decelerates the driving lower extremity and trunk.


Two common errors that should be avoided in this phase are “pie throwing” and “opening up” too soon. First, if the hand is rotated under the ball (the “pie-throwing” position seen in Fig. 20-4B ) instead of remaining on top ( Fig. 20-4A ), the humerus externally rotates and places the humeral head in a vulnerable position for anterior subluxation and instability. Second, the lead foot should land pointing toward home plate ( Fig. 20-5A ). Flaws observed in inexperienced pitchers include abduction of the lead leg when landing on it. For example, a right-handed pitcher with poor form would place the lead left foot on the first-base side of the mound ( Fig. 20-5B ). This premature opening causes early pelvis rotation with a consequent loss of velocity and increased anterior shoulder strain. Movement of the lower extremity and trunk with their substantial mass creates maximal energy in the lower body that is transferred to the upper extremity and finally to the ball. This requires timed and delayed upper body rotation that allows the energy to develop in the lower extremity and trunk.




FIGURE 20-4


A, The mature player keeps his hand on top of the ball during early cocking. B, The immature player brings his hand under the ball during early cocking.



FIGURE 20-5


A, The mature player keeps his hips closed, and his lead foot is directed toward home plate. B, The immature player opens his pelvis, and his lead foot is directed inside of home plate.


Late Cocking


The left foot hits the ground pointing in the direction of home plate, leaving the legs stretched apart (see Fig. 20-2C ). The weight of the body is evenly distributed on both legs, and the torso balances in an upright position between the legs. Trunk rotation is delayed as long as possible while the right humerus externally rotates from approximately 45 degrees to 170 degrees in its position in the scapular plane. At this time, the periscapular muscles, including the trapezius, rhomboids, levator scapulae, and serratus anterior, keep the scapula stabilized, and the biceps brachii keeps the elbow flexed at slightly more than 90 degrees. Eccentric contraction of the subscapularis muscle decelerates the externally rotating humerus.


Most injured pitchers experience pain during the late cocking phase. During this phase, at maximal external rotation (nearing 170 degrees), the arm should be abducted 90 to 100 degrees. Throwing with reduced external rotation at the time the foot makes contact with the ground may be associated with increased strain on the anterior shoulder during acceleration and ball release.


Periscapular muscular weakness may also predispose to injury during the late cocking phase. The serratus anterior is significantly less active in pitchers with shoulder instability than in those with normal shoulders. To compensate for diminished serratus anterior strength, the thrower might drop the elbow thus decreasing the degree of scapular rotation and the elevation needed. If this pathologic process continues, the player might attempt to compensate further by moving the humerus behind the scapular plane. If symptoms arise, the player reduces the amount of external rotation to protect against shoulder pain and arches the back into hyperlordosis to compensate for the decreased humeral external rotation. Early recognition of muscle imbalances in the thrower allows the surgeon to institute an early, focused physical therapy program to strengthen the affected structures and protect against the vicious cycle of compensatory pathologic throwing.


The elbow should reach its highest point in late cocking ( Fig. 20-6A ); inexperienced throwers often have their elbows in a suboptimal lower position ( Fig. 20-6B ).




FIGURE 20-6


A, The mature player keeps his throwing elbow high (arrow). B, The immature player drops his throwing elbow (arrow).


Acceleration


Once the humerus reaches maximal external rotation, the hand carrying the ball accelerates in a rapid arc of internal rotation (see Fig. 20-2D ). The energy of the lower extremity and trunk is transferred through the shoulder to the elbow and wrist as the body falls forward. Immediately prior to the release of the ball, the arm internally rotates 80 degrees, reaching peak angular velocities near 7000 degrees per second. Within 0.05 seconds, the ball is released with speeds exceeding 90 mph.


A pitcher with a painful shoulder may lead with the elbow during the acceleration phase, or reduce horizontal abduction while increasing elbow flexion to bring the ball closer to the shoulder. Although this maladaptive position reduces the load on the shoulder, it increases the load on the medial elbow, predisposing it to injury. If the thrower opens up too quickly, positioning the elbow behind the plane of the scapula, the glenohumeral joint hyperangulates, resulting in more pronounced internal impingement ( Fig. 20-7 ).




FIGURE 20-7


When the elbow moves posterior to the plane of the scapula, the shoulder is hyperabducted, increasing the risk of internal impingement.


Deceleration


After the ball release, the right hip rises up and over the left leg. The right foot lifts off the mound and the pitcher performs a controlled fall forward (see Fig. 20-2E ). In this phase the teres minor, infraspinatus, and scapular rotator muscles contract eccentrically to dissipate the kinetic energy that was not transferred to the ball. The glenohumeral distraction forces at this time can reach 1 to 1.5 times body weight; these forces are absorbed by the shoulder capsule and posterior rotator cuff.


Follow-through


The arm continues to descend, and the right leg lands on the ground in a controlled fashion (see Fig. 20-2F ). Eccentric contraction by the scapular rotator muscles continues to decelerate the arm, and the posterior capsule experiences tension as the arm adducts. During the follow-through, the shoulder should internally rotate and horizontally adduct across the body. If the arm instead finishes facing home plate, excessive stresses are transferred to the shoulder.


Football Throwing


Although similar in some respects, the overhead throwing motion in football has fundamental differences in shoulder position and stresses compared with the overhead throwing motion in baseball. This is largely attributable to the greater weight of the football (0.42 kg versus 0.14 kg for the baseball). The observed injury patterns also differ, with predilection towards overuse disorders, such as biceps tendonitis and rotator cuff injury, as well as traumatic conditions, including rupture of the pectoralis major (PM) muscle.


Electromyographic analysis demonstrates four distinct phases in football throwing. Early cocking is initiated at rear foot plant and continued to maximal shoulder abduction and internal rotation. Late cocking starts at maximal shoulder abduction and internal rotation and ends with maximal shoulder external rotation. Acceleration begins with maximal shoulder external rotation and completes with release of the ball. Finally, the follow-through phase is the period from ball release to maximal horizontal adduction.


The kinematics and kinetics of the baseball pitch and football pass have been compared; pitchers produce significantly greater forces and torques in the shoulder during arm deceleration. Quarterbacks demonstrate less motion in their legs, pelvis, and torso, which limits the force transmission compared with that experienced in pitchers. When combined with a lower throwing frequency, fewer games in a season, and greater rest periods between games, quarterbacks are also less prone to many of the overuse injuries characteristic of pitchers.




Nonthrowing Overhead Athletes


Tennis


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.


The tennis serve has five distinct phases ( Fig. 20-8 ), 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.




FIGURE 20-8


The tennis serve has been divided into five phases, akin to those of the baseball pitch. These include the wind-up, early cocking, late cocking, acceleration, and follow-through. The shoulder kinematics resemble those of the overhead throw.

(Courtesy Nicholas Frankfurt.)


Swimming


The demands on the shoulders of competitive swimmers are immense, and the number of strokes exceeds 500,000 per arm per year. The freestyle swimming stroke has been subdivided into five distinct phases: hand entry, catch, in-sweep, finish, and recovery ( Fig. 20-9 ). 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.




FIGURE 20-9


The swimming stroke is divided into five phases: hand entry, catch, in-sweep, finish, and recovery.

(Courtesy Nicholas Frankfurt.)


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


Hand Entry


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 in order 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, PM, 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.


Catch


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 and colleagues 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.


In-Sweep


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.


Finish


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.


Recovery


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 in order to achieve full abduction. Otherwise, the greater tuberosity comes in contact with the acromion at about 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. Whereas a normal shoulder might be able to compensate for these muscle imbalances, 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.


Impingement in Swimmers


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 hand 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 (NSAIDs), 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.


Golf


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).


The golf swing is divided into five phases ( Fig. 20-10 ): 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).




FIGURE 20-10


The golf swing is divided into five phases: 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 the horizontal to ball impact), and follow-through (from ball contact to the end of the swing).

(From Kim DH, Millett PJ, Warner JJ, Jobe FW. Shoulder injuries in golf. Am J Sports Med. 2004;32[5]:1324-1330.)


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 Impingement and Rotator Cuff Injury


The golfer’s lead shoulder is placed in the position of impingement at the extremes of 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. 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.


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 about 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.


Glenohumeral Instability


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.


Glenohumeral Arthritis


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.




Asymptomatic Throwing Shoulder Adaptation


Overall Motion


The dominant shoulder of a thrower exhibits adaptive changes. It is well documented in throwers that with the shoulder abducted to 90 degrees, external rotation significantly increases by as much as 10 degrees compared with that of the contralateral arm, and internal rotation is diminished; this is known as glenohumeral internal rotation deficit (GIRD). The gain in external rotation is often associated with an equal loss in internal rotation. In asymptomatic throwers therefore the total arc of shoulder motion is maintained, but it is shifted in external rotation by 10 degrees. There is controversy regarding the anatomic changes responsible for the observed glenohumeral rotation changes, with studies examining soft tissue and bone adaptations.


Bone Adaptations


Developmental changes in the proximal humerus occur in young throwers. Mair and colleagues found that 55% of asymptomatic and 62% of symptomatic skeletally immature baseball players had radiographic evidence of physeal widening. Krahl and colleagues observed that pitching arms underwent a significant increase in humeral length. The developmental bone changes in young throwers also include increased humeral retroversion, which shifts the shoulder arc of motion, with the greatest change occurring in those aged 13 to 14 years. These early changes lead to permanent change in the proximal humerus anatomy. Crockett and colleagues showed that professional pitchers’ dominant shoulders have 17 degrees greater humeral retroversion compared with their nondominant shoulders and that there may also be adaptive changes in retroversion within the glenoid. Wyland and colleagues further suggested that concurrent increases in dominant shoulder humeral retroversion and glenoid retroversion are coupled during skeletal development; these were observed as a 2 : 1 “thrower’s ratio” in 32 professional pitchers.


As the normal humeral retroversion angle decreases from 78 degrees to 30 degrees during development, Yamamoto and colleagues hypothesized that repetitive throwing did not increase retroversion in dominant shoulders but rather restricted the physiologic de-rotation of the humeral head during growth. Humeral osseous adaptation may therefore explain the decrease in internal rotation and most of the increase in external rotation in asymptomatic throwers.


Capsuloligamentous Changes


Soft tissue adaptations are also thought to occur. The anterior capsule and glenohumeral ligaments become more lax in throwing shoulders, and the posterior capsule and glenohumeral ligaments become stiffer. The etiology of these changes remains a controversial subject. Two major theories exist, each proposing different inciting capsular adaptations to repetitive throwing. One argues that throwers initially develop a posterior capsular contracture; the other proposes that they develop an adaptive anterior capsular laxity.


Posterior Capsular Contracture Theory


Burkhart and colleagues proposed that a fundamental adaptation in throwers is a posterior capsular contracture that, although initially asymptomatic, can eventually have significant pathologic implications. They reasoned that in the overhead thrower, the posterior capsule must withstand tensile forces of up to 750 N during the deceleration and follow-through phases. These posterior tensile forces are resisted by the eccentric contraction of the rotator cuff, primarily the infraspinatus, and by the posteroinferior capsule (the posterior band of the inferior glenohumeral ligament) ( Fig. 20-11 ). With repetitive infraspinatus eccentric contraction during deceleration and follow-through, the muscle belly loses active tension, gains passive muscle tension, and develops disturbed proprioception. As a result, higher loads are imposed on the posteroinferior capsule, which then becomes hypertrophied and stiffer.




FIGURE 20-11


The posterior capsule and posterior rotator cuff are stressed by tensile forces during the follow-through and deceleration phases of throwing. Repetitive throwing can instigate a focal fibroblastic response in the posterior capsule, and the capsule reacts by becoming hypertrophied and stiff. If the capsule becomes stiff, the center of rotation of the shoulder is shifted to a more posterosuperior location. A, The figure shows the original center of rotation of the humeral head (c). B, The center of rotation is shifted posterosuperiorly. C, A further shift posterosuperiorly as the posterior capsule becomes hypertrophied and stiff. A, Anterior; P, posterior.


The theory proposes that this posterior contracture shifts the center of rotation of the shoulder to a more posterosuperior location, creating posterosuperior instability and functional consequences for the shoulder in abduction and external rotation. Grossman and colleagues created a posterior capsular contracture in a cadaveric model and found that the shoulder center of rotation did in fact shift posterosuperiorly in abduction and external rotation, allowing increased clearance of the greater tuberosity over the posterior glenoid rim. The humeral head could consequently externally hyperrotate, producing increased shear in the rotator cuff tendon and internal impingement that is more pronounced.


The rationale for this hypothesis is based on O’Brien’s concept of the inferior glenohumeral ligament complex ( Fig. 20-12 ) acting as a hammock to support the humeral head with the arm in abduction. In abduction and external rotation, the posterior band of the inferior glenohumeral ligament is shifted under the humeral head. Posterior band contracture exerts a posterosuperior force on the humeral head, shifting it in that direction. The shift creates a relative anteroinferior capsular redundancy. The net effect of the capsular changes (contracted posterior capsule and relative lengthening of the anteroinferior capsule) and the posterosuperior humeral head shift is increased external and decreased internal rotation. However, other studies have documented significant posterior laxity instead of tightness in throwers, supporting the idea that GIRD likely arises from both ligamentous and osseous adaptations.




FIGURE 20-12


A model of the inferior glenohumeral ligament (IGHL) adaptation complex helps explain glenohumeral internal rotation deficit and hyperexternal rotation in the throwing athlete. A, The IGHL complex. B, The complex can be simplified into two bands: the anterior IGHL (AIGHL) and the posterior IGHL (PIGHL). In abduction and external rotation, the posterior band of IGHL is shifted under the humeral head. C, If the posterior band has a contracture, it will push the humeral head in a posterosuperior direction. D, This allows the greater tuberosity to clear the glenoid rim and the humerus to externally rotate more easily.

(From Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: Spectrum of pathology. Part I: Pathoanatomy and biomechanics. Arthroscopy. 2003;19[4]:404-420.)


Adaptive Capsular Laxity Theory


Other authors have proposed that repetitive shoulder microtrauma to the anterior capsule, particularly during the cocking phase of throwing, can lead to stretched anterior capsuloligamentous structures. The stretched anterior capsule allows the greater external rotation routinely seen in overhead throwers; it can also lead to symptomatic anterior microinstability. These authors attribute the loss of internal rotation to two factors: the aforementioned osseous adaptation of the humerus and posterior muscle tightness resulting from eccentric posterior muscle contraction during the deceleration phase of throwing.


Several studies have quantified capsular laxity in the context of throwing. Sethi and colleagues found an increased anteroposterior glenohumeral translation of more than 3 mm in pitchers’ dominant shoulders compared with the nondominant arm. Borsa and colleagues found that posterior translation was consistently greater than anterior translation in throwers’ dominant shoulders. These studies suggest that throwing shoulders are generally lax instead of stiff, contradicting the theory that posterior capsular tightness is a universal phenomenon in the asymptomatic thrower.


Combining the two proposed mechanisms would lead to the conclusion that in the asymptomatic thrower, increased external rotation results from osseous changes with a component of increased anterior capsular laxity, whereas decreased internal rotation primarily results from increased humeral retroversion with the addition of posterior muscular and capsular tightness.


Muscle Strength and Proprioception


Pitchers have been shown to exhibit decreased external rotation strength and increased internal rotation strength in their dominant shoulder compared with their nondominant shoulder. Magnusson and colleagues showed that professional baseball pitchers had weaker external rotation and supraspinatus strength in their throwing shoulder compared with their nondominant shoulder as well as the dominant shoulder of age-matched nonathlete controls. Some authors have proposed that if external rotator muscle strength is not between 65% and 75% of internal rotator strength, the glenohumeral joint becomes unbalanced and destabilized during throwing. The periscapular musculature also responds to repetitive throwing. Most throwers have hypertrophied scapular elevator and protraction muscles on their throwing side.


It has been shown that proprioception is significantly diminished in shoulders with excessive laxity, although it is heightened to at least normal levels in extreme external rotation. Elite pitchers retain a proprioceptive sense of the degree of external rotation (the slot) they must achieve to produce the required pitch velocity.


Scapulothoracic Motion


The scapula plays a critical role in transferring energy from the trunk to the humerus. Adaptive scapulothoracic changes leading to scapular asymmetry have been described in the asymptomatic thrower. Changes in static and dynamic scapular mechanics arise from overuse and weakness of the scapular stabilizers and posterior rotator cuff muscles. The major findings are as follows: with the arm hanging at the side, the throwing shoulder’s scapula has increased upward rotation (abduction), internal rotation (protraction), antetilting in the sagittal plane, and inferior translation ( Fig. 20-13 ). During forward arm elevation, the scapula upwardly and internally rotates and retracts. Scapular upward rotation has been theorized to be a key adaptation to the cocking phase of throwing. During cocking, when the humerus is terminally externally rotated and abducted, upward scapular rotation helps to maintain glenohumeral articular congruency. This altered scapular positioning, although initially asymptomatic, can nevertheless predispose the shoulder to injury.




FIGURE 20-13


With repetitive throwing, the overhead athlete’s scapula shows increased upward rotation (abduction), internal rotation (protraction), antetilting in the sagittal plane, and inferior translation. This has been termed as SICK (scapular malposition, inferior medial border prominence, coracoid pain, and scapular dyskinesis) scapula.

(From Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: Spectrum of pathology. Part III: The SICK scapula, scapular dyskinesis, the kinetic chain, and rehabilitation. Arthroscopy. 2003;19[6]:641-661.)




Throwing Shoulder Conditions


Various paradigms have been used to describe the constellation of injuries and pathologic syndromes in the throwing shoulder. The concepts of instability and impingement apply uniquely to the thrower’s shoulder. Instability and internal impingement in throwers should be viewed as syndromes of collective common pathologies occurring in the static and dynamic stabilizing elements of the shoulders that ultimately lead to pain during throwing. The injury cascade tends to form a continuum of pathology and pathomechanics. When considered separately, current theories regarding the etiology of specific throwing-related shoulder injuries may appear to contradict one another, but in actuality, they are complementary when considered as elements of a pathologic continuum.


Injuries are often secondary to the accumulation of repetitive microtrauma in the throwing shoulder, which causes attrition and gradual failure. Typical sites of pathoanatomy include the superior and posterosuperior labrum, the articular surface of the supraspinatus and infraspinatus, and the posterior capsule. The current understanding of conditions of the throwing shoulder is based on biomechanical analysis of sports-specific shoulder motions, intraoperative correlation with symptoms, and reports from imaging and clinical studies on the outcomes of different treatments.


Injury to the thrower’s shoulder joint occurs most commonly during the late cocking or early acceleration phases. When pain or symptoms disturb pitch acceleration, velocity, or efficacy, the symptomatic shoulder is called a dead arm. Historically, the dead arm has been ascribed to a multitude of pathologic processes. These have included psychiatric disease involving voluntary dislocators, acromial osteophytes, coracoacromial impingement, rotator cuff tendinitis and tears, biceps tendinits, acromioclavicular joint pathology, microinstability, posterior glenoid calcifications, and SLAP lesions. However, the exact etiology and sequence of injury in throwers has not yet been confirmed in vivo, although there is evidence that a combination of abnormal scapulothoracic and glenohumeral motion can injure the superior and posterosuperior labrum as well as the undersurface of the rotator cuff and posterior capsule. Several distinct processes appear to play a role in the development of throwing pathology, with these processes considered to be a continuum ( Fig. 20-14 ).




FIGURE 20-14


Continuum flow chart illustrating how shoulder adaptations to repetitive throwing and poor throwing mechanics can generate shoulder pathology that leads to clinical symptoms. SLAP, Superior labrum anterior and posterior lesion.


Internal Impingement


Walch and colleagues initially described internal impingement that occurs in 90 degrees of abduction and 90 degrees of external rotation where the posterosuperior rotator cuff contacts the posterosuperior glenoid labrum ( Fig. 20-15 ). Although physiologic in a static position, excessive contact of the undersurface of the rotator cuff and the superior labrum during repetitive overhead activity can lead to articular-sided rotator cuff tears and SLAP lesions in throwers. Andrews and colleagues noted that labral tears were present in 100% of 36 competitive athletes with articular-sided, partial-thickness rotator cuff tears of whom 64% were baseball pitchers. Guidi and colleagues found superior labral fraying in 90% of patients with partial-thickness rotator cuff tears.




FIGURE 20-15


Internal impingement results in the 90-degree abducted, 90-degree externally rotated position when the posterosuperior rotator cuff presses against the posterosuperior glenoid labrum.

(From Jobe CM, Pink MM, Jobe FW, et al. Anterior shoulder instability, impingement and rotator cuff tear: Theories and concepts. In: Jobe FW, Pink MM, Glousman RE, Kvitne RS, eds . Operative Techniques in Upper Extremity Sports Injuries. St. Louis: Mosby; 1996:164-176.)


Jobe extrapolated internal impingement to throwing athletes and detailed a spectrum of injuries that included rotator cuff, glenoid labrum, and bone pathologies. He suggested that with repetitive hyperangulation of the humerus in the scapular plan, as seen in throwers with pathologic pitching mechanics, internal impingement might be aggravated by gradual stretching of the anterior capsuloligamentous structures with resultant microinstability . He believed that this microinstability leads to exacerbation of the internal impingement, which increases contact of the posterior rotator cuff, greater tuberosity, and glenoid. After limited success with subacromial decompression in overhead athletes, Jobe recommended anterior capsulolabral reconstruction when surgery was indicated.


The other predominant theory of the pathophysiologic mechanism of internal impingement was described by Burkhart and Morgan. They postulated that the shoulder dysfunction in the overhead throwing athlete was primarily due to a torsional SLAP lesion resulting from an acquired posterosuperior instability caused by posteroinferior capsular tightness. They described this phenomenon as the “peel-back” mechanism. With the arm in the externally rotated and abducted position, the biceps is brought into a more posterior and vertical position, and with further external rotation it transmits a torsional force to the posterior labrum, peeling it back ( Fig. 20-16 ). With repetitive throwing, the biceps tendon can further peel the biceps anchor off the glenoid lip.




FIGURE 20-16


A, At rest, the biceps tendon does not transmit torsional forces. B, In humeral external rotation and abduction, the long head of the biceps tendon transmits a torsional force to the posterior labrum, peeling it back.


Panossian demonstrated in a cadaver model that creation of a type II SLAP lesion resulted in increases in both humeral internal-to-external rotation and anterior-to-posterior translations. After arthroscopic repair, total range of motion, internal rotation, external rotation, and translation significantly decreased, returning to expected values. These findings suggest that type II SLAP lesions cause significant glenohumeral instability, which can be effectively treated with current arthroscopic repair techniques.


Burkhart and colleagues further argued that the existence of internal impingement is physiologic and that it is GIRD that allows supraphysiologic external rotation with fatigue failure of the rotator cuff fibers, potentially leading to a pathologic state. Another study highlighted the significant coexistence of undersurface rotator cuff tears and labral fraying in 73.3% of non-overhead athletes as evidence that internal impingement may not be a phenomenon unique to throwers.


Posterior Capsular Contracture


The theory describing adaptive changes to the posterior capsule has been outlined earlier. In the context of throwing pathology, the contracture of the posterior capsule initiates a cascade that some authors believe explains most overhead arm pathology. Once there is posterosuperior instability and the humeral head is shifted posterosuperiorly, kinetic chain dynamics are affected. The arm loses even more internal rotation and arm acceleration, and therefore ball velocity is lost. Over time, posterior SLAP tears can occur from posterosuperior contact of the labrum and the greater tuberosity. The posterior cuff undersurface begins to fail, and the picture of internal impingement arises. In a small cohort of mainly older patients, attenuation of the anterior capsule occurred with continued throwing, leading to eventual permanent deformation and anterior microinstability.


Glenohumeral Internal Rotation Deficit


As described earlier in the discussion on shoulder adaptations to throwing, over time the throwing shoulder develops increased external rotation and disproportionately decreased internal rotation (GIRD). By convention, glenohumeral rotation is measured with the patient either supine or sitting and with the shoulder abducted 90 degrees in the plane of the body. The scapula must be stabilized either against the examination table, if the patient is supine, or by the examiner’s hand, if the patient is sitting. Glenohumeral rotation is then measured up to the point that the scapula begins to move on the posterior chest wall or provides resistance ( Fig. 20-17 ). Failure to stabilize the scapula incorporates scapulothoracic motion into the total rotational arc, leading to confounding measurements.




FIGURE 20-17


Measurement of internal (A) and external (B) rotation with the arm at 90 degrees of abduction and the scapula stabilized in the supine position.


GIRD resulting in a loss of total rotational arc of greater than 20 degrees compared with the contralateral side puts the shoulder at risk for injury. Indeed, severe GIRD is more prevalent in symptomatic shoulders. Verna studied 39 professional pitchers with GIRD greater than 35 degrees (with 25 degrees or less of total internal rotation) during a baseball season. He found that 60% of them developed shoulder problems that required them to stop pitching. In a case series of overhead athletes with arthroscopically proven type II SLAP lesions, Kibler found that severe GIRD (average, 33 degrees; range, 26 to 58 degrees) was present in all of them.


Wilk and colleagues prospectively evaluated passive ROM and shoulder injuries in 122 professional baseball pitchers and found that pitchers with GIRD were at almost twice the risk of sustaining shoulder injuries compared with those without GIRD. The authors further noted that when the total rotational motion deficit between the dominant throwing arm and the nonthrowing arm was greater than 5 degrees, pitchers were 2.5 times more likely to sustain a shoulder injury. In a subsequent investigation Wilk and colleagues examined 296 professional pitchers over eight seasons, and found that pitchers with total rotational motion deficits more than 5 degrees in their throwing shoulders were 2.6 times more likely to suffer an elbow injury. This was consistent with previous studies that suggested that a loss of internal rotation increased the load on the medial compartment of the elbow, leading to potential ulnar collateral ligament injury.


Symptomatic GIRD likely has a component of posterior capsular or muscular contracture. In a prospective study Kibler and colleagues reported that tennis players who performed daily posteroinferior capsular stretching to minimize GIRD increased their dominant shoulder internal rotation and had a 38% lower incidence of shoulder problems compared with those in a control group who did not stretch. Burkhart and colleagues reported that 90% of throwers with symptomatic GIRD (>25 degrees), and almost all young collegiate or high school athletes, responded well to a posteroinferior capsular stretching program (over as little as 2 weeks) that reduced GIRD to an acceptable level (defined as either <20 degrees or <10% of the total rotation in the nonthrowing shoulder).


Alternatively, various developmental adaptations seen in the glenohumeral joint of the overhead throwing athlete have also been suggested as possible reasons for losses in internal rotation, with osseous adaptations (retroversion) and muscular adaptations both being implicated. In a study of adolescent baseball players by Hibberd and colleagues, age-related increases in GIRD were primarily attributed to humeral retrotorsion rather than to soft tissue tightness. When the GIRD measurements of players of various age groups were adjusted for retrotorsion, no differences in GIRD were detected. Noonan and colleagues further investigated the relationship between GIRD and humeral retrotorsion in 222 professional baseball pitchers. Pitchers with GIRD displayed significantly less humeral torsion (i.e., greater retrotorsion) in their dominant arm compared with those without GIRD as well as greater side-to-side difference in humeral torsion. These authors suggested that greater humeral retrotorsion may place greater stress on the posterior shoulder, resulting in motion deficits and may predispose these pitchers to shoulder injury.


SICK Scapula and Scapular Dyskinesis


The scapula has three main functions during throwing that maximize force transmission from the trunk and torso to the humerus while avoiding risk of labral and rotator cuff injury. First, the scapula must optimize the position of the glenoid with respect to the rapidly rotating humeral head. Second, it must fluidly retract and protract around the thoracic wall as the arm moves through the phases of throwing, maintaining glenohumeral angulation within a safe zone. Third, it must act as a stable base for the origin of the extrinsic and intrinsic shoulder muscles that provide glenohumeral compression and regulate arm motion. These functions require optimal strength and coordination of the periscapular muscles. Weakness, inflexibility, or an imbalance of the periscapular and posterior rotator cuff muscles disturbs the normal anatomic static and dynamic relationships of the scapula. Burkhart and colleagues called the abnormally positioned thrower’s scapula a SICK scapula (scapular malposition, inferior medial border prominence, coracoid pain, and dyskinesis of scapular movement). Aberrant scapulothoracic motion has been called scapular dyskinesis .


The SICK scapula is an extreme form of scapular dyskinesis. Morgan also used the term “SICK scapula” to specifically define the static asymmetrical position of the thrower’s scapula, in contrast to “scapular dyskinesis,” which describes abnormal scapular motion. The hallmark of the SICK scapula is an asymmetrically drooping throwing shoulder and medial scapular winging ( Fig. 20-18 ). The scapular malposition is a combination of four changes in position: upward tilting, protraction, forward tilting in the sagittal plane, and inferior translation. Burkhart and colleagues have described three different subtypes of this syndrome depending on the structures fatigued. The first two are associated with posterosuperior labral tears and internal impingement, and the third is associated with rotator cuff tears. Type I stems from weak lower trapezius and serratus anterior muscles and inflexibility of pectoralis major and minor. This causes inferomedial scapular winging at rest and greater winging on cocking. Type II is predominantly caused by upper and lower trapezius and rhomboid weakness and does not have a large inflexibility component. It is identified by complete medial winging at rest, which worsens with cocking. Type III is associated with impingement lesions and involves superomedial winging of the scapula.




FIGURE 20-18


A, A patient with a SICK scapula (scapular malposition, inferior medial border prominence, coracoid pain, and scapular dyskinesis) demonstrates scapular asymmetry with inferior medial border prominence. B, After a therapy regimen consisting of scapular stabilizer muscle strengthening and reeducation, the scapulae are symmetrical.

(From Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: Spectrum of pathology. Part III: The SICK scapula, scapular dyskinesis, the kinetic chain, and rehabilitation. Arthroscopy. 2003;19[6]:641-661.)


The SICK scapula predisposes the shoulder to labral and rotator cuff tears because the scapula sits in a more protracted and upwardly tilted orientation, positioning the glenoid so it faces more anteriorly and superiorly. This position leads to three developments: anterior tension, posterior compression, and increased glenohumeral angulation. First, with glenoid protraction, the anterior band of the inferior glenohumeral ligament tightens, limiting anterior translation of the humeral head; over time, the ligament becomes susceptible to chronic strain. Second, simultaneously, the posterior edge of the glenoid is brought toward the humerus, placing the posterosuperior labrum and rotator cuff at risk of injury. Finally, excessive protraction increases glenohumeral angulation, which in a thrower will result in the arm lagging behind the body.


Excessive external rotation in this setting has two deleterious consequences: it exacerbates the aforementioned biceps peel-back effect, and with preexisting scapular protraction, external rotation and abduction can result in posterosuperior glenoid impingement. One study examined throwers with proven posterosuperior labral tears and found that a total of 60 out of 64 (94%) showed patterns of dynamic scapular dyskinesis.


Morgan has described a cascade of events that explains many pathologies associated with the SICK scapula: coracoid pain due to pectoralis minor traction tendinopathy, superior medial angle scapular pain from levator scapulae insertional tendinopathy, subacromial origin pain from acromial malposition and decreased subacromial space from upward tilting, acromioclavicular joint pain caused by anterior joint incongruity, sternoclavicular pain, thoracic outlet syndrome radicular pain, and subclavian vascular problems, such as arterial pseudoaneurysm or venous thrombosis.


Treatment for SICK scapula consists of scapular stabilizer muscular strengthening and reeducation. The kinetic chain is incorporated into the rehabilitation. The involved side is addressed first using closed-chain exercises followed by open-chain exercises. Scapular rehabilitation has been successful in returning patients with SICK scapula to their previous level of competitive play ( Fig. 20-19 ).




FIGURE 20-19


In the active compression test, the patient’s arm is forward-flexed to 90 degrees, adducted 10 to 15 degrees, and maximally internally rotated. The patient resists as the examiner applies a uniform downward force. The patient then maximally supinates the arm and the maneuver is repeated.

(Modified from O’Brien SJ, Pagnani MJ, Fealy S, et al. The active compression test: A new and effective test for diagnosing labral tears and acromioclavicular joint abnormality. Am J Sports Med. 1998;26[5]:610-613.)




Evaluation of the Overhead Athlete


The evaluation of the overhead athlete can be a diagnostic challenge that requires the close integration of history and physical examination findings while utilizing a systematic approach. 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.


History


A sport-specific approach should be used when evaluating the shoulder in an athlete. 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.


In throwers a detailed history with the chronology of symptoms is essential. In many cases the athlete only describes vague discomfort associated with throwing and a decrease in performance. Pitchers commonly complain of loss of pitch control and loss of velocity and also describe symptoms distant from the shoulder joint. A preseason examination is also critical to document baseline shoulder stability, strength, and ROM, which can be used as a reference when evaluating a mid-season injury. Instability often exists in these patients, but they do not present with symptoms of frank subluxation or dislocation. The throwing phase in which the pain occurs gives direct clues to the underlying pathoanatomy. For example, pain during cocking is often a result of instability or internal impingement with a type II SLAP lesion, whereas pain during follow-through arises from rotator cuff or posterior capsular problems.


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 impingement.


Athletes can also 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 (such as 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. The location of pain or instability, its duration, and response to prior treatment should be noted for all athletes.


Physical Examination


As outlined in the biomechanics section, pathology related to overuse injuries is a continuum and the result of a highly coordinated cascade of movements. Therefore when investigating shoulder complaints, the clinician should also perform a global assessment of related joints, including the spine, elbow, hips, and core area.


Inspection


Both upper extremities should be exposed. The examination begins with inspection of the shoulders for symmetry, with special attention to the acromioclavicular joints, scapular asymmetry, and hypertrophy of the muscles of the dominant arm. Muscle atrophy, particularly the infraspinatus in baseball players, and scapular winging should be noted, as should any surgical incisions.


Range of Motion


Both active and passive ranges of motion (ROM) of the glenohumeral and scapulothoracic joints are measured. Forward elevation in the plane of the scapula, external rotation, and internal rotation in both 0 degrees and 90 degrees of abduction should be documented (in 0 degrees of abduction this is the highest spinal level the patient can reach with the thumb behind the back). During forward elevation with the arm at the side, the 2 : 1 glenohumeral/scapular motion ratio should be maintained. (The first half of the motion is primarily glenohumeral, and the second half of the elevation arc should move in a 1 : 1 glenohumeral/scapulothoracic ratio.) As noted previously, the dominant arm in many overhead athletes may demonstrate an increase in external rotation and a concomitant loss in internal rotation. These rotational values should be compared with those of the contralateral limb, and the total arc of motion for both shoulders recorded.


Examination of the scapula should include observing the cervical and thoracic posture, scapular symmetry at rest and with ascending and descending arm motion in both flexion and abduction, and active scapular retraction and elevation.


The scapular lateral slide measurements, devised by Kibler, are used to assess scapular asymmetry by comparing the distance from the inferior angle of the scapula to the spinous process of the thoracic vertebra in the same horizontal plane (the reference vertebra) in three test positions. In position 1 the arm is at the side. In position 2 the humerus is internally rotated and abducted 45 degrees, as the hands are placed on the hips. In position 3 the shoulder is abducted further to 90 degrees. An asymmetrical difference of greater than 1.5 cm determines a positive lateral scapular slide test.


Palpation


Several structures can be easily palpated, including the glenohumeral joint lines, the acromioclavicular joint, the long head of the biceps (LHB) tendon, and the coracoid process. Tenderness over the acromioclavicular joint is suggestive of acromioclavicular joint pathology. Tenderness over the LHB tendon may indicate tendinitis or a SLAP tear. Coracoid process tenderness suggests pectoralis minor tendinitis or tightness, which has been correlated with scapular protraction and dyskinesis.


Strength


Manual muscle strength testing should aim to isolate the muscle being tested, comparing the injured with the uninjured side. The supraspinatus can be isolated in the empty can position. The subscapularis is best assessed either by the lift-off test described by Gerber and Krushell or by the internal rotation lag sign, which is more sensitive.


Internal Impingement


Apprehension Relocation


The patient is positioned supine on a table. The shoulder is brought into the classic position of internal impingement (≥90 degrees of external rotation, ≥90 degrees of abduction). An anteriorly directed force applied on the posterior aspect of the shoulder will elicit pain but not apprehension. The pain is then relieved with the examiner’s hand applying a posteriorly directed force on the anterior aspect of the shoulder.


Active Compression Test


The active compression test, also known as the O’Brien test (see Fig. 20-19 ), evaluates pathology of the biceps and superior labrum complex. The shoulder is brought to 90 degrees of forward flexion and 15 degrees of adduction. Resisted forward elevation is then performed with the thumb pointing down (internal rotation) and pointing up (external rotation). Deep pain during internal rotation but not during external rotation indicates a biceps-labrum complex problem. Pain on top of the shoulder is likely to be due to acromioclavicular joint pathology.


Impingement


Neer Impingement Sign


The shoulder is forcibly elevated while stabilizing the scapula. If there is impingement, pain is classically reproduced at about 90 degrees of forward elevation.


Hawkins Impingement Sign


The shoulder is placed in 90 degrees of forward elevation and 30 degrees of forward flexion and is forcibly internally rotated. Pain evoked in this position is considered a further evidence of impingement.


Acromioclavicular Joint


Acromioclavicular joint pathology is a clinical diagnosis. Pain in the acromioclavicular joint with cross-body adduction and tenderness over the acromioclavicular joint are relatively sensitive and specific. Pain in the acromioclavicular joint area during the active compression test can also denote acromioclavicular joint pathology.


Scapular Provocative Maneuvers


Scapular Assistance Test


Scapular upward rotation is assisted by manually stabilizing the upper medial scapular border and rotating the inferomedial border as the arm is abducted. A positive test relieves symptoms of impingement, clicking, or rotator cuff weakness that are present without the manual assistance.


Scapular Retraction Test


The entire medial border of the scapula is manually stabilized. In patients with apparent rotator cuff weakness and a protracted scapula, if the manual stabilization increases strength, this is positive for scapular dyskinesis. In patients with a positive apprehension relocation test, if the stabilization reduces the pain of impingement during the test, this also suggests that the scapula should be included in the rehabilitation protocol.


Imaging


Standard radiographs and magnetic resonance imaging (MRI) are a critical part of the diagnostic armamentarium for treating athletes’ shoulders. Imaging interpretation and diagnoses are discussed in detail in another chapter.




Treatment


Posterior Capsule Contracture


Nonoperative Treatment


Nonoperative management has proven successful in managing excessive GIRD (greater than 20 degrees). Some authors have described a series of exercises that theoretically improve posterior capsular contracture and reduce GIRD with some reliability. These include sleeper stretches ( Fig. 20-20 ), in which the athlete lies on one side with the shoulder in 90 degrees of flexion, in neutral rotation, with the elbow in 90 degrees of flexion as well. The shoulder is then passively internally rotated by pushing the forearm toward the table around the fixed point of the elbow.




FIGURE 20-20


A, The sleeper stretch stretches the posterior capsule. The patient lies on one side with the shoulder neutrally rotated and in 90 degrees of flexion. The elbow is held in 90 degrees of flexion. The forearm is pushed down toward the table to stretch the posterior capsule. B, The rollover sleeper stretch in which the patient is lying on the stomach, thereby adducting the arm. As with the sleeper stretch, the forearm is pushed toward the table to stretch the posterior capsule. C, In the doorway stretch, the patient stands in a doorway with the shoulder abducted 90 degrees and maximally internally rotated. The door frame is used to apply leverage to the forearm to further internally rotate the shoulder and stretch the posterior capsule. D, The cross-arm adduction stretch stretches the posterior rotator cuff and the posterior capsule.


Others have recommended stretches to improve posterior shoulder flexibility, although they have cited posterior muscle contracture rather than capsule tightness as the component that requires stretching. These stretches include the internal rotation stretch and the horizontal adduction stretch. In the internal rotation stretch, the arm is placed in the throwing (cocked) position and then internally rotated to stretch the posterior rotator cuff. In the horizontal adduction stretch, the arm is horizontally adducted while the scapula is stabilized. The pectoralis minor should also be stretched. This can be effected by placing a rolled towel between the supine athlete’s shoulder blades and steadily pushing posteriorly on the shoulders. In addition to the aforementioned stretches, the trapezius muscle and the periscapular retractor and protractor muscles should be strengthened.


In one specific rehabilitation program four phases have been outlined. Phase I is the acute phase and calls for modalities, such as ice, ultrasound, electrical stimulation, and NSAIDs. During this phase, internal rotation stretches and periscapular strengthening are instituted. Phase II is the intermediate phase and involves more aggressive isotonic strengthening activities with the goal of restoring muscle balance. Stretching is continued. Phase III is the advanced strengthening phase and employs plyometric exercises to enhance power and endurance and gradually incorporates throwing drills. Finally, phase IV is the return to throwing phase and involves progression of an interval throwing program.


Operative Management


The rate of failure of conservative measures, such as sleeper stretches, is exceedingly low, and operative management should only be pursued after aggressive physiotherapy. A thorough examination under anesthesia should be performed prior to diagnostic arthroscopy, documenting bilateral shoulder ranges of motion at 0 and 90 degrees of abduction to confirm the presence of a posterior capsule contracture. The procedure consists of an arthroscopic posteroinferior quadrant capsulotomy, from the 6 o’clock position to the 3 o’clock or 9 o’clock position. The capsule should be incised until the muscle belly of the external rotators can be visualized. Morgan found an average of 62 degrees (range, 55 to 68 degrees) of increase in internal rotation after the capsulotomy. Yoneda and colleagues performed posterior capsular releases on 16 patients and reported that 11, including all four who had no other concomitant lesions, returned to their preinjury level of performance.


SLAP Lesions


Variations in Normal Superior Labrum Anatomy


Appreciating the normal anatomic variants of the superior labrum and biceps insertion is critical to recognizing abnormal pathology. First, the labrum inferior to the glenoid equator is consistently a rounded, fibrous structure continuous with the articular cartilage, whereas the superior labrum has a high degree of normal variation, typically either rounded ( Fig. 20-21A ) or meniscoid (see Fig. 20-21B ), with the meniscal component overlying but not attached to the glenoid articular surface. In one series 49 of 191 patients demonstrated a mobile meniscoid type of superior labrum at arthroscopy and were treated with observation alone. Only one of these patients became clinically symptomatic, which highlights the nonpathologic nature of this anatomic variant.




FIGURE 20-21


A, Round morphology of the superior labrum. B, Meniscoid morphology of the superior labrum.


Second, there are three predominant labral variations that occur in over 10% of the population as reported by Rao and colleagues. The sublabral recess represents a small potential space under the biceps anchor and the anterosuperior labrum and is often present at the 12 o’clock position. The Buford complex is a normal variant that consists of a cordlike middle glenohumeral ligament that originates directly from the superior labrum at the base of the biceps tendon. As a result, there is an absence of anterosuperior labral tissue ( Fig. 20-22 ). The sublabral foramen also involves a cordlike middle glenohumeral ligament that attaches directly to the anterosuperior labrum, creating a hole between the ligament and the glenoid. Inappropriate surgical attachment of this cordlike middle glenohumeral ligament to this void on the anterosuperior glenoid results in painful restriction of external rotation and elevation. The incidence of the cordlike middle glenohumeral ligament in isolation (18%) is more common than that in combination with the Buford complex (1% to 2%).




FIGURE 20-22


Example of a Buford complex with a cord-like middle glenohumeral ligament (double dots) underneath the probe attaching to the anterior biceps (single dot) and a sublabral foramen inferior to the middle glenohumeral ligament.


Superior Labrum-Biceps Complex and Stability


The labrum adds stability to the glenohumeral joint by providing depth and surface area to the glenoid. The function of the LHB tendon in glenohumeral stability remains controversial. For example, studies using EMG suggest that the biceps muscle is active with elbow function only. Other biomechanical studies however suggest that the biceps tendon might act as an anterior and inferior dynamic stabilizer of the glenohumeral joint. One study found that isolated lesions of the anterosuperior portion of the labrum that do not involve LHB had no significant effect on anteroposterior or superoinferior glenohumeral translation. In contrast, complete lesions of the superior labrum and biceps insertion resulted in significant increases in glenohumeral translation. Biomechanical studies have demonstrated that repair of type II SLAP lesions restores glenohumeral stability in both anterior-posterior and inferior translations.


Classification


Snyder originally described four types of SLAP lesions :




  • Type I lesions consist of fraying and degeneration of the superior labrum without instability of LHB attachment ( Fig. 20-23A ).




    FIGURE 20-23


    A, Type I SLAP (scapular malposition, inferior medial border prominence, coracoid pain, and scapular dyskinesis) lesion. Fraying (arrow) of the superior labrum without degeneration of the biceps anchor. B, Type II SLAP lesion. Detachment (arrow) of the biceps tendon anchor from the superior glenoid tubercle. C, Type III SLAP lesion. Bucket-handle tear of a meniscoid labrum (single dot) with an intact biceps tendon anchor (double dots). D, Type IV SLAP lesion. A superior labral tear that extends into biceps tendon. The arrow points to superior labral detachment extending into the split biceps.



  • Type II lesions consist of detachment of the biceps tendon anchor from the superior glenoid tubercle ( Fig. 20-23B ). Morgan and colleagues later subclassified type II SLAP lesions into anterior, posterior, and combined anterior-posterior lesions.



  • Type III lesions consist of a bucket-handle tear of a meniscoid superior labrum with an intact biceps tendon anchor ( Fig. 20-23C ).



  • Type IV lesions consist of a superior labral tear that extends into the biceps tendon ( Fig. 20-23D ).



Historically, the incidence of each type of lesion has been reported as 74% type I, 21% type II, 0.7% type III, and 4% type IV. In addition, most SLAP lesions (123 of 139, 88%) can be associated with other intra-articular lesions. Different SLAP types may also coexist as complex lesions; typically, type III or IV lesions manifest in conjunction with a significantly detached biceps anchor (a type II lesion).


Several modifications have been made to the original Snyder classification. Maffet and colleagues expanded the criteria to include three additional subtypes: type V lesions where an anteroinferior Bankart labral lesion exists in continuity with a SLAP tear, type VI lesions with biceps tendon separation and an unstable flap tear of the labrum, and type VII lesions with separation of the biceps tendon–superior labrum complex that extends anteriorly to the middle glenohumeral ligament. Powell and colleagues added three further types: type VIII lesions, where a type II tear has a posterior extension to the 6 o’clock position; type IX lesions, representing a more extensive tear with circumferential involvement of the labrum; and type X lesions, where a superior labral tear is combined with a posteroinferior labral tear (a reverse Bankart lesion).


SLAP Lesions and Throwing


Andrews and colleagues first observed anterosuperior glenoid labrum tears in throwers and postulated that these resulted from traction injuries that occurred in the follow-through phase of throwing, with the biceps eccentrically decelerating the rapidly extending elbow. Burkhart and Morgan described the “peel-back” phenomenon occurring during late cocking, reproducible during an arthroscopic examination, consisting of a torsional force applied to the biceps anchor. Torsional forces in the biceps-labral complex increase as the arm moves into abduction and hyperexternal rotation. The biceps tendon changes from a relative horizontal to a vertical position, producing a twist at the base and thus transmitting the torsional forces to the posterosuperior labrum.


Biomechanical studies have further improved our understanding of the various mechanisms by which SLAP lesions are created. Bey and colleagues found that traction on the biceps tendon can reproducibly create type II SLAP lesions if the glenohumeral joint is inferiorly subluxated. Clavert and colleagues simulated falls on an outstretched hand and found that falling forward on an outstretched hand reliably produced type II SLAP lesions. They postulated that shearing forces were critical to the pathogenesis of these lesions. Kuhn and colleagues studied the throwing motion and found SLAP lesions occurred more commonly in the late cocking position than in the early deceleration position, further supporting the “peel-back” mechanism of injury.


Diagnosis


History


The clinical presentation of the SLAP tear varies; it may be the result of a single traumatic event or it can be more subtle as seen in the overhead athletes. Anterior shoulder pain is the most common complaint, but throwing athletes may present with impaired performance or a loss of velocity and control. Anterosuperior or posterosuperior shoulder pain may be exacerbated by overhead activities, and mechanical symptoms, including popping, locking, and snapping, can occur with unstable tears. Frank instability symptoms are rare, but may be present if the tear extends into the anterior ligament and labrum, resulting in a Bankart lesion.


Anterior traction injuries result from sports, such as water skiing, where the shoulder is pulled forward. Superior traction injuries result from attempting to break a fall from a height. Inferior traction injuries result from a sudden inferior pull. Compression of the glenohumeral joint as a result of a fall onto an outstretched hand in forward flexion and abduction or a direct blow to the glenohumeral joint causes an impaction injury of the humeral head against the superior labrum and the biceps anchor. A type II lesion results when the biceps tendon is avulsed from the superior glenoid as it is tensioned over the humeral head. If a meniscoid-type superior labrum is present, a type III or IV lesion can result with the formation of a bucket-handle fragment.


Physical Examination


The clinical diagnosis of superior labral lesions is challenging, and numerous examination maneuvers have been described for them. Most of these tests are relatively sensitive, but often lack specificity. They include the active compression, compression-rotation, Speed, and apprehension-relocation tests. For the active compression test, the arm is positioned in 15 degrees of adduction and 90 degrees of forward elevation. The examiner applies a downward force on the forearm while the hand is pronated and supinated and compares the resulting pain and weakness. A positive test occurs when the patient reports pain that is worse in the pronated position.


The compression-rotation test is similar to McMurray’s test of the knee. It is performed by compressing the glenohumeral joint and then rotating the humerus in an attempt to trap the labrum in the joint. This test should be performed in the supine position, where the patient is more relaxed. Speed’s biceps tension test is also sensitive for SLAP lesions. This is performed by having the patient resist downward pressure with his or her arm in 90 degrees of forward elevation with the elbow extended and the forearm supinated. Although this test is more suggestive of biceps tendon damage, an unstable biceps anchor causes the test to elicit pain. A positive apprehension-relocation sign for posterior shoulder pain might suggest a SLAP lesion in the posterior labrum as part of a spectrum of internal impingement.


Many other tests have been described, including the biceps load test II, the anterior slide test, and the pain provocation test, but their utility has been questioned. Meserve and colleagues performed a meta-analysis that evaluated the sensitivity and specificity of physical exam maneuvers for SLAP lesions. They suggested that the active compression test is the most sensitive and also the most predictive for ruling out SLAP tears. Furthermore, Cook and colleagues conducted a prospective case-control study testing the diagnostic accuracy of five unique tests (the active compression, Speed, biceps load II, dynamic labral shear, and labral tension tests) and concluded that each of these provided little or no value for the diagnosis of SLAP tears.


One study has evaluated the Speed test, the Yergason test, the active compression test (O’Brien’s), the apprehension relocation test, the crank test, and tenderness of the bicipital groove. The examination results were compared with surgical findings and analyzed for sensitivity and specificity in the diagnosis of SLAP lesions and other glenoid labral tears. The results of the O’Brien test (63% sensitive, 73% specific) and apprehension-relocation test (44% sensitive, 87% specific) were statistically correlated with the presence of a labral tear, and a positive apprehension test (pain) approached statistical significance. Performing all three tests and accepting a positive result for any of them increased the statistical value, although the sensitivity and specificity were still disappointingly low (72% and 73%, respectively). The other four tests were not found to be useful for labral tears, and none of the tests or combinations was statistically valid for the specific detection of a SLAP lesion.


Imaging


Radiographic evaluation includes anteroposterior, axillary, and outlet views of the shoulder. No specific radiographic abnormalities are pathognomonic for SLAP tears, but concomitant bony lesions including posterior labral ossification, outlet impingement, and acromioclavicular joint disease can be detected. MRI-enhanced arthrography is superior to plain MRI for diagnosing SLAP lesions as the intra-articular contrast medium provides a clearer delamination of the normal anatomic variants of the superior labrum. The diagnostic feature of the MR arthrogram is contrast between the superior labrum and the glenoid that extends around and under the biceps anchor on the coronal oblique image ( Fig. 20-24 ). The axial views visualize possible extension into the anterior and or posterior labrum. MR arthrography is also helpful in identifying the presence of a spinoglenoid cyst and provides the best differentiation between a type II SLAP tear and a normal sublabral recess. Bencardino and colleagues demonstrated a sensitivity of 89%, specificity of 91%, and accuracy of 90% for detecting labral lesions using MR arthrography.




FIGURE 20-24


Coronal image of a magnetic resonance arthrogram demonstrating a superior labral tear (arrow).


However, despite excellent sensitivity in identifying SLAP lesions, not all abnormalities are clinically significant, and thus careful correlation with physical examination and clinical history is warranted. There can be a high incidence of clinically false-positive MRI findings in the dominant shoulder of the overhead athlete, including partial- or full-thickness rotator cuff tears, labral ossification, and partial tears of the anteroinferior or superior glenoid labrum.


Arthroscopic Evaluation


Although the history, physical examination, and MRI can provide useful information in the diagnosis of SLAP lesions, diagnostic arthroscopy remains the gold standard. It is essential to view the joint from both the anterior and posterior portals to thoroughly assess the degree of involvement. Diagnosis of type II lesions can be challenging as the normal superior labrum often has a small cleft between it and the glenoid, especially in the setting of a meniscoid labrum. The stability of the biceps anchor is determined by probing and attempting to elevate the labrum and biceps. The glenoid articular cartilage usually extends medially over the superior corner of the glenoid. An absence of cartilage in this region indicates labral detachment. Traction on the biceps tendon is indicative of a loss of integrity at the superior labral attachment. Burkhart and Morgan have described an arthroscopic examination for “peel back.” The arm is placed in a throwing position with humeral external rotation, and the labrum peels away from the posterosuperior glenoid.


Treatment


Nonoperative Management


The role of nonoperative management of unstable SLAP lesions remains controversial. Snyder has argued that nonoperative treatment generally yields poor results, although few studies have focused on the natural history of nonsurgical SLAP tears. In one study patients were treated with an extended trial of activity modification, rehabilitation exercises, corticosteroid injections, and NSAIDs without any significant relief of their symptoms. In contrast, Edwards and colleagues demonstrated that 10 (67%) of 15 overhead throwing athletes treated with a nonoperative regimen were able to return to the same or improved level of play compared with preinjury.


For patients with an acute injury, initial treatment should be directed at eliminating pain, restoring motion, correcting strength deficits, and restoring normal synchronous muscle activity. This includes rest from provocative activities, antiinflammatory medication, and therapeutic modalities. Strengthening is initiated once the pain is resolved. For throwing athletes, a gradual return to throwing may begin as muscle balance and ROM are restored. Treatment may be directed toward surgical intervention if there is failure of the nonoperative program, early suspicion of significant mechanical dysfunction, or a seasonal timing issue.


In throwing athletes, SLAP lesions may coexist with articular-sided tears of the rotator cuff and posterior capsular contractures. Classic subacromial bursitis symptoms and external impingement might also be present. Kibler and colleagues found a high incidence of scapular dyskinesis associated with SLAP lesions. Nonoperative management should therefore include stretching maneuvers for the posterior capsule and rotator cuff as well as exercises for balance and for restoring scapular dynamic stability. Symptoms of subacromial bursitis may be treated with NSAIDs or subacromial corticosteroid injection. Rotator cuff strengthening may proceed only after the restoration of proper capsular elasticity and scapular dynamics. This process can require 6 to 12 weeks before throwing can be initiated. Treatment may be directed toward earlier surgical intervention if there is failure of the nonoperative program, persistent pain, mechanical symptoms and dysfunction, or seasonal timing issues.


Operative Management


The surgical management of SLAP lesions continues to evolve. Treatment options include debridement, labral repair, biceps tenodesis, and combinations of these. Labral repair is performed using suture anchors with either traditional knots or knotless techniques.


Type I SLAP lesions are typically treated with debridement alone. Type II SLAP lesions can be debrided or repaired back to the glenoid rim with suture anchors. For type III SLAP lesions, if the unstable bucket-handle fragment is small, simple resection suffices, but repair is preferable if the unstable fragment is large. Type IV SLAP lesions are treated similarly to type III lesions, and the tendon split is managed with tenotomy, tenodesis, or repair. Management options for the biceps tendon depend on the age and activity level of the patient and on the condition of the remainder of the tendon. Superior labral tears should not be repaired in the face of adhesive capsulitis and should be repaired with caution in patients with significant glenohumeral chondromalacia. Further tightening these shoulders with labral repair can significantly aggravate pain, further compromise their ROM, and accelerate the development of glenohumeral arthrosis.


Surgical Repair Technique


Although labral repairs may be performed in either the beach chair or the lateral decubitus position, we prefer the lateral decubitus position with traction to improve superior visualization and provide better access to the posterior labrum ( Fig. 20-25 ). The patient is positioned in approximately 20 degrees of reverse Trendelenburg position and tilted slightly posteriorly to bring the glenoid parallel to the floor. Typically, 10 lb of traction is applied to the arm with a modular joint distractor or a limb positioner, with care taken to avoid overdistraction in order to prevent brachial plexus injury.




FIGURE 20-25


The patient is placed in the lateral decubitus position to facilitate visualization of the anterior and posterior labrum.


Diagnostic arthroscopy is used to confirm the diagnosis of a SLAP lesion. The superior labrum is probed to test the integrity of the biceps-labral attachment to the glenoid. True avulsion of the superior labrum is indicated by fraying and irregularity of the labral undersurface as well as visible chondromalacia of the normally smooth hyaline cartilage of the underlying superior glenoid rim. Arthroscopic examination should include placing the shoulder in the late cocking position of throwing and examining the posterosuperior labrum for possible peel back. During this test, pathologic hypermobility of the posterosuperior labrum and traction of the posterior capsule causes the biceps-labral complex to be pulled medially off the articular edge of the glenoid. The articular surface of the rotator cuff is also examined in this position for delamination and tears. The stability of the entire circumference of the labrum as well as that of anterior and posterior capsule is examined.


Degenerative tissue is debrided from the labrum, biceps, and articular surface of the rotator cuff. This facilitates visualization of damaged tissue that might require repair. In cases of extensive labral tearing or concomitant rotator cuff pathology, our preferred order of repair is as follows: the anteroinferior labrum, proceeding superiorly along the anterior glenoid to the glenoid sulcus; the posteroinferior labrum, proceeding from inferior to superior; the anterosuperior labrum; and finally the rotator cuff.


Care should be taken not to overtighten the tissue or over-constrain the biceps anchor. Placement of anchors anterior to the biceps tendon should be avoided to prevent inadvertent tightening of the middle glenohumeral ligament or closure of a sublabral forearm, which can cause loss of external rotation. Sutures should be placed so as to include the labrum and just enough of the capsular reflection to ensure tissue integrity. Likewise, anchors and sutures should not be placed directly at the biceps-labral base in order to preserve maximal biceps excursion with external and internal rotation.


For a reparable superior labral lesion, the anterior and posterior extent of the labral avulsion is determined. An anterior portal high within the rotator interval provides the best angle of inclination for placing anchors in the anterosuperior glenoid rim ( Fig. 20-26 ). Prior to anchor insertion, the bony surface should be debrided to enhance healing. A motorized shaver is introduced through the anterior working portal to prepare the superior neck of the glenoid beneath the detached labrum. Preferably, percutaneous techniques that minimize morbidity to the supraspinatus tendon should be used. A spinal needle is used to find a position at the desired angle on the glenoid at the location of the Wilmington portal, posterior to the biceps. A small stab incision allows introduction of the drill guide, which penetrates the supraspinatus tendon ( Fig. 20-27 ). The anchor is placed adjacent to the biceps tendon at the glenoid articular margin. The suture anchor must be visualized and confirmed to be in bone, and it must be tested with tension to confirm its security. Suture passage through the labrum is next; we prefer the suture-shuttling technique as the instruments have low profiles and are less traumatic to the labral tissue. In this technique the suture limb facing the labrum is retrieved from the anterior portal. The suture-passing device is passed through the labrum, and the suture shuttle is retrieved through the anterior portal ( Fig. 20-27D ). The suture is then shuttled through the labrum and out the posterior cannula. If a vertical mattress stitch is elected for a meniscoid labrum, the second suture limb is passed through the labrum. Both suture limbs are then retrieved through the anterior cannula, with the cannula placed posterior to the biceps to facilitate knot tying. Knot tying should aim to ensure the knots are kept away from the glenohumeral articulation. A probe is used to assess the stability and tension of the repair. The process of anchor placement, suture passing, and knot tying is repeated anteriorly and posteriorly as needed ( Fig. 20-27F ).




FIGURE 20-26


Portals used for labral repair include anterior (A) , posterior (B) , and the portal of Wilmington (C) .



FIGURE 20-27


Percutaneous SLAP (scapular malposition, inferior medial border prominence, coracoid pain, and scapular dyskinesis) lesion repair technique. A, Anchor guide in position on the glenoid. B, Anchor placed. C, Suture passer introduced percutaneously. D, Suture passing. E, Knot tying with the anterior cannula placed posterior to the biceps tendon. F, First anchor complete.


Knotless fixation devices have the advantages of eliminating the need for knot-tying and reducing potential chondral irritation from the knots themselves ( Fig. 20-28 ). The results of SLAP repairs have not been as consistent in throwing athletes as in other patient populations. Dines and ElAttrache have suggested that the limited glenohumeral joint space combined with the bulky knots used to secure the labrum to the anchor may be a cause of discomfort. They prefer a horizontal mattress-knotless anchor technique that better recreates the normal meniscoid appearance of the superior labrum.




FIGURE 20-28


Knotless SLAP (scapular malposition, inferior medial border prominence, coracoid pain, and scapular dyskinesis) lesion repair. A, Probe demonstrating tear. B, Two knotless vertical mattress sutures have been placed.


Rehabilitation


Postoperatively, the shoulder should be protected in a sling for 3 weeks to prevent undue stress on the biceps tendon. The patient begins elbow, wrist, and hand exercises immediately postoperatively and gentle pendulum exercises in 1 week. Strengthening exercises for the rotator cuff, scapular stabilizers, and deltoid are initiated with the goal of restoring full ROM at 6 weeks. Biceps strengthening is initiated 8 weeks postoperatively. Vigorous or strenuous lifting activities are implemented after 3 months, and at 4 months, throwing athletes can begin an interval throwing program on a level surface. They continue a stretching and strengthening program, with particular emphasis on posteroinferior capsular stretching. At 6 months, pitchers may begin throwing full speed, and at 7 months they are allowed maximal effort throwing from the mound.


Outcomes


Historically, simple debridement yielded poor results for unstable SLAP lesions. As fixation techniques evolved, outcomes of surgical repair have improved. Stapling and absorbable tack devices initially yielded good outcomes compared with debridement alone, but these were later abandoned due to implant-related complications, including synovitis, foreign body reaction, adhesive capsulitis, and breakage.


Suture anchors have emerged as the gold standard for repair, achieving more reliable results compared with previous devices. Kim and colleagues reported 94% satisfactory results after repair with suture anchors in 34 patients with isolated SLAP lesions; 91% regained their preinjury level of shoulder function. Similarly, 87% of throwing athletes in a study by Morgan and colleagues were able to return to preinjury levels of throwing after suture anchor repair. However, although these studies demonstrated a high level of success following repair, more recent investigations indicate that returning overhead athletes to their preinjury level of performance may be more difficult than previously thought. Yung and colleagues reported that elite overhead athletes may take longer to rehabilitate before returning to sport. Of the 13 patients involved in overhead sports in their cohort, 4 took more than 11 months to return and 1 never returned to competitive play. Sayde and colleagues published a systematic review involving 506 patients with type II SLAP tears from 14 studies. Although “good to excellent” satisfaction was reported for the patient population as a whole, only 63% of overhead athletes were able to return to their previous level of play. The authors did note that there may also be a high incidence of concomitant pathology (such as rotator cuff tears or instability), especially in the throwing athletes, which may have affected the final outcomes. Furthermore, most studies included a mixed population of young competitive athletes with older recreational athletes and reported outcomes as an initial “return to sport” rather than full return to the prior level of performance. In an investigation of SLAP repairs in elite overhead athletes, Neri and colleagues showed a return to preinjury level of competition in only 57% of the patients. Inability to return to competition was correlated with the presence of partial-thickness rotator cuff tears.


Other studies have implicated age as a risk factor for SLAP repair failure. Provencher and colleagues prospectively evaluated 179 patients with type II SLAP tears and demonstrated a 37% repair failure rate with 28% of patients requiring revision surgery. Age over 36 years was cited as an independent risk factor for failure. Despite these recent reports, SLAP repairs in this subset of patients continue to increase.


Biceps Tenodesis


Tenodesis of LHB for lesions associated with rotator cuff tears has yielded satisfactory results. As the reported results of SLAP repairs in overhead athletes have been inconsistent, some authors have suggested biceps tenodesis as an alternative to reinsertion (labral repair). There has been speculation over the rationale for why some overhead athletes have difficulty returning to sport following SLAP repair. Alpantaki and colleagues showed that LHB is innervated by a dense network of sensory sympathetic fibers, and these fibers may serve as a source of residual pain following arthroscopic SLAP repair. Rigid fixation of the superior labrum using suture anchors may also restrict the physiologic excursion of the biceps anchor during shoulder elevation, abduction, and rotation, generating pain in throwing movements. Studies have also demonstrated reduced vascularity in the superior osseous glenoid and the superior labral complex. A biceps tenodesis can be advantageous in this environment as it eliminates the pull of the biceps on the repair site and does not require healing in the relatively avascular superior glenoid.


A biceps tenodesis attempts to circumvent potential sources of residual biceps pain in the athlete and can be performed using an all-arthroscopic suprapectoral or an open subpectoral technique. The optimal surgical approach, tenodesis location, and choice of fixation have been the subject of considerable research, but there is a lack of consensus over these in the orthopedic community.


Arthroscopic Biceps Tenodesis Technique


Our preferred technique places the tenodesis location distal to the bicipital groove and is performed according to the method previously described by Lutton and colleagues ( Fig. 20-29 ). The procedure is completed in the modified beach chair position using regional (interscalene) anesthesia. The surgical arm is positioned and adjusted with the use of a limb positioner. Standard arthroscopic portals including a posterior viewing and anterior working portal through the rotator interval are utilized. LHB is released from its superior labral attachment using arthroscopic scissors and the remaining stump and superior labrum are debrided. A tagging suture is not routinely placed in LHB prior to tenotomy. The arthroscope is inserted into the subacromial space and a lateral portal is created using an outside-in technique. Bursectomy of the subdeltoid space is completed to facilitate visualization.


Jun 9, 2019 | Posted by in ORTHOPEDIC | Comments Off on The Shoulder in Athletes

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