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 ).

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.

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.

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.

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 ).

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 ).

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.

Phases of Freestyle Swimming

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.

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.

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.

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.

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.)

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

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

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.

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.

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.

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%).

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 :

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

  
  

  
  

  
  

  

  
  

  
  

  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.

  
  
  
  
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  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.

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

  
  
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  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

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.

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.

Treatment

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.

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 ).

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

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.

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.

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