Throwing exerts great stress on the shoulder. As a result, the shoulder is a common site of pathology and disability in these athletes. Conte et al. reported that shoulder injuries accounted for 28% of all injuries sustained by professional baseball pitchers. Each athlete presents unique diagnostic and therapeutic challenges, and an understanding of sport-specific biomechanics and pathology is essential. Throwing athletes repeatedly accelerate and decelerate their shoulders over a wide arc of rotation, causing repetitive microtrauma to the static and dynamic stabilizers of the glenohumeral and scapulothoracic joints. 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. This chapter provides a comprehensive overview of the pathophysiology, evaluation, and management of shoulder injuries specific to the throwing athlete.
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. 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 knee and hip 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, 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.
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 the 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. 7.1 ). 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.
Wind-up
The wind-up ( Fig. 7.2 ) 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. 7.3 A). Inexperienced throwers often have flawed form with poor trunk tilt and less hip advancement toward home plate ( Fig. 7.3 B).
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 ( Fig. 7.2 B). 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. 7.4 B) instead of remaining on top ( Fig. 7.4 A), 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. 7.5 A). 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. 7.5 B). 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.
Late cocking
The left foot hits the ground pointing in the direction of home plate, leaving the legs stretched apart ( Fig. 7.2 C). 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 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. 7.6 A); inexperienced throwers often have their elbows in a suboptimal lower position ( Fig. 7.6 B).
Acceleration
Once the humerus reaches maximal external rotation, the hand carrying the ball accelerates in a rapid arc of internal rotation ( Fig. 7.2 D). 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. 7.7 ).
Deceleration
After 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 ( Fig. 7.2 E). 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 ( Fig. 7.2 F). 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 vs. 0.14 kg for the baseball). , The observed injury patterns also differ, with predilection toward overuse disorders, such as biceps tendinitis 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 continues 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.
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 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. 7.8 ). 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 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. 7.9 ) 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 shift of the posterosuperior humeral head 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.
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. 7.10 ). 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.
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. *
* References , , , , , .
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 superior labrum anterior and posterior (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. †
† References , , , , , .
Several distinct processes appear to play a role in the development of throwing pathology, with these processes considered to be a continuum ( Fig. 7.11 ).
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. 7.12 ). 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.
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. 7.13 ). With repetitive throwing, the biceps tendon can further peel the biceps anchor off the glenoid lip.
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 (ROM), 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 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 undersurface of the posterior cuff begins to fail, and the picture of internal impingement arises.
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. 7.14 ). Failure to stabilize the scapula incorporates scapulothoracic motion into the total rotational arc, leading to confounding measurements.
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. 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. 7.15 ). 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 rotator cuff tears and involves superomedial winging of the scapula.
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. 7.16 ).
Evaluation of the throwing athlete
The evaluation of the throwing 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
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.
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.
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 and scapular winging should be noted, as should any surgical incisions.
Range of motion
Both active and passive 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 and 90 degrees of abduction should be documented (in 0 degree 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.
Relocation test
Described by Jobe as pain with a posteriorly directed force with the shoulder in 90 degrees of abduction and maximal external rotation. An anterior load relieves the pain.
Active compression test
The active compression test, also known as the O’Brien test (see Fig. 7.16 ), 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.
Internal impingement sign.
Pain in the deep posterior shoulder when the arm is placed into maximal external rotation with the arm abducted 90 to 110 degrees and 10 to 15 degrees of extension.
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. The test is not specific as it tends to be positive with a number of different shoulder conditions.
Hawkins impingement sign
The shoulder is placed in 90 degrees of forward flexion with the elbow flexed 90 degrees. The shoulder is then forcibly internally rotated. Pain evoked in this position is considered further evidence of impingement. The test is not specific as it tends to be positive with a number of different shoulder conditions.
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 (>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. 7.17 ), 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.
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 nonsteroidal antiinflammatory drugs (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
Failure of conservative measures is exceedingly rare, 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 ROM 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 (left shoulder) or 9 o’clock (right shoulder) position. The capsule should be incised until the muscle belly of the external rotators can be visualized. 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.
Superior labrum anterior and posterior 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. 7.18 A) or meniscoid ( Fig. 7.18 B), 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.
