Chapter 8 Pathophysiology of Injury to the Overhead-Throwing Athlete

Michael S. Zazzali, Robert A. Donatelli, Vijay B. Vad ^*,

In recent decades there has been a dramatic rise in the number of participants in overhead-throwing sports. The increase in participation has developed a concurrent increase in incidence of injury to the upper extremity. The skill of throwing a baseball with extremely high velocities and precision requires years of practice and advanced neuromuscular efficiency, not to mention natural ability to reach the upper echelons of professional competition.

The professional baseball pitcher most likely starts out early in life during Little League to begin the development of his musculoskeletal and neuromuscular systems. However, no matter how blessed the individual may be to pitch a baseball upwards of 90 miles an hour, the repetitive microtrauma that stresses the athlete’s shoulder complex during the throwing motion challenges the physiological limits of the surrounding tissues. Frequently the repetitive act of throwing a baseball has led to a variety disabilities arising from alterations in throwing mechanics secondary to fatigue, capsular shortening, or contracture versus capsular laxity; glenohumeral labral tears; muscle weakness; and imbalances around the shoulder complex, all of which can lead to tissue compromise and eventual injury.

Conte et al ¹ performed a study over a 5-year period from 1995 to 1999 that determined the prevalence of upper extremity injuries in Major League Baseball. They found an injury rate of 27.8% and 22% involving the shoulder and elbow, respectively. The authors also reported in a prior study between 1989 and 1999 that 48.4% of all injuries in Major League Baseball involved pitchers.¹ The data suggest that half of all Major League Baseball injuries that necessitated removal of the athlete from the active roster and placed on the disabled list were related to pathology to the upper extremity.^1,²

This chapter reviews the phases of throwing and details the most current concepts in the pathophysiology of the throwing shoulder compared with the past theories and practices from conservative, as well as surgical, perspectives.

The act of throwing a baseball involves a transfer of kinetic energy from the legs, through the hips, spine, shoulder, elbow, and wrist. The forces are generated through the trunk and core and expressed in the extremities. The stages of overhand throwing as it relates to pitching have been divided into the following phases: (1) windup, (2) early cocking, (3) late cocking, (4) acceleration, and (5) follow-through.

STAGES OF OVERHAND THROWING

Windup

The purpose of the windup is to organize the body beneath the arm to form a stable platform. The body must perform in sequential links to enable the hand to be in the correct position in space to complete the assigned task. The scapulohumeral rhythm must place the hand in an optimal position for propulsion. The humeral head is centered in the glenoid during the first initial phase of elevation via the supraspinatus. Due to the windup phase having such individualistic styles among athletes, there is no consistent pattern of muscle activity.

Early Cocking

Early cocking is the temporal period when the dominant hand is separated from the gloved hand, and it ends when the forward foot makes contact with the mound. The scapula is fully retracted at this time and stabilized against the chest wall by the rhomboids and the serratus anterior. The humerus is brought into position of 90-degree abduction and horizontal extension, with external rotation of only approximately 50 degrees. This is accomplished with the activation of the anterior, middle, and posterior deltoid. The external rotators of the cuff are activated toward the end of early cocking, with the supraspinatus being more active than the infraspinatus and teres minor as it steers the humeral head in the glenoid. The biceps brachii and brachialis act on the forearm to develop the necessary angle of the elbow.

As the body moves forward, the humerus is supported by the anterior and medial deltoid as the posterior deltoid pulls the humerus into approximately 30 degrees of horizontal extension. At this time the static stability of the humeral head becomes dependent on the restraints of the anterior margin of the glenoid, notably the anterior band of the inferior glenohumeral ligament (IGHL) and the inferior portion of the glenoid labrum.

Late Cocking

Late cocking is the interval in the throwing motion when the lead foot makes contact with the mound, and it ends when the humerus begins internal rotation. The lead foot applies an anterior shear to slow the lower extremity and to transfer energy. The foot serves as an anchor. The forward and vertical momentum is transformed into rotational components. During this time the humerus is moved into a position more forward in relation to the trunk and begins to come into alignment with the upper body. The extreme of external rotation, an additional 125 degrees, is achieved to provide positioning for the power or acceleration phase.

The supraspinatus, infraspinatus, and teres minor are active in this phase but become quiet once external rotation is achieved. Deceleration of the externally rotating humerus is accomplished by contraction of the subscapularis. The subscapularis remains active until the completion of late cocking. The serratus anterior and the clavicular head of the pectoralis major have their greatest activity during deceleration. The biceps brachii aids in maintaining the humerus in the glenoid by producing a compressive axial load. At the end of this phase, the triceps begins activity and provides compressive axial loading to replace the force of the biceps. The capsule winds tightly in preparation for acceleration. The humeral head experiences a force of anterior translation equivalent to 40% of body weight.³

Acceleration

Acceleration is a ballistic action lasting less than one tenth of a second. The ball is accelerated from 4 mph to 90 mph or higher.⁴ This rapid acceleration produces angular velocities that have reported as high as 9198 degrees/sec.⁵ The scapula is protracted, rotated downward, and held to the chest wall by the serratus anterior. The arm continues into forward flexion and is marked by the maximal internal rotation of the humerus. The humerus travels forward in 100 degrees of abduction but adducts about 5 degrees just before release. The latissimus dorsi and pectoralis major deliver the power to the forward-moving shoulder. The subscapularis activity is at maximum levels as the humerus travels into medial rotation. The triceps develops strong action in accelerating the extension of the elbow.

The forces developed in this instant reflect the body’s ability to generate power and encase itself in a protective mechanism. Pappas et al ⁵ reported peak accelerations approaching 6000 degrees/sec. Gainer et al⁶ reported 14,000 inch lbs of rotatory torque produced at the shoulder. This torque develops 27,000 inch lbs of kinetic energy in the humerus.

Control of the ball is lost approximately midway through the acceleration phase, when the humerus is positioned slightly behind the forward-flexing trunk and at an angle of about 110 degrees of external rotation. The hand follows the ball after release and is unable to apply further force.

Follow-Through

Follow-through begins with release of the ball. Within the first tenth of a second the humerus travels across the midline of the body and undergoes a slight external rotation before finishing in internal rotation. This is an active phase for all glenohumeral muscles because the arm is decelerated. The deltoid and upper trapezius have strong activity, as does the latissimus dorsi. The infraspinatus, teres minor, supraspinatus, and subscapularis are all active while eccentric loads are produced. The biceps develops peak activity in decelerating the forearm and imposing a traction force within the glenohumeral joint.

The task of documenting the sequence of muscle activity during the act of pitching has allowed the musculature acting on the glenohumeral joint to be divided into two groups.⁷ The first group of muscles consists of those that are most active during the second and third phases of throwing and early and late cocking. They are least active during the acceleration phase. The deltoid, trapezius, external rotators, supraspinatus, teres minor, and biceps brachii comprise this first group.

The second group of muscles consists of those used primarily for the fourth phase of throwing—acceleration. These muscles are necessary to protract the scapula, horizontally flex forward and internally rotate the humerus, and extend the elbow. This group consists of the subscapularis, serratus anterior, pectoralis major, latissimus dorsi, and triceps brachii. The first phase of throwing is not included in either group because of its nonspecific generalized activity.

It has been postulated that in order for the elite pitcher to reach velocities of mid to upper 90s, excessive external rotation of the glenohumeral joint must occur during the late cocking and acceleration phase of throwing. This hyperexternal rotation is often seen in elite pitchers who appear to have a set point of external rotation that they know they need to attain to throw with maximum velocities. These high-level pitchers have a proprioceptive sense of reaching their set point of hyperexternal rotation, which they call the slot.⁸

The amount of external rotation at the glenohumeral joint has been measured to reach upwards of 130 to 170 degrees during this phase of throwing.⁸ The arm has been clocked at moving from 7000 to 9000 degrees/sec during the acceleration phase of throwing as it moves into internal rotation at the glenohumeral joint.⁹ Jobe et al¹⁰ described that one of the main reasons shoulder pain occurred during the act of throwing was an impingement-instability overlap. They postulated that repetitive throwing and this hyperexternal rotation gradually induced a serial stretching of the anterior capsuloligamentous complex. According to Jobe et al,¹⁰ this would then lead to the anterosuperior migration of the humeral head during throwing, thus inducing subacromial impingement symptoms, and affect the athletes’ throwing ability. However, these authors reported only a 50% success rate of pitchers returning to sport for 1 year following open capsulolabral reconstruction.¹¹

In the past the primary rationale for the ability to reach these amounts of hyperexternal rotation was thought to be due to serial laxity of the anterior capsuloligamentous tissues.¹² This repetitive microtrauma eventually could lead to subluxation and eventually dislocation or the so-called “dead arm syndrome.”

INTERNAL IMPINGEMENT

Walch et al ¹³ were the first to describe a condition known as internal impingement, which relates to intra-articular compression that occurs in all shoulders when they are in the abducted and hyperexternally rotated position. Walch described that in the position of 90 degrees of abduction and 90 degrees of external rotation position, the posterosuperior rotator cuff, mainly the supraspinatus, contacts the posterosuperior glenoid labrum and may become impinged between the labrum and the greater tuberosity (Figure 8-1). Jobe extrapolated this observation to the throwing athlete and described the propensity of internal impingement to possibly lead to injury to the rotator cuff, glenoid labrum, and osseous structures.¹⁴ Jobe also hypothesized that internal impingement in throwers might worsen over time due to the serial stretching of the anterior capsuloligamentous structures. Jobe believed there was a hyperangulation occurring at the humeral head as opposed to hypertranslation that needed to be kept in check by the subscapularis during the act of throwing to help control this hyperexternal rotation.¹⁴

Figure 8-1 Cross section (A) and artist’s tracing (B) of a cadaver shoulder frozen in forward elevation and internal rotation to mimic the impingement sign. The tuberosity and cuff are already past the acromion. The structures at risk for this mechanism are (1) greater tuberosity, (2) supraspinatus tendon, (3) superior labrum, (4) inferior glenohumeral ligament, and (5) superior glenoid bone.

(From Jobe CM: J Shoulder Elbow Surg 11:530-536, 1995.)

The thrower with internal impingement will most often complain of pain in the posterior aspect of the shoulder in the late cocking and early acceleration phases of throwing.¹⁵ The posterior impingement sign can confirm a diagnosis of tears into the posterior labrum or rotator cuff, or both.^16,¹⁷ In this test the patient is positioned supine with the shoulder in 90 degrees of abduction and maximum external rotation (Figure 8-2). Re-creation of the patient’s symptoms with the arm in this position elicits pain of a deep nature within the posterior aspect of the shoulder. Applying a posteriorly directed force (as in the relocation test) to the humeral head while in the position of 90 degrees of abduction and maximum external rotation that reduces or eliminates the posterior pain may also be diagnostic.¹⁷ The surgical approach to address the previous description of internal impingement led to anterior capsulolabral reconstruction under the hypothesis that the anterior microinstability was the underlying mechanism of the internal impingement. However, the results of this surgical intervention for throwing athletes remained unpredictable.^11,¹⁸

Figure 8-2 A and B, Test for internal impingement. The arm is placed in the plane of the scapula and in maximal external rotation of the undersurface of the rotator cuff between the humeral head and the posterosuperior glenoid, and the labrum occurs in this position. The patient will experience pain in the posterior aspect of the shoulder at the level of the glenohumeral joint if internal impingement is present.

(From DeLee JC, Drez D, Miller MD: DeLee & Drez’s orthopaedic sports medicine: principles and practice, ed 2, Philadelphia, 2002, Saunders.)

Gerber and Sebesta ¹⁹ arthroscopically assessed 16 individuals who were not described as throwing athletes with moderate to severe and primarily unexplained shoulder pain provoked by anterior elevation and internal rotation and who were unresponsive to subacromial injection. None of the patients had signs of instability. The authors determined that when the subjects’ arms were internally rotated and elevated below 90 degrees, impingement occurred between the deep surface of the subscapularis tendon and the anterior glenoid labrum and rim. Gerber and Sebesta’s study suggests that in addition to the posterosuperior impingement of the supraspinatus tendon originally described by Walch, anterosuperior impingement of the deep surface of the subscapularis is a form of intra-articular impingement.¹⁹ This impingement may be related to a lack of deceleration control or eccentric strength of the external rotators during the follow-through phase of throwing, which could result in an excessive amount of flexion and coupled internal rotation leading to the intra-articular subscapularis impingement.

Other authors such as Halbrecht et al ²⁰ and Burkhart et al⁸ disagreed with the premise that anterior instability would aggravate internal impingement. They felt that an anterior instability would most likely lessen the posterosuperior glenoid contact with the rotator cuff due to the fact that the unstable shoulder is subluxing anteriorly. This could be an underlying reason why anterior stabilization procedures did not appear to have predictable and promising results in the overhead-throwing athlete.

More recently, Burkhart and Morgan,^21,²² on the basis of two arthroscopic studies, clinical observation, and biomechanical data, have questioned the role of microinstability as the universal cause of throwing injuries. Burkhart et al reported on 53 baseball players, 44 of whom were pitchers, who had Type II superior labrum anterior to posterior (SLAP) lesions that were surgically repaired after failed conservative rehabilitation. Arthroscopic repair of these Type II SLAP lesions returned 87% of these athletes to a preinjury level of performance.²¹ This was superior to the reported successful return of athletes after open anterior capsulolabral repairs, which ranged from 50% to 68% return to sport.^11,¹⁸ Burkhart et al do not believe that the underlying lesion is the anterior capsular laxity or microinstability but that the SLAP lesion induces a “pseudolaxity,” which has led to the erroneous diagnosis of microinstability.⁸

Pitchers and throwing athletes are believed to be at risk of developing SLAP lesions due to the obligatory tightening of the posteroinferior glenohumeral capsule.⁸ In studying 372 professional baseball players, Wilk and Meister²³ have reported that external rotation on average is 7 degrees greater in the throwing shoulder and internal rotation is 7 degrees greater in the nonthrowing shoulder. The average total shoulder range of motion was reported as 129.9 plus or minus 10 degrees of external rotation and 62.6 plus or minus 9 degrees of internal rotation. The authors coined the term total motion concept to describe total shoulder motion being equal to the summation of external and internal rotation. Thus an individual with an imbalance of external to internal rotation as such would lend to dynamic instability with overhead throwing.

In 1991, Verna was the first to recognize the relationship between gross internal rotation deficit (GIRD) and shoulder dysfunction in the throwing athlete.²⁴ During a baseball season he assessed 39 professional pitchers who were determined to have 25 degrees or less of total internal rotation at spring training (GIRD, ≥35 degrees in each of these pitchers). During the course of the study and season, 60% developed shoulder problems requiring them to stop pitching. These findings of restricted internal rotation correlate with a tight posteroinferior capsule but can also be attributed to tightness of the external rotators and osseous adaptations of the humeral head or glenoid.²

Cooper manually stretched 22 Major League pitchers daily to minimize GIRD to less than 20 degrees during the 1997, 1998, and 1999 professional baseball seasons.⁸ During those seasons, he reported innings lost, no intra-articular problems, and no surgical procedures in the study group. These reports help substantiate that a prophylactic-focused posteroinferior capsular stretching program is successful in minimizing GIRD and is effective in preventing secondary intra-articular problems, particularly posterior Type II SLAP lesions.⁸

According to Burkhart et al,⁸ this acquired loss of internal rotation caused by the posteroinferior capsule contracture is the “essential lesion” that leads to a secondary resultant increase in external rotation. They believe this occurs via two mechanisms by which a tight posterior capsule induces hyperexternal rotation of the humerus. First, the tethering effect of the posterior capsular contracture shifts the glenohumeral contact point posterosuperiorly, allowing the greater tuberosity to clear the glenoid rim through a greater arc of external rotation before internal impingement occurs (Figure 8-3). Second, the shift in the glenohumeral contact point reduces the cam effect of the proximal humerus on the anteroinferior capsule to allow greater external rotation due to the redundancy in the capsule (Figure 8-4). They define GIRD as a loss in degrees of glenohumeral internal rotation of the throwing shoulder compared with the nonthrowing shoulder. Glenohumeral internal rotation deficits of 15 to 20 degrees have been associated with nonsymptomatic pitchers, while symptomatic pitchers have reported deficits as high as 45 degrees.^2,²²