The four main categories of overhead athletes that we treat are baseball players, tennis players, volleyball players, and football quarterbacks. Although all four groups have common factors that contribute to injury, there are also specific differences to consider in each type of athlete. Although superior labrum anterior and posterior (SLAP) lesions have been implicated as a primary cause of the disabled throwing shoulder, we know that many high-level overhead athletes, including baseball pitchers, have been able to adapt to SLAP lesions and return to a high level of competition without surgery. Therefore, surgery is not our first line of treatment.

There are three categories of baseball players that all have different functional demands for throwing. The highestdemand category comprises pitchers, who place the highest demand on their shoulders of all the overhead athletes. In fact, pitchers’ shoulders routinely achieve angular velocities of 7,000° per second, the fastest motion in all of sports. The next category, outfielders and long infielders (short stop and third base) must also achieve high velocities to their throws and may achieve angular velocities of the shoulder approaching those of the pitcher. The third category, short infielders (second and first base) do not need to throw with such high velocities and may function adequately at their positions even with significant shoulder pathology. Catchers, who have a less extreme cocked position to the arm during the throwing motion, do not fit into any of these categories. The less extreme cocked position may actually be protective, as catchers seem to have a lower rate of injury to their throwing shoulders than do other categories of baseball players.

Volleyball players have a similar cocking mechanism to baseball players. However, the fact that the volleyball player is airborne when striking the ball for a spike probably protects the shoulder by not having the lower extremity kinetic chain maximally engaged.

Tennis players can achieve ball speeds of >120 miles per hour, compared to 95+ miles per hour for top baseball pitchers. However, this increased ball velocity does not directly correlate with higher forces on the shoulder in tennis than in baseball, because the angular momentum is imparted to the tennis ball through a very long lever arm that includes the length of the racket plus the upper arm and the forearm. The racket length is an important biomechanical variable that can help the tennis player compensate in ways that are not available to a baseball player.

Football quarterbacks, despite the collision nature of their sport, seem to have very durable throwing shoulders. They do not hyper-externally rotate to the extent that baseball pitchers do, and their angular velocities are much lower than baseball pitchers. Furthermore, we have all heard of high-performance football quarterbacks, such as John Elway, who could throw as hard, as far, and as
accurately after rupture of the long head of the biceps as before, with no noticeable difference from their prerupture performance level.

On the other hand, there are no major league baseball pitchers that have returned to their preinjury or preoperative performance level after losing the origin of the long head of the biceps, either by rupture or by tenodesis. Why the difference between baseball and football? The answer may well lie in the ability of the root of the biceps to control perturbations of motion at high angular velocities. Without this control function of the biceps, it may be impossible to throw a high-velocity baseball pitch, whereas the more low-angular-velocity shoulder motion of the football quarterback may not require this dampening effect of the biceps root for high-level function.

Particularly in baseball players, the pathologic cascade seems to begin with a glenohumeral internal rotation deficit (GIRD), which is probably secondary to a posteroinferior capsular contracture. GIRD can then contribute to biomechanical imbalances that contribute to the creation of SLAP lesions that may become disabling by virtue of loss of the stabilizing influence of the biceps root.

GIRD can contribute to hyper-external rotation of the humerus by causing a posterosuperior shift in the glenohumeral contact point (Fig. 5-1).

There is also a dynamic peel-back mechanism that occurs with the arm in the cocked position of combined abduction and external rotation. This creates a torsional force that can disrupt the attachment of the biceps root, thereby creating a SLAP lesion (Fig. 5-2).

The pathologic cascade is best understood by examining the interplay of forces that occurs with the shoulder in the cocked position of 90° abduction and full external rotation (Fig. 5-3). At that point, the posterior band of the inferior glenohumeral ligament (PIGHL) is beneath the humeral head, causing a posterosuperior shift in the glenohumeral contact point. The posterosuperior shift of the humeral head causes increased shear stresses at the posterosuperior labrum at the point in the throwing cycle where the torsional peelback forces are at their highest, subjecting the biceps root and superior labrum to forces that could create a SLAP lesion. Furthermore, this concentration of forces on the superior labrum and biceps root is occurring at exactly the point in the kinetic chain where maximum acceleration forces are being funneled from the trunk to the shoulder. This confluence of forces onto a vulnerable “shoulder-at-risk” can produce functionally devastating injuries in the overhead athlete.

Once nonoperative management has failed, the surgical options must be considered. There seems to be little, if any, consensus on surgical treatment of the disabled throwing shoulder.

We have developed a surgical treatment paradigm based on our arthroscopic and clinical observations. This treatment paradigm has evolved from three observations:

1. Hyper-external rotation of the humerus is functionally desirable, but it can contribute to repetitive damage to the posterosuperior labrum and to the rotator cuff. At the time of diagnostic arthroscopy, we dynamically bring the arm into the cocked position
of abduction and external rotation while viewing through an anterosuperolateral portal. Most throwers have an internal impingement point (where the greater tuberosity/cuff contacts the labrum) in the posterosuperior quadrant of the glenoid. If that internal impingement point is in the posteroinferior quadrant, we believe that this is indicative of hyper-external rotation, which may contribute to repetitive structural damage to the labrum and/or the rotator cuff (Fig. 5-1B).

2. SLAP lesions within the posterosuperior quadrant can cause decreased performance; when this happens, it is likely due to loss of the biceps root’s function in dampening the perturbations of motion that occur at high angular velocities.

3. A thickened and tight posteroinferior capsule can contribute to the pathologic cascade as previously described in this chapter. Although some patients respond to a stretching program, if a patient is a “stretch nonresponder” the patient may need to have the tight posteroinferior capsule addressed at the time of surgery.

As a result of these three observations, we have developed an arthroscopic treatment paradigm that has worked well in those patients who have not responded to nonoperative management.

Our arthroscopic treatment paradigm is based on our observations that the pathologic processes that need to be looked for and addressed arthroscopically are

1. SLAP lesions, especially those that extend posteriorly

2. Tight posteroinferior capsule

3. Hyper-external rotation of the humerus, defined as an internal impingement contact point in the posteroinferior (rather than posterosuperior) quadrant (Fig. 5-4).

So, in the case of an overhead athlete who has failed nonoperative management, we first look for a SLAP lesion. Arthroscopically, we typically observe a positive peel-back sign (Fig. 5-5) and an unstable biceps root (Fig. 5-6). We prefer to repair SLAP lesions as a first step, before significant swelling occurs that can obscure the superior capsular sulcus. We avoid trauma to the superior capsule that could cause excessive scarring, and we repair the labrum with knotless suture anchors (Fig. 5-7). We believe that avoidance of labral knots is important in order to prevent iatrogenic injury to the rotator cuff from knot impingement. We use a simple shuttling technique for suture passage through the superior labrum by placing a spinal needle through the modified Neviaser location. We have found this to be the most atraumatic technique for suture passage in this very sensitive area.

After SLAP repair, we address hyper-external rotation if we think it is a part of the problem. As previously stated, we do this only if we have confirmed that the internal impingement contact point is in the posteroinferior quadrant (Fig. 5-8). Obviously, the surgeon does not want to decrease external rotation by very much, or it could decrease pitch velocity and performance. However, we have found it beneficial in some cases to slightly restrict external rotation by means of a “mini-plication.” This “mini-plication” comprises only two sutures that are passed to suture the middle glenohumeral ligament (MGHL) to the anterior band of the inferior glenohumeral ligament (IGHL) (Fig. 5-9). No suture anchors are


used for this “mini-plication,” as we do not want to tether the capsule.