The Overhead Athlete

The Overhead Athlete


The overhead athlete’s quest for excellence is itself a major conundrum. On the one hand, the athlete must have a perfectly conditioned and coordinated kinetic chain that can function efficiently and painlessly. On the other hand, he or she must willfully subject the shoulder to extreme loads at extreme angles on such a regular repetitive basis that breakdown of vital anatomic structures in the shoulder seems all but inevitable.

Functional Comparison of Overhead Athletics

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.

The Pathologic Cascade

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).

FIGURE 5-1 A: The glenoid has four quadrants: anterosuperior (AS), anteroinferior (AI), posterosuperior (PS), and posteroinferior (PI). Ordinarily, internal impingement in which the greater tuberosity of the humerus abuts the glenoid occurs in the posterosuperior quadrant. A posterosuperior shift of the contact point can “delay” internal impingement so that it occurs in the posteroinferior quadrant. B: Right shoulder of a 20-year-old baseball pitcher, from an anterosuperolateral viewing portal. The arm has been dynamically positioned into maximal external rotation while at 90° abduction. Posterosuperior shift of the glenohumeral contact point delays internal impingement of the greater tuberosity against the glenoid rim from the normal location in the posterosuperior quadrant to the posteroinferior quadrant (as we see in this patient with hyper-external rotation). H, humeral head; GT, greater tuberosity; RC, rotator cuff; AI, anteroinferior; PI, posteroinferior; PS, posterosuperior.

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.


This chapter is not intended to be an exhaustive resource on the step-by-step management of the overhead athlete, but rather is intended to show how we have reached our decisions to treat specific athletes in a certain way. For a more comprehensive overview of the throwing shoulder, the reader is referred to our previous work on this subject.1,2,3

FIGURE 5-2 Schematic of the peel-back maneuver for intraoperative demonstration of a superior labrum anterior and posterior (SLAP) tear. A: Appearance of the biceps root with the arm at the side. B: Placing the arm in 90° of abduction and maximal external rotation creates a torsional force on the biceps root. In the setting of a SLAP tear, the biceps root and the labrum just posterior to the biceps root displace medially during this maneuver.

For the athlete with a shoulder that becomes so painful that he can no longer participate in his sport, we always begin with a nonoperative regimen. This begins with a thorough investigation of potential causes, and this investigation usually includes both physical examination and imaging.

FIGURE 5-3 The diagram shows the shift in position that occurs in the major tendon and capsuloligamentous structures of the glenohumeral joint between the resting position (solid lines) and the abducted externally rotated (ABER) position (dotted lines). In abduction and external rotation, the bowstrung posterior band of the inferior glenohumeral ligament (PIGHL) is beneath the humeral head, causing a shift in the glenohumeral rotation point; and the biceps vector shifts posteriorly as the peel-back forces are maximized. The result is a posterosuperior shift of the glenohumeral contact point. SGHL, superior glenohumeral ligament; AIGHL, anterior band of the inferior glenohumeral ligament; MGHL, middle glenohumeral ligament.

Thorough evaluation of each segment of the kinetic chain is essential, so that deficiencies in strength or mobility at each level can be addressed. We frequently find that seemingly unrelated pathology, such as stiffness in one of the hips, has caused the athlete to try to compensate with the shoulder. By correcting the kinetic chain dysfunction, the shoulder dysfunction will resolve by nonoperative means. Surgery is seldom necessary.

Even the overhead athletes with MRI evidence of SLAP lesions or cuff tears can be satisfactorily treated without surgery in most cases. In many pitchers, SLAP lesions and cuff tears are adaptive lesions that occur over time due to the athlete’s need to hyper-externally rotate the shoulder in order to achieve maximal speed when throwing a ball. Many pitchers can maintain a high performance level despite long-standing SLAP or cuff lesions. Even in patients with imaging evidence of such lesions, nonoperative treatment can be successful and should always be tried before considering surgery.

Operative Management

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

FIGURE 5-4 A: Internal impingement in the posteroinferior quadrant. There is damage to the posteroinferior labrum that could be mistaken for a posterior instability lesion. B: With the arm in 90° abduction and full external rotation (late cocking position), the internal impingement point (i.e., the point on the glenoid labrum where the greater tuberosity strikes with full external rotation) is seen to be in the posteroinferior quadrant, exactly at the point of labral damage. Therefore, the labral damage has been caused by repetitive striking of that segment of the labrum by the greater tuberosity (internal impingement), and it is not a sign of posterior instability.

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.

Only gold members can continue reading. Log In or Register to continue

Oct 27, 2018 | Posted by in ORTHOPEDIC | Comments Off on The Overhead Athlete
Premium Wordpress Themes by UFO Themes