Shoulder & Elbow

I am very honored that Dr. Rob Bell, past president of the American Shoulder and Elbow Surgeons, invited me to give last year’s Neer Lecture. Dr. Bell asked me to specifically address my role in the development of arthroscopic rotator cuff repair and to recount the significant resistance that the early arthroscopic shoulder surgeons faced from the shoulder establishment as we struggled to achieve mainstream acceptance for this new technology. Tasked with such a personal topic, I find myself in a position analogous to that of Winston Churchill at the end of World War II. When a journalist asked him to speculate on how historians would portray his role in the war, he replied without hesitation, “History will be kind to me because I intend to write it.”

So let’s start at the beginning. And for me it makes the most sense to travel back to the year I started my practice: 1981. The world then was very different from today’s world. On January 20, 1981, Ronald Reagan was inaugurated President of the United States. The same day, 52 US hostages in Iran were released after having been held captive for 442 days. In March 1981, Reagan survived an assassination attempt; 3 months earlier, John Lennon had not been so lucky. Lennon’s hit song “Starting Over” garnered the highest musical awards posthumously.

The world of shoulder surgery was also very different in 1981. The arthroscope was the “instrument of the devil,” according to Dr. Rockwood. And shoulder surgery was ruled by the Charlies—Dr. Charles Neer, Dr. Charlie Rockwood, and any other Charlie who felt compelled to marginalize shoulder arthroscopy.

My personal world in the early 1980s was daunting as well. I had just completed my residency at the Mayo Clinic and my sports medicine fellowship in Eugene, Oregon. I had a young son, a new daughter, and a new job with the San Antonio Orthopaedic Group. I had a new house with a 21% mortgage loan and a “new” used car with a 23% car loan.

I was simultaneously energized and intimidated by my new job, where I was doing general orthopedics with a “special interest” in shoulder surgery and sports medicine. I was initially very proud and humbled by the fact that my senior partners had entrusted me with the care of the most difficult shoulder cases within the practice. But that pride got cut down to its appropriate size the day after I had thanked one of my partners, Dr. Lamar Collie, for his confidence in my potential as a shoulder surgeon. Dr. Collie replied matter-of-factly, “Sure … but you need to understand that we always make the new guy the shoulder expert because shoulders never do worth a damn.”

For shoulder arthroscopy, the early 1980s were exciting. Most of us who were scoping shoulders had already been doing knee arthroscopy and were trying to adapt knee instruments to the shoulder. This worked for some simple excisional cases. For example, I recall excising the bucket-handle portion of a type III SLAP (superior labral tear from anterior to posterior) lesion in 1983. In general, however, shoulder problems were different from knee problems and usually involved repair rather than excision of damaged tissues. Therefore, the technology used in knee arthroscopy was often not directly transferable to the shoulder. Furthermore, treatment of the rotator cuff necessitated development of arthroscopic techniques in a virtual space, the subacromial space, and this was an entirely new arthroscopic concept.

Development of Arthroscopic Rotator Cuff Repair

A major mind-expanding turning point for me occurred in 1984 when I attended one of Dr. Jim Esch’s early San Diego shoulder courses. During that course, Dr. Harvard Ellman of Los Angeles demonstrated to me on a cadaver shoulder how he created a virtual subacromial working space that allowed enough visualization for an arthroscopic acromioplasty. At that moment, I knew that arthroscopic rotator cuff repair was just around the corner. Up until then, I had not been able to envision complex extra-articular reconstructive surgery, as all previous arthroscopic surgery had been intra-articular. But now, having realized a virtual working space could always be created, I knew it would be relatively straightforward to develop the portals to approach the cuff as well as the implants and the instruments to repair it. But I also knew that progression to all-arthroscopic repair techniques would have to be stepwise and that the final repair constructs would need to be at least as strong as those of open repair in order to be acceptable. With an undergraduate degree in mechanical engineering, I had a reasonably clear idea of the concepts I wanted to apply to the instrumentation and techniques, though I could never have envisioned how circuitous the route to the end result would be.

First Steps

I sketched out my ideas for arthroscopic suture passers and knot-tying instruments and presented them to a couple of the major arthroscopy companies in the United States, but the companies were not interested. They did not believe arthroscopy would have any meaningful applications in the shoulder. So, I enlisted the services of a local San Antonio aircraft machinist to fabricate instruments for me. By 1987, I was doing arthroscopic side-to-side margin convergence¹ cuff repairs for U-shape tears on a regular basis. And I was doing these at the most hostile point in the universe for arthroscopic shoulder surgery: San Antonio, Texas.

Only a few surgeons were doing arthroscopic shoulder surgery in the 1980s and early 1990s, and without exception these surgeons became the leader-pioneers in the new discipline. In general, these were young surgeons who were in private practice and removed from academia and professional organizations, and thus relatively sheltered from the actions of the shoulder rule-makers of the day. They accepted their status as pariahs as they developed their techniques out of the view of mainstream orthopedics. These leaders included Jim Esch, Steve Snyder, Dick Caspari, Lanny Johnson, Gene Wolf, Gary Gartsman, Rob Bell, and Howard Sweeney. We shared our techniques and our ideas with one another, encouraged one another, and generally became good friends.

Thomas Kuhn, in his classic book The Structure of Scientific Revolutions,² observed that paradigm shifts within a given field were usually achieved by practitioners who were either very young (naïve) or outside the established hierarchy in the field. The surgeons who contributed most to the shift of shoulder surgery from open to arthroscopic techniques were generally young men who were in private practice and had little to lose by inciting the disdain of the shoulder establishment. Predictably, resistance from the mainstream open shoulder surgeons increased as arthroscopic techniques became more successful and more threatening to the primacy of the open shoulder surgeons. The disdain yielded to disruption and finally to transformation as the paradigm shift occurred. The conflict between the open shoulder surgeons and the arthroscopic shoulder surgeons passed through all the phases that Mahatma Gandhi had described many years before. “First they ignore you; then they laugh at you; then they fight you; then you win.”

Building a Ship in a Bottle

At the start of the 1990s, I recognized that my progress in arthroscopic rotator cuff repair would be extremely slow unless I could find an industry partner who shared my vision for full-scale conversion to arthroscopic means of repair and would be willing to help make it a reality. In 1991, I happened to meet Reinhold Schmieding, the owner of Arthrex, a small arthroscopic device company in Naples, Florida. Reinhold invited me to visit him to discuss the feasibility of developing arthroscopic repair systems for the shoulder. At the time, the world headquarters of Arthrex was a 20×30-ft storage room in an office service center, and there were 2 employees. One employee, Don Grafton, was a talented engineer without medical experience. By the end of my first day there, Reinhold and Don and I had agreed that developing arthroscopic repair systems for shoulder instability and rotator cuff repair would become a top priority for Arthrex.

My initial bias toward arthroscopic cuff repair was that a transosseous bone tunnel technique not only would be possible but would be superior to suture anchor fixation. In fact, my first 2 patents with Arthrex were for instrumentation for an arthroscopic transosseous repair technique. I tested my hypothesis with 2 successive biomechanical studies. The first examined cyclic loading of bone tunnel repairs, and the second examined cyclic loading of anchor-based repairs.^3,4 Evaluating the data from these 2 studies, I was surprised to find that anchor-based repairs were significantly stronger than bone tunnel repairs. In addition, anchors shifted the weak link from the bone–suture interface to the tendon–suture interface; in essence, anchors optimized bone fixation by shifting the weak link in the construct to the tendon. I was then completely convinced of the superiority of suture anchors over bone tunnels, and that conviction has become even stronger over the years. After these 2 cyclic loading studies, I shifted my focus, and that of Arthrex, toward arthroscopic suture anchor repair of the rotator cuff.

Reconciling Technique and Instrumentation With Anatomy and Biomechanics

Having recognized the importance of the rotator cable attachments both anatomically⁵ and biomechanically,^6,7 I thought it important to reinforce them as a routine part of performing rotator cuff repairs. Our anatomical and biomechanical studies had had great translational implications in the development of our techniques and instrumentation.

As mentioned earlier, Don Grafton was the chief (and for a long time only) engineer at Arthrex. As he had no medical experience, I invited him to come to San Antonio to observe surgery. During Don’s many visits, I showed him pathology in the operating room and pointed out what I could do with the instruments I had and what I could not do. Then in the evening we went to my house and brainstormed how to perform the “missing” surgical manipulations, how to improve manipulations that were suboptimal, and how to optimize final surgical constructs.

Passing suture through tendon was an early challenge. One must remember that, in the early 1990s, it was not possible for machinists to fabricate complex shapes. Therefore, straight tubular retrograde suture passers were the logical first option. We initially developed spring-loaded retrograde hook retrievers (Figure 1) and then curved suture hooks with shuttling wires (Lasso). To me, the most unappealing feature of retrograde suture passage was the oblique angle of approach through the tendon, which caused a length–tension mismatch between the upper fibers and the lower fibers of the muscle–tendon unit. We recognized we could eliminate the mismatch if we passed the suture antegrade, such that it would pass perpendicular to the tendon fibers. These insights and efforts culminated in development of the Viper suture passer and then the FastPass Scorpion suture passer, which has a spring-loaded trapdoor on the upper jaw for ergonomic self-retrieving of the suture once it is passed through the tendon.

To develop a knot pusher that optimized knot tying (yielding the highest knot security and the tightest loop security), we used prototype instruments to tie and test literally thousands of knots in the laboratory. We were thus able to verify that the Surgeon’s Sixth Finger Knot Pusher (Arthrex) reproducibly tied optimized knots^8,9 and also optimized knot fixation and bone fixation. However, our suture was not yet optimized and was prone to breakage, and our suture–tendon interface was not yet optimized. Clearly, improvement was needed in 2 more areas.

Don came up with the idea for a virtually unbreakable suture and developed that idea into FiberWire.¹⁰ Shortly thereafter, I contributed the idea and design for FiberTape, which dramatically enhanced suture pullout strength and footprint compression.

Anchor designs improved rapidly and dramatically. We made the second-generation BioCorkscrew fully threaded, which virtually eliminated anchor failure, even in soft bone.

Optimization of the suture–tendon interface took a giant step forward when Park and colleagues^11,12 introduced linked double-row rotator cuff repair. Much as with a Chinese finger trap, the harder you pull, the stronger it becomes, with yield load approaching ultimate load.

At this point, it seemed we had optimized virtually every segment of the rotator cuff repair construct. Each component was just about as good as it could be. Or was it?

The Accidental Quest for Knotless Fixation

In November 1998, I made my first trip to China as a guest speaker at the Congress of the Hong Kong Orthopaedic Association. My first view of the magnificent Hong Kong skyline across Victoria Harbour was truly breathtaking. As I admired the gleaming glass towers and the concrete canyons of the city, I had no idea that the very next day these modern skyscrapers would reveal an ancient secret that would change my approach to arthroscopic rotator cuff repair.

The day after my arrival, Dr. James Lam took me to lunch. As we approached the restaurant, he pointed across the street to a tall building that was being renovated and had scaffolding supporting workers alongside the first 9 stories of the exterior wall. Dr. Lam said that, after lunch, he would take me to the construction site for a closer look at the scaffolding.

After lunch, we walked to the base of the scaffolding. Dr. Lam told me it was constructed entirely of bamboo poles held together with lashings but no knots (Figure 2). Lashings were secured by turning them back on themselves and wrapping them in an entirely knotless manner.¹³ I found it incredible that this knotless fixation was so secure that it could support the weight of workers many stories above the ground. I resolved to determine how this fixation method worked and see if the same mechanism might help us achieve reliable knotless fixation in surgery.

When I returned home, I broke out my college engineering books and reacquainted myself with the concept of cable friction. As has happened so often in the past, however, it took a practical lesson from the ranch to truly illustrate for me how cable friction works.

Every cowboy knows that a spirited horse cannot be restrained with only one lead rope. However, a cowboy can wrap a lead rope around a “snubbing post” and thereby gain complete control over the animal, despite the horse’s superior size and strength. The cable friction between the rope and the post creates such a large restraining force that the cowboy can easily hold the animal without the help of a knotted rope (Figure 3). In similar fashion in the Hong Kong scaffolding, fixation strength results from the significant amount of cable friction produced when the lashings wrap around one another and around the bamboo poles.

The cable friction concept was pivotal in the development of knotless fixation in arthroscopic rotator cuff repair. In lateral row fixation, the eyelet of the PushLock and SwiveLock suture anchors (Arthrex) produces significant cable friction at the eyelet–suture interface, in addition to frictional force wedging the suture between anchor and bone.

As with so many other devices in shoulder arthroscopy, the SwiveLock suture anchor developed in stages. In the first stage, a chainlike suture with consecutive intersecting links was used (FiberChain). The idea for an adjustable fixation construct came to me because I thought that a forked eyelet on a SwiveLock would provide a firm fixation point when inserted into the appropriate suture link, yet would be totally adjustable simply by choosing a tighter or looser link (Figure 4). Although the system worked very well, it was technically challenging. The process was greatly simplified after Don Grafton and I developed FiberTape and recognized that the power of cable friction was dramatically increased by the larger contact area between the eyelet and the braided FiberTape. The SpeedBridge construct (Arthrex), which enhanced cable friction fixation by means of passing FiberTape through the anchor eyelets, also provided a larger compressive interface at the repair site by using FiberTape rather than conventional suture. These incremental improvements led to what I would characterize as today’s gold standard for arthroscopic rotator cuff repair: a largely knotless linked double-row construct using FiberTape, with cinch-loop sutures at the anterior and posterior margins of the tear to reinforce the cable attachments and simultaneously reduce the dog-ears that typically occur in those locations, and a double-pulley medial mattress if tendon quality is poor (Figure 5).

The Burden of Craft

With all the recent enthusiasm for level I studies, I think we need to examine whether they will accelerate technological advancement in rotator cuff repair. The answer, in my opinion, is a resounding no. This answer is based on a major disconnect I have detected in how we evaluate these studies in rotator cuff disease and repair.

An irony related to technological advancement in surgery is that the more technically advanced the surgery becomes, the more skill is required. This fact is completely at odds with the public’s perception that technological advances make procedures easier. In arthroscopic rotator cuff repair, the surgeon must look, feel, and be aware to a greater degree than in open surgery.

Edward Tenner, in his book Why Things Bite Back, described the burden of the practitioner of any advanced technology as the burden of craft.¹⁴ The burden of craft is the inherent demand on all craftspeople, but particularly surgeons, to “up our game” if we are to be successful in our craft. For arthroscopic rotator cuff repair, the burden of craft requires patience, attention to detail, and the ability to work in a virtual space. Not everyone has these skills. But anyone who wants to practice in this discipline has an obligation to learn the skills required, and then to teach them to others and assess how well they are being applied.

The problem with relying on level I studies to assess the efficacy of a surgical procedure is that they are inherently biased by the surgeons involved. As results depend on surgeons’ skills, and surgeons’ skill levels are not equal, level I studies cannot prove what is possible, cannot demonstrate the limits of a technique, and cannot demonstrate the equivalence of techniques.

Amazingly enough, there are still rotator cuff repair “deniers” who confidently assert from the podium that a large percentage of massive cuff tears cannot be repaired and that, even if they can be repaired, they do not have the biological potential to heal. Given the disparity in surgeons’ skills and results, however, one must ask whether poor results are a consequence of a biological deficit in the patient, or of a skill deficit in the surgeon.

What I know is that we have techniques for predictable arthroscopic repair and healing of the vast majority of rotator cuff tears, even massive tears,^15-17 and patients do very well clinically. Yet, among many orthopedic surgeons, there is a trend to go straight to reverse total shoulder arthroplasty (rTSA) for massive tears—despite the evidence against it. As reported in the literature, rTSA results are not as good as arthroscopic cuff repair results, and the complication rate for rTSA is much higher.

Why has this trend toward rTSA for massive tears gained so much momentum? The only reason I can surmise is that, for the average surgeon, rTSA is easier and quicker than arthroscopic repair for massive tears. But the reason for choosing a specific type of surgery for a given problem should not be that it is easiest for the surgeon; it should be that it is best for the patient.

The surgeon should start by asking what procedure he or she would want if the roles were reversed—if the surgeon were the patient with the massive rotator cuff tear. If a surgeon does not have the skill set for the best procedure for a particular patient, he or she is obligated to send that patient to a surgeon who does have the skills. In addition, given that infection is the most feared complication in most shoulder surgeries, the surgeon should ask which infection rate would be personally acceptable. Arthroscopic rotator cuff repair has a reported infection rate of 1.6 per 1000, or .0016,¹⁸ whereas rTSA has an infection rate about 25 times higher, or .04.¹⁹ Further, the surgeon must consider the relative severity of the consequences of infection. By any measure, an infected arthroscopy is a straightforward treatable complication, but an infected shoulder replacement is a human tragedy. Patients vastly prefer the minimally invasive arthroscopic approach, and through online searches can easily identify who can offer an arthroscopic solution.

To reproducibly achieve successful arthroscopic repair of massive rotator cuff tears, the surgeon must know advanced techniques, including subscapularis repair techniques,^20,21 interval slides,^22,23 and self-reinforcing constructs.^24,25

“It’s a poor carpenter who blames his tools.” This 18th-century English proverb is as true today as it was 300 years ago. The tools for arthroscopic cuff repair exist, and they are excellent. The burden of craft is the surgeon’s burden and obligation. As surgeons, we must accept that obligation and the responsibility of that burden.

As mentioned earlier, Dr. Rob Bell’s charge to me when he invited me to give the Neer Lecture was to sum up my involvement in the development of arthroscopic shoulder surgery. The short version is that I have been doing shoulder arthroscopy for 31 years; have received 28 US patents related to shoulder instruments and implants and have 12 US patents pending; have published 167 peer-reviewed articles, a couple dozen book chapters, and 2 textbooks on shoulder arthroscopy; have trained 25 fellows; and have hosted approximately 3000 visiting surgeons in my operating room. My greatest professional dream was to see the standard of care for rotator cuff repair and shoulder instability transition from open to arthroscopic techniques, and I have been fortunate enough to have observed that paradigm shift during my career.

What do I envision over the next 31 years? As we all know, history runs in both directions, and some things simply have not happened yet. In terms of rotator cuff treatment, I think over the next few years the guiding principle of treatment will be joint preservation. All rotator cuff tears, even massive tears, will be repaired arthroscopically. Patients and insurers will demand arthroscopic repair, and surgeons without the skill set will migrate to other subspecialties. As for the role of arthroplasty in the treatment of rotator cuff tears, rTSA will be indicated only for pseudoparalysis after failed cuff repair in low-demand elderly patients.

In rotator cuff treatment, I envision a standard of care that is almost entirely arthroscopic. This standard will demand that surgeons who treat rotator cuff tears be proficient in arthroscopic repair of the full range of tears. Acquiring the skills for arthroscopic repair may not be easy, but then “there’s the easy way, and there’s the Cowboy Way.” As my dad used to tell me when I complained about working too hard, “No man ever drowned in his own sweat.” We shoulder surgeons must accept the burden of craft that accompanies the new standard of arthroscopic cuff repair, and we must offer our patients the same level of care we would choose for ourselves.

Happy trails!

I am very honored that Dr. Rob Bell, past president of the American Shoulder and Elbow Surgeons, invited me to give last year’s Neer Lecture. Dr. Bell asked me to specifically address my role in the development of arthroscopic rotator cuff repair and to recount the significant resistance that the early arthroscopic shoulder surgeons faced from the shoulder establishment as we struggled to achieve mainstream acceptance for this new technology. Tasked with such a personal topic, I find myself in a position analogous to that of Winston Churchill at the end of World War II. When a journalist asked him to speculate on how historians would portray his role in the war, he replied without hesitation, “History will be kind to me because I intend to write it.”

So let’s start at the beginning. And for me it makes the most sense to travel back to the year I started my practice: 1981. The world then was very different from today’s world. On January 20, 1981, Ronald Reagan was inaugurated President of the United States. The same day, 52 US hostages in Iran were released after having been held captive for 442 days. In March 1981, Reagan survived an assassination attempt; 3 months earlier, John Lennon had not been so lucky. Lennon’s hit song “Starting Over” garnered the highest musical awards posthumously.

The world of shoulder surgery was also very different in 1981. The arthroscope was the “instrument of the devil,” according to Dr. Rockwood. And shoulder surgery was ruled by the Charlies—Dr. Charles Neer, Dr. Charlie Rockwood, and any other Charlie who felt compelled to marginalize shoulder arthroscopy.

My personal world in the early 1980s was daunting as well. I had just completed my residency at the Mayo Clinic and my sports medicine fellowship in Eugene, Oregon. I had a young son, a new daughter, and a new job with the San Antonio Orthopaedic Group. I had a new house with a 21% mortgage loan and a “new” used car with a 23% car loan.

I was simultaneously energized and intimidated by my new job, where I was doing general orthopedics with a “special interest” in shoulder surgery and sports medicine. I was initially very proud and humbled by the fact that my senior partners had entrusted me with the care of the most difficult shoulder cases within the practice. But that pride got cut down to its appropriate size the day after I had thanked one of my partners, Dr. Lamar Collie, for his confidence in my potential as a shoulder surgeon. Dr. Collie replied matter-of-factly, “Sure … but you need to understand that we always make the new guy the shoulder expert because shoulders never do worth a damn.”

For shoulder arthroscopy, the early 1980s were exciting. Most of us who were scoping shoulders had already been doing knee arthroscopy and were trying to adapt knee instruments to the shoulder. This worked for some simple excisional cases. For example, I recall excising the bucket-handle portion of a type III SLAP (superior labral tear from anterior to posterior) lesion in 1983. In general, however, shoulder problems were different from knee problems and usually involved repair rather than excision of damaged tissues. Therefore, the technology used in knee arthroscopy was often not directly transferable to the shoulder. Furthermore, treatment of the rotator cuff necessitated development of arthroscopic techniques in a virtual space, the subacromial space, and this was an entirely new arthroscopic concept.

Development of Arthroscopic Rotator Cuff Repair

A major mind-expanding turning point for me occurred in 1984 when I attended one of Dr. Jim Esch’s early San Diego shoulder courses. During that course, Dr. Harvard Ellman of Los Angeles demonstrated to me on a cadaver shoulder how he created a virtual subacromial working space that allowed enough visualization for an arthroscopic acromioplasty. At that moment, I knew that arthroscopic rotator cuff repair was just around the corner. Up until then, I had not been able to envision complex extra-articular reconstructive surgery, as all previous arthroscopic surgery had been intra-articular. But now, having realized a virtual working space could always be created, I knew it would be relatively straightforward to develop the portals to approach the cuff as well as the implants and the instruments to repair it. But I also knew that progression to all-arthroscopic repair techniques would have to be stepwise and that the final repair constructs would need to be at least as strong as those of open repair in order to be acceptable. With an undergraduate degree in mechanical engineering, I had a reasonably clear idea of the concepts I wanted to apply to the instrumentation and techniques, though I could never have envisioned how circuitous the route to the end result would be.

First Steps

I sketched out my ideas for arthroscopic suture passers and knot-tying instruments and presented them to a couple of the major arthroscopy companies in the United States, but the companies were not interested. They did not believe arthroscopy would have any meaningful applications in the shoulder. So, I enlisted the services of a local San Antonio aircraft machinist to fabricate instruments for me. By 1987, I was doing arthroscopic side-to-side margin convergence¹ cuff repairs for U-shape tears on a regular basis. And I was doing these at the most hostile point in the universe for arthroscopic shoulder surgery: San Antonio, Texas.

Only a few surgeons were doing arthroscopic shoulder surgery in the 1980s and early 1990s, and without exception these surgeons became the leader-pioneers in the new discipline. In general, these were young surgeons who were in private practice and removed from academia and professional organizations, and thus relatively sheltered from the actions of the shoulder rule-makers of the day. They accepted their status as pariahs as they developed their techniques out of the view of mainstream orthopedics. These leaders included Jim Esch, Steve Snyder, Dick Caspari, Lanny Johnson, Gene Wolf, Gary Gartsman, Rob Bell, and Howard Sweeney. We shared our techniques and our ideas with one another, encouraged one another, and generally became good friends.

Thomas Kuhn, in his classic book The Structure of Scientific Revolutions,² observed that paradigm shifts within a given field were usually achieved by practitioners who were either very young (naïve) or outside the established hierarchy in the field. The surgeons who contributed most to the shift of shoulder surgery from open to arthroscopic techniques were generally young men who were in private practice and had little to lose by inciting the disdain of the shoulder establishment. Predictably, resistance from the mainstream open shoulder surgeons increased as arthroscopic techniques became more successful and more threatening to the primacy of the open shoulder surgeons. The disdain yielded to disruption and finally to transformation as the paradigm shift occurred. The conflict between the open shoulder surgeons and the arthroscopic shoulder surgeons passed through all the phases that Mahatma Gandhi had described many years before. “First they ignore you; then they laugh at you; then they fight you; then you win.”

Building a Ship in a Bottle

At the start of the 1990s, I recognized that my progress in arthroscopic rotator cuff repair would be extremely slow unless I could find an industry partner who shared my vision for full-scale conversion to arthroscopic means of repair and would be willing to help make it a reality. In 1991, I happened to meet Reinhold Schmieding, the owner of Arthrex, a small arthroscopic device company in Naples, Florida. Reinhold invited me to visit him to discuss the feasibility of developing arthroscopic repair systems for the shoulder. At the time, the world headquarters of Arthrex was a 20×30-ft storage room in an office service center, and there were 2 employees. One employee, Don Grafton, was a talented engineer without medical experience. By the end of my first day there, Reinhold and Don and I had agreed that developing arthroscopic repair systems for shoulder instability and rotator cuff repair would become a top priority for Arthrex.

My initial bias toward arthroscopic cuff repair was that a transosseous bone tunnel technique not only would be possible but would be superior to suture anchor fixation. In fact, my first 2 patents with Arthrex were for instrumentation for an arthroscopic transosseous repair technique. I tested my hypothesis with 2 successive biomechanical studies. The first examined cyclic loading of bone tunnel repairs, and the second examined cyclic loading of anchor-based repairs.^3,4 Evaluating the data from these 2 studies, I was surprised to find that anchor-based repairs were significantly stronger than bone tunnel repairs. In addition, anchors shifted the weak link from the bone–suture interface to the tendon–suture interface; in essence, anchors optimized bone fixation by shifting the weak link in the construct to the tendon. I was then completely convinced of the superiority of suture anchors over bone tunnels, and that conviction has become even stronger over the years. After these 2 cyclic loading studies, I shifted my focus, and that of Arthrex, toward arthroscopic suture anchor repair of the rotator cuff.

Reconciling Technique and Instrumentation With Anatomy and Biomechanics

Having recognized the importance of the rotator cable attachments both anatomically⁵ and biomechanically,^6,7 I thought it important to reinforce them as a routine part of performing rotator cuff repairs. Our anatomical and biomechanical studies had had great translational implications in the development of our techniques and instrumentation.

As mentioned earlier, Don Grafton was the chief (and for a long time only) engineer at Arthrex. As he had no medical experience, I invited him to come to San Antonio to observe surgery. During Don’s many visits, I showed him pathology in the operating room and pointed out what I could do with the instruments I had and what I could not do. Then in the evening we went to my house and brainstormed how to perform the “missing” surgical manipulations, how to improve manipulations that were suboptimal, and how to optimize final surgical constructs.

Passing suture through tendon was an early challenge. One must remember that, in the early 1990s, it was not possible for machinists to fabricate complex shapes. Therefore, straight tubular retrograde suture passers were the logical first option. We initially developed spring-loaded retrograde hook retrievers (Figure 1) and then curved suture hooks with shuttling wires (Lasso). To me, the most unappealing feature of retrograde suture passage was the oblique angle of approach through the tendon, which caused a length–tension mismatch between the upper fibers and the lower fibers of the muscle–tendon unit. We recognized we could eliminate the mismatch if we passed the suture antegrade, such that it would pass perpendicular to the tendon fibers. These insights and efforts culminated in development of the Viper suture passer and then the FastPass Scorpion suture passer, which has a spring-loaded trapdoor on the upper jaw for ergonomic self-retrieving of the suture once it is passed through the tendon.

To develop a knot pusher that optimized knot tying (yielding the highest knot security and the tightest loop security), we used prototype instruments to tie and test literally thousands of knots in the laboratory. We were thus able to verify that the Surgeon’s Sixth Finger Knot Pusher (Arthrex) reproducibly tied optimized knots^8,9 and also optimized knot fixation and bone fixation. However, our suture was not yet optimized and was prone to breakage, and our suture–tendon interface was not yet optimized. Clearly, improvement was needed in 2 more areas.

Don came up with the idea for a virtually unbreakable suture and developed that idea into FiberWire.¹⁰ Shortly thereafter, I contributed the idea and design for FiberTape, which dramatically enhanced suture pullout strength and footprint compression.

Anchor designs improved rapidly and dramatically. We made the second-generation BioCorkscrew fully threaded, which virtually eliminated anchor failure, even in soft bone.

Optimization of the suture–tendon interface took a giant step forward when Park and colleagues^11,12 introduced linked double-row rotator cuff repair. Much as with a Chinese finger trap, the harder you pull, the stronger it becomes, with yield load approaching ultimate load.

At this point, it seemed we had optimized virtually every segment of the rotator cuff repair construct. Each component was just about as good as it could be. Or was it?

The Accidental Quest for Knotless Fixation

In November 1998, I made my first trip to China as a guest speaker at the Congress of the Hong Kong Orthopaedic Association. My first view of the magnificent Hong Kong skyline across Victoria Harbour was truly breathtaking. As I admired the gleaming glass towers and the concrete canyons of the city, I had no idea that the very next day these modern skyscrapers would reveal an ancient secret that would change my approach to arthroscopic rotator cuff repair.

The day after my arrival, Dr. James Lam took me to lunch. As we approached the restaurant, he pointed across the street to a tall building that was being renovated and had scaffolding supporting workers alongside the first 9 stories of the exterior wall. Dr. Lam said that, after lunch, he would take me to the construction site for a closer look at the scaffolding.

After lunch, we walked to the base of the scaffolding. Dr. Lam told me it was constructed entirely of bamboo poles held together with lashings but no knots (Figure 2). Lashings were secured by turning them back on themselves and wrapping them in an entirely knotless manner.¹³ I found it incredible that this knotless fixation was so secure that it could support the weight of workers many stories above the ground. I resolved to determine how this fixation method worked and see if the same mechanism might help us achieve reliable knotless fixation in surgery.

When I returned home, I broke out my college engineering books and reacquainted myself with the concept of cable friction. As has happened so often in the past, however, it took a practical lesson from the ranch to truly illustrate for me how cable friction works.

Every cowboy knows that a spirited horse cannot be restrained with only one lead rope. However, a cowboy can wrap a lead rope around a “snubbing post” and thereby gain complete control over the animal, despite the horse’s superior size and strength. The cable friction between the rope and the post creates such a large restraining force that the cowboy can easily hold the animal without the help of a knotted rope (Figure 3). In similar fashion in the Hong Kong scaffolding, fixation strength results from the significant amount of cable friction produced when the lashings wrap around one another and around the bamboo poles.

The cable friction concept was pivotal in the development of knotless fixation in arthroscopic rotator cuff repair. In lateral row fixation, the eyelet of the PushLock and SwiveLock suture anchors (Arthrex) produces significant cable friction at the eyelet–suture interface, in addition to frictional force wedging the suture between anchor and bone.

As with so many other devices in shoulder arthroscopy, the SwiveLock suture anchor developed in stages. In the first stage, a chainlike suture with consecutive intersecting links was used (FiberChain). The idea for an adjustable fixation construct came to me because I thought that a forked eyelet on a SwiveLock would provide a firm fixation point when inserted into the appropriate suture link, yet would be totally adjustable simply by choosing a tighter or looser link (Figure 4). Although the system worked very well, it was technically challenging. The process was greatly simplified after Don Grafton and I developed FiberTape and recognized that the power of cable friction was dramatically increased by the larger contact area between the eyelet and the braided FiberTape. The SpeedBridge construct (Arthrex), which enhanced cable friction fixation by means of passing FiberTape through the anchor eyelets, also provided a larger compressive interface at the repair site by using FiberTape rather than conventional suture. These incremental improvements led to what I would characterize as today’s gold standard for arthroscopic rotator cuff repair: a largely knotless linked double-row construct using FiberTape, with cinch-loop sutures at the anterior and posterior margins of the tear to reinforce the cable attachments and simultaneously reduce the dog-ears that typically occur in those locations, and a double-pulley medial mattress if tendon quality is poor (Figure 5).

The Burden of Craft

With all the recent enthusiasm for level I studies, I think we need to examine whether they will accelerate technological advancement in rotator cuff repair. The answer, in my opinion, is a resounding no. This answer is based on a major disconnect I have detected in how we evaluate these studies in rotator cuff disease and repair.

An irony related to technological advancement in surgery is that the more technically advanced the surgery becomes, the more skill is required. This fact is completely at odds with the public’s perception that technological advances make procedures easier. In arthroscopic rotator cuff repair, the surgeon must look, feel, and be aware to a greater degree than in open surgery.

Edward Tenner, in his book Why Things Bite Back, described the burden of the practitioner of any advanced technology as the burden of craft.¹⁴ The burden of craft is the inherent demand on all craftspeople, but particularly surgeons, to “up our game” if we are to be successful in our craft. For arthroscopic rotator cuff repair, the burden of craft requires patience, attention to detail, and the ability to work in a virtual space. Not everyone has these skills. But anyone who wants to practice in this discipline has an obligation to learn the skills required, and then to teach them to others and assess how well they are being applied.

The problem with relying on level I studies to assess the efficacy of a surgical procedure is that they are inherently biased by the surgeons involved. As results depend on surgeons’ skills, and surgeons’ skill levels are not equal, level I studies cannot prove what is possible, cannot demonstrate the limits of a technique, and cannot demonstrate the equivalence of techniques.

Amazingly enough, there are still rotator cuff repair “deniers” who confidently assert from the podium that a large percentage of massive cuff tears cannot be repaired and that, even if they can be repaired, they do not have the biological potential to heal. Given the disparity in surgeons’ skills and results, however, one must ask whether poor results are a consequence of a biological deficit in the patient, or of a skill deficit in the surgeon.

What I know is that we have techniques for predictable arthroscopic repair and healing of the vast majority of rotator cuff tears, even massive tears,^15-17 and patients do very well clinically. Yet, among many orthopedic surgeons, there is a trend to go straight to reverse total shoulder arthroplasty (rTSA) for massive tears—despite the evidence against it. As reported in the literature, rTSA results are not as good as arthroscopic cuff repair results, and the complication rate for rTSA is much higher.

Why has this trend toward rTSA for massive tears gained so much momentum? The only reason I can surmise is that, for the average surgeon, rTSA is easier and quicker than arthroscopic repair for massive tears. But the reason for choosing a specific type of surgery for a given problem should not be that it is easiest for the surgeon; it should be that it is best for the patient.

The surgeon should start by asking what procedure he or she would want if the roles were reversed—if the surgeon were the patient with the massive rotator cuff tear. If a surgeon does not have the skill set for the best procedure for a particular patient, he or she is obligated to send that patient to a surgeon who does have the skills. In addition, given that infection is the most feared complication in most shoulder surgeries, the surgeon should ask which infection rate would be personally acceptable. Arthroscopic rotator cuff repair has a reported infection rate of 1.6 per 1000, or .0016,¹⁸ whereas rTSA has an infection rate about 25 times higher, or .04.¹⁹ Further, the surgeon must consider the relative severity of the consequences of infection. By any measure, an infected arthroscopy is a straightforward treatable complication, but an infected shoulder replacement is a human tragedy. Patients vastly prefer the minimally invasive arthroscopic approach, and through online searches can easily identify who can offer an arthroscopic solution.

To reproducibly achieve successful arthroscopic repair of massive rotator cuff tears, the surgeon must know advanced techniques, including subscapularis repair techniques,^20,21 interval slides,^22,23 and self-reinforcing constructs.^24,25

“It’s a poor carpenter who blames his tools.” This 18th-century English proverb is as true today as it was 300 years ago. The tools for arthroscopic cuff repair exist, and they are excellent. The burden of craft is the surgeon’s burden and obligation. As surgeons, we must accept that obligation and the responsibility of that burden.

As mentioned earlier, Dr. Rob Bell’s charge to me when he invited me to give the Neer Lecture was to sum up my involvement in the development of arthroscopic shoulder surgery. The short version is that I have been doing shoulder arthroscopy for 31 years; have received 28 US patents related to shoulder instruments and implants and have 12 US patents pending; have published 167 peer-reviewed articles, a couple dozen book chapters, and 2 textbooks on shoulder arthroscopy; have trained 25 fellows; and have hosted approximately 3000 visiting surgeons in my operating room. My greatest professional dream was to see the standard of care for rotator cuff repair and shoulder instability transition from open to arthroscopic techniques, and I have been fortunate enough to have observed that paradigm shift during my career.

What do I envision over the next 31 years? As we all know, history runs in both directions, and some things simply have not happened yet. In terms of rotator cuff treatment, I think over the next few years the guiding principle of treatment will be joint preservation. All rotator cuff tears, even massive tears, will be repaired arthroscopically. Patients and insurers will demand arthroscopic repair, and surgeons without the skill set will migrate to other subspecialties. As for the role of arthroplasty in the treatment of rotator cuff tears, rTSA will be indicated only for pseudoparalysis after failed cuff repair in low-demand elderly patients.

In rotator cuff treatment, I envision a standard of care that is almost entirely arthroscopic. This standard will demand that surgeons who treat rotator cuff tears be proficient in arthroscopic repair of the full range of tears. Acquiring the skills for arthroscopic repair may not be easy, but then “there’s the easy way, and there’s the Cowboy Way.” As my dad used to tell me when I complained about working too hard, “No man ever drowned in his own sweat.” We shoulder surgeons must accept the burden of craft that accompanies the new standard of arthroscopic cuff repair, and we must offer our patients the same level of care we would choose for ourselves.

Happy trails!

I am very honored that Dr. Rob Bell, past president of the American Shoulder and Elbow Surgeons, invited me to give last year’s Neer Lecture. Dr. Bell asked me to specifically address my role in the development of arthroscopic rotator cuff repair and to recount the significant resistance that the early arthroscopic shoulder surgeons faced from the shoulder establishment as we struggled to achieve mainstream acceptance for this new technology. Tasked with such a personal topic, I find myself in a position analogous to that of Winston Churchill at the end of World War II. When a journalist asked him to speculate on how historians would portray his role in the war, he replied without hesitation, “History will be kind to me because I intend to write it.”

So let’s start at the beginning. And for me it makes the most sense to travel back to the year I started my practice: 1981. The world then was very different from today’s world. On January 20, 1981, Ronald Reagan was inaugurated President of the United States. The same day, 52 US hostages in Iran were released after having been held captive for 442 days. In March 1981, Reagan survived an assassination attempt; 3 months earlier, John Lennon had not been so lucky. Lennon’s hit song “Starting Over” garnered the highest musical awards posthumously.

The world of shoulder surgery was also very different in 1981. The arthroscope was the “instrument of the devil,” according to Dr. Rockwood. And shoulder surgery was ruled by the Charlies—Dr. Charles Neer, Dr. Charlie Rockwood, and any other Charlie who felt compelled to marginalize shoulder arthroscopy.

My personal world in the early 1980s was daunting as well. I had just completed my residency at the Mayo Clinic and my sports medicine fellowship in Eugene, Oregon. I had a young son, a new daughter, and a new job with the San Antonio Orthopaedic Group. I had a new house with a 21% mortgage loan and a “new” used car with a 23% car loan.

I was simultaneously energized and intimidated by my new job, where I was doing general orthopedics with a “special interest” in shoulder surgery and sports medicine. I was initially very proud and humbled by the fact that my senior partners had entrusted me with the care of the most difficult shoulder cases within the practice. But that pride got cut down to its appropriate size the day after I had thanked one of my partners, Dr. Lamar Collie, for his confidence in my potential as a shoulder surgeon. Dr. Collie replied matter-of-factly, “Sure … but you need to understand that we always make the new guy the shoulder expert because shoulders never do worth a damn.”

For shoulder arthroscopy, the early 1980s were exciting. Most of us who were scoping shoulders had already been doing knee arthroscopy and were trying to adapt knee instruments to the shoulder. This worked for some simple excisional cases. For example, I recall excising the bucket-handle portion of a type III SLAP (superior labral tear from anterior to posterior) lesion in 1983. In general, however, shoulder problems were different from knee problems and usually involved repair rather than excision of damaged tissues. Therefore, the technology used in knee arthroscopy was often not directly transferable to the shoulder. Furthermore, treatment of the rotator cuff necessitated development of arthroscopic techniques in a virtual space, the subacromial space, and this was an entirely new arthroscopic concept.

Development of Arthroscopic Rotator Cuff Repair

A major mind-expanding turning point for me occurred in 1984 when I attended one of Dr. Jim Esch’s early San Diego shoulder courses. During that course, Dr. Harvard Ellman of Los Angeles demonstrated to me on a cadaver shoulder how he created a virtual subacromial working space that allowed enough visualization for an arthroscopic acromioplasty. At that moment, I knew that arthroscopic rotator cuff repair was just around the corner. Up until then, I had not been able to envision complex extra-articular reconstructive surgery, as all previous arthroscopic surgery had been intra-articular. But now, having realized a virtual working space could always be created, I knew it would be relatively straightforward to develop the portals to approach the cuff as well as the implants and the instruments to repair it. But I also knew that progression to all-arthroscopic repair techniques would have to be stepwise and that the final repair constructs would need to be at least as strong as those of open repair in order to be acceptable. With an undergraduate degree in mechanical engineering, I had a reasonably clear idea of the concepts I wanted to apply to the instrumentation and techniques, though I could never have envisioned how circuitous the route to the end result would be.

First Steps

I sketched out my ideas for arthroscopic suture passers and knot-tying instruments and presented them to a couple of the major arthroscopy companies in the United States, but the companies were not interested. They did not believe arthroscopy would have any meaningful applications in the shoulder. So, I enlisted the services of a local San Antonio aircraft machinist to fabricate instruments for me. By 1987, I was doing arthroscopic side-to-side margin convergence¹ cuff repairs for U-shape tears on a regular basis. And I was doing these at the most hostile point in the universe for arthroscopic shoulder surgery: San Antonio, Texas.

Only a few surgeons were doing arthroscopic shoulder surgery in the 1980s and early 1990s, and without exception these surgeons became the leader-pioneers in the new discipline. In general, these were young surgeons who were in private practice and removed from academia and professional organizations, and thus relatively sheltered from the actions of the shoulder rule-makers of the day. They accepted their status as pariahs as they developed their techniques out of the view of mainstream orthopedics. These leaders included Jim Esch, Steve Snyder, Dick Caspari, Lanny Johnson, Gene Wolf, Gary Gartsman, Rob Bell, and Howard Sweeney. We shared our techniques and our ideas with one another, encouraged one another, and generally became good friends.

Thomas Kuhn, in his classic book The Structure of Scientific Revolutions,² observed that paradigm shifts within a given field were usually achieved by practitioners who were either very young (naïve) or outside the established hierarchy in the field. The surgeons who contributed most to the shift of shoulder surgery from open to arthroscopic techniques were generally young men who were in private practice and had little to lose by inciting the disdain of the shoulder establishment. Predictably, resistance from the mainstream open shoulder surgeons increased as arthroscopic techniques became more successful and more threatening to the primacy of the open shoulder surgeons. The disdain yielded to disruption and finally to transformation as the paradigm shift occurred. The conflict between the open shoulder surgeons and the arthroscopic shoulder surgeons passed through all the phases that Mahatma Gandhi had described many years before. “First they ignore you; then they laugh at you; then they fight you; then you win.”

Building a Ship in a Bottle

At the start of the 1990s, I recognized that my progress in arthroscopic rotator cuff repair would be extremely slow unless I could find an industry partner who shared my vision for full-scale conversion to arthroscopic means of repair and would be willing to help make it a reality. In 1991, I happened to meet Reinhold Schmieding, the owner of Arthrex, a small arthroscopic device company in Naples, Florida. Reinhold invited me to visit him to discuss the feasibility of developing arthroscopic repair systems for the shoulder. At the time, the world headquarters of Arthrex was a 20×30-ft storage room in an office service center, and there were 2 employees. One employee, Don Grafton, was a talented engineer without medical experience. By the end of my first day there, Reinhold and Don and I had agreed that developing arthroscopic repair systems for shoulder instability and rotator cuff repair would become a top priority for Arthrex.

My initial bias toward arthroscopic cuff repair was that a transosseous bone tunnel technique not only would be possible but would be superior to suture anchor fixation. In fact, my first 2 patents with Arthrex were for instrumentation for an arthroscopic transosseous repair technique. I tested my hypothesis with 2 successive biomechanical studies. The first examined cyclic loading of bone tunnel repairs, and the second examined cyclic loading of anchor-based repairs.^3,4 Evaluating the data from these 2 studies, I was surprised to find that anchor-based repairs were significantly stronger than bone tunnel repairs. In addition, anchors shifted the weak link from the bone–suture interface to the tendon–suture interface; in essence, anchors optimized bone fixation by shifting the weak link in the construct to the tendon. I was then completely convinced of the superiority of suture anchors over bone tunnels, and that conviction has become even stronger over the years. After these 2 cyclic loading studies, I shifted my focus, and that of Arthrex, toward arthroscopic suture anchor repair of the rotator cuff.

Reconciling Technique and Instrumentation With Anatomy and Biomechanics

Having recognized the importance of the rotator cable attachments both anatomically⁵ and biomechanically,^6,7 I thought it important to reinforce them as a routine part of performing rotator cuff repairs. Our anatomical and biomechanical studies had had great translational implications in the development of our techniques and instrumentation.

As mentioned earlier, Don Grafton was the chief (and for a long time only) engineer at Arthrex. As he had no medical experience, I invited him to come to San Antonio to observe surgery. During Don’s many visits, I showed him pathology in the operating room and pointed out what I could do with the instruments I had and what I could not do. Then in the evening we went to my house and brainstormed how to perform the “missing” surgical manipulations, how to improve manipulations that were suboptimal, and how to optimize final surgical constructs.

Passing suture through tendon was an early challenge. One must remember that, in the early 1990s, it was not possible for machinists to fabricate complex shapes. Therefore, straight tubular retrograde suture passers were the logical first option. We initially developed spring-loaded retrograde hook retrievers (Figure 1) and then curved suture hooks with shuttling wires (Lasso). To me, the most unappealing feature of retrograde suture passage was the oblique angle of approach through the tendon, which caused a length–tension mismatch between the upper fibers and the lower fibers of the muscle–tendon unit. We recognized we could eliminate the mismatch if we passed the suture antegrade, such that it would pass perpendicular to the tendon fibers. These insights and efforts culminated in development of the Viper suture passer and then the FastPass Scorpion suture passer, which has a spring-loaded trapdoor on the upper jaw for ergonomic self-retrieving of the suture once it is passed through the tendon.

To develop a knot pusher that optimized knot tying (yielding the highest knot security and the tightest loop security), we used prototype instruments to tie and test literally thousands of knots in the laboratory. We were thus able to verify that the Surgeon’s Sixth Finger Knot Pusher (Arthrex) reproducibly tied optimized knots^8,9 and also optimized knot fixation and bone fixation. However, our suture was not yet optimized and was prone to breakage, and our suture–tendon interface was not yet optimized. Clearly, improvement was needed in 2 more areas.

Don came up with the idea for a virtually unbreakable suture and developed that idea into FiberWire.¹⁰ Shortly thereafter, I contributed the idea and design for FiberTape, which dramatically enhanced suture pullout strength and footprint compression.

Anchor designs improved rapidly and dramatically. We made the second-generation BioCorkscrew fully threaded, which virtually eliminated anchor failure, even in soft bone.

Optimization of the suture–tendon interface took a giant step forward when Park and colleagues^11,12 introduced linked double-row rotator cuff repair. Much as with a Chinese finger trap, the harder you pull, the stronger it becomes, with yield load approaching ultimate load.

At this point, it seemed we had optimized virtually every segment of the rotator cuff repair construct. Each component was just about as good as it could be. Or was it?

The Accidental Quest for Knotless Fixation

In November 1998, I made my first trip to China as a guest speaker at the Congress of the Hong Kong Orthopaedic Association. My first view of the magnificent Hong Kong skyline across Victoria Harbour was truly breathtaking. As I admired the gleaming glass towers and the concrete canyons of the city, I had no idea that the very next day these modern skyscrapers would reveal an ancient secret that would change my approach to arthroscopic rotator cuff repair.

The day after my arrival, Dr. James Lam took me to lunch. As we approached the restaurant, he pointed across the street to a tall building that was being renovated and had scaffolding supporting workers alongside the first 9 stories of the exterior wall. Dr. Lam said that, after lunch, he would take me to the construction site for a closer look at the scaffolding.

After lunch, we walked to the base of the scaffolding. Dr. Lam told me it was constructed entirely of bamboo poles held together with lashings but no knots (Figure 2). Lashings were secured by turning them back on themselves and wrapping them in an entirely knotless manner.¹³ I found it incredible that this knotless fixation was so secure that it could support the weight of workers many stories above the ground. I resolved to determine how this fixation method worked and see if the same mechanism might help us achieve reliable knotless fixation in surgery.

When I returned home, I broke out my college engineering books and reacquainted myself with the concept of cable friction. As has happened so often in the past, however, it took a practical lesson from the ranch to truly illustrate for me how cable friction works.

Every cowboy knows that a spirited horse cannot be restrained with only one lead rope. However, a cowboy can wrap a lead rope around a “snubbing post” and thereby gain complete control over the animal, despite the horse’s superior size and strength. The cable friction between the rope and the post creates such a large restraining force that the cowboy can easily hold the animal without the help of a knotted rope (Figure 3). In similar fashion in the Hong Kong scaffolding, fixation strength results from the significant amount of cable friction produced when the lashings wrap around one another and around the bamboo poles.

The cable friction concept was pivotal in the development of knotless fixation in arthroscopic rotator cuff repair. In lateral row fixation, the eyelet of the PushLock and SwiveLock suture anchors (Arthrex) produces significant cable friction at the eyelet–suture interface, in addition to frictional force wedging the suture between anchor and bone.

As with so many other devices in shoulder arthroscopy, the SwiveLock suture anchor developed in stages. In the first stage, a chainlike suture with consecutive intersecting links was used (FiberChain). The idea for an adjustable fixation construct came to me because I thought that a forked eyelet on a SwiveLock would provide a firm fixation point when inserted into the appropriate suture link, yet would be totally adjustable simply by choosing a tighter or looser link (Figure 4). Although the system worked very well, it was technically challenging. The process was greatly simplified after Don Grafton and I developed FiberTape and recognized that the power of cable friction was dramatically increased by the larger contact area between the eyelet and the braided FiberTape. The SpeedBridge construct (Arthrex), which enhanced cable friction fixation by means of passing FiberTape through the anchor eyelets, also provided a larger compressive interface at the repair site by using FiberTape rather than conventional suture. These incremental improvements led to what I would characterize as today’s gold standard for arthroscopic rotator cuff repair: a largely knotless linked double-row construct using FiberTape, with cinch-loop sutures at the anterior and posterior margins of the tear to reinforce the cable attachments and simultaneously reduce the dog-ears that typically occur in those locations, and a double-pulley medial mattress if tendon quality is poor (Figure 5).

The Burden of Craft

With all the recent enthusiasm for level I studies, I think we need to examine whether they will accelerate technological advancement in rotator cuff repair. The answer, in my opinion, is a resounding no. This answer is based on a major disconnect I have detected in how we evaluate these studies in rotator cuff disease and repair.

An irony related to technological advancement in surgery is that the more technically advanced the surgery becomes, the more skill is required. This fact is completely at odds with the public’s perception that technological advances make procedures easier. In arthroscopic rotator cuff repair, the surgeon must look, feel, and be aware to a greater degree than in open surgery.

Edward Tenner, in his book Why Things Bite Back, described the burden of the practitioner of any advanced technology as the burden of craft.¹⁴ The burden of craft is the inherent demand on all craftspeople, but particularly surgeons, to “up our game” if we are to be successful in our craft. For arthroscopic rotator cuff repair, the burden of craft requires patience, attention to detail, and the ability to work in a virtual space. Not everyone has these skills. But anyone who wants to practice in this discipline has an obligation to learn the skills required, and then to teach them to others and assess how well they are being applied.

The problem with relying on level I studies to assess the efficacy of a surgical procedure is that they are inherently biased by the surgeons involved. As results depend on surgeons’ skills, and surgeons’ skill levels are not equal, level I studies cannot prove what is possible, cannot demonstrate the limits of a technique, and cannot demonstrate the equivalence of techniques.

Amazingly enough, there are still rotator cuff repair “deniers” who confidently assert from the podium that a large percentage of massive cuff tears cannot be repaired and that, even if they can be repaired, they do not have the biological potential to heal. Given the disparity in surgeons’ skills and results, however, one must ask whether poor results are a consequence of a biological deficit in the patient, or of a skill deficit in the surgeon.

What I know is that we have techniques for predictable arthroscopic repair and healing of the vast majority of rotator cuff tears, even massive tears,^15-17 and patients do very well clinically. Yet, among many orthopedic surgeons, there is a trend to go straight to reverse total shoulder arthroplasty (rTSA) for massive tears—despite the evidence against it. As reported in the literature, rTSA results are not as good as arthroscopic cuff repair results, and the complication rate for rTSA is much higher.

Why has this trend toward rTSA for massive tears gained so much momentum? The only reason I can surmise is that, for the average surgeon, rTSA is easier and quicker than arthroscopic repair for massive tears. But the reason for choosing a specific type of surgery for a given problem should not be that it is easiest for the surgeon; it should be that it is best for the patient.

The surgeon should start by asking what procedure he or she would want if the roles were reversed—if the surgeon were the patient with the massive rotator cuff tear. If a surgeon does not have the skill set for the best procedure for a particular patient, he or she is obligated to send that patient to a surgeon who does have the skills. In addition, given that infection is the most feared complication in most shoulder surgeries, the surgeon should ask which infection rate would be personally acceptable. Arthroscopic rotator cuff repair has a reported infection rate of 1.6 per 1000, or .0016,¹⁸ whereas rTSA has an infection rate about 25 times higher, or .04.¹⁹ Further, the surgeon must consider the relative severity of the consequences of infection. By any measure, an infected arthroscopy is a straightforward treatable complication, but an infected shoulder replacement is a human tragedy. Patients vastly prefer the minimally invasive arthroscopic approach, and through online searches can easily identify who can offer an arthroscopic solution.

To reproducibly achieve successful arthroscopic repair of massive rotator cuff tears, the surgeon must know advanced techniques, including subscapularis repair techniques,^20,21 interval slides,^22,23 and self-reinforcing constructs.^24,25

“It’s a poor carpenter who blames his tools.” This 18th-century English proverb is as true today as it was 300 years ago. The tools for arthroscopic cuff repair exist, and they are excellent. The burden of craft is the surgeon’s burden and obligation. As surgeons, we must accept that obligation and the responsibility of that burden.

As mentioned earlier, Dr. Rob Bell’s charge to me when he invited me to give the Neer Lecture was to sum up my involvement in the development of arthroscopic shoulder surgery. The short version is that I have been doing shoulder arthroscopy for 31 years; have received 28 US patents related to shoulder instruments and implants and have 12 US patents pending; have published 167 peer-reviewed articles, a couple dozen book chapters, and 2 textbooks on shoulder arthroscopy; have trained 25 fellows; and have hosted approximately 3000 visiting surgeons in my operating room. My greatest professional dream was to see the standard of care for rotator cuff repair and shoulder instability transition from open to arthroscopic techniques, and I have been fortunate enough to have observed that paradigm shift during my career.

What do I envision over the next 31 years? As we all know, history runs in both directions, and some things simply have not happened yet. In terms of rotator cuff treatment, I think over the next few years the guiding principle of treatment will be joint preservation. All rotator cuff tears, even massive tears, will be repaired arthroscopically. Patients and insurers will demand arthroscopic repair, and surgeons without the skill set will migrate to other subspecialties. As for the role of arthroplasty in the treatment of rotator cuff tears, rTSA will be indicated only for pseudoparalysis after failed cuff repair in low-demand elderly patients.

In rotator cuff treatment, I envision a standard of care that is almost entirely arthroscopic. This standard will demand that surgeons who treat rotator cuff tears be proficient in arthroscopic repair of the full range of tears. Acquiring the skills for arthroscopic repair may not be easy, but then “there’s the easy way, and there’s the Cowboy Way.” As my dad used to tell me when I complained about working too hard, “No man ever drowned in his own sweat.” We shoulder surgeons must accept the burden of craft that accompanies the new standard of arthroscopic cuff repair, and we must offer our patients the same level of care we would choose for ourselves.

Happy trails!

The overhead athlete’s shoulder is exposed to extremes of stress and range of motion (ROM), predisposing this joint to unique injury patterns. Prompt diagnosis and management begin with a comprehensive history and a physical examination, supplemented by imaging studies as needed. Furthermore, the throwing shoulder undergoes adaptive changes, such as partial undersurface rotator cuff tears and capsular laxity. Imaging studies typically demonstrate abnormalities in asymptomatic throwers. Therefore, clinicians must be skilled in history taking and physical examination in throwing athletes to accurately determine the cause of symptoms and provide optimal treatment. This primer provides orthopedic surgeons with the key points in performing a thorough physical examination of the shoulder in overhead athletes.

When working with overhead athletes, surgeons must elicit the precise nature of symptoms. For example, it is important to distinguish pain from fatigue, as well as complaints related purely to decline in performance. Often, collaboration with the player’s parent or coach may help clarify the chief complaint. In addition, surgeons must have an intricate knowledge of the various stages of the overhead motion, as symptoms in specific stages (late cocking/early acceleration) may raise suspicion for distinctive pathology (labral/biceps complex). Last, it is imperative to understand that the shoulder represents only one part of the kinetic chain in overhead athletes. Successful throwing relies on integrity of the entire kinetic chain, starting with the lower extremity and trunk, extending through the spine, scapula, and shoulder, and terminating with the hand and fingers. Pathology anywhere in the chain must be evaluated and addressed.

When examining the shoulder in overhead athletes, surgeons must address several anatomical structures, both bony and soft tissue. Proper examination begins with comprehensive assessment of the ROM and strength of the various muscles around the shoulder, along with visual inspection to identify any asymmetry of these structures. In addition, the scapulothoracic structures must be examined in detail to rule out underlying dyskinesis. The capsular and ligamentous components of the shoulder joint must be further assessed to note any capsular contracture causing glenohumeral internal rotation deficit (GIRD) or any pathology with the rotator cuff or labral/biceps complex. Last, a comprehensive neurovascular examination should be performed to rule out any compression or neuropathy affecting the shoulder and overhead motion. Findings from the physical examination may then require further imaging to correlate the history and physical examination findings.

1. Inspection, palpation, strength testing

Every examination of the shoulder must begin with visual inspection, along with assessment of basic ROM and strength. The patient must be positioned and exposed adequately to promote visualization of the entire shoulder and scapular girdle, from both anterior and posterior. Visual inspection focuses on identifying any areas of asymmetry, such as position of the bony prominences or bulk of the muscular fossae. Asymmetry of the bony architecture may indicate prior trauma, and atrophy of the muscular fossae may indicate nerve compression. For example, atrophy of the infraspinatus fossa may be caused by compression of the suprascapular nerve at the spinoglenoid notch (likely by a cyst, often associated with labral pathology, but infraspinatus atrophy can result even without the presence of a compressive cyst¹). Alternatively, atrophy of both the supraspinatus and infraspinatus fossae may indicate underlying compression of the suprascapular nerve at the suprascapular notch (either by a cyst or by the transverse scapular ligament). Static and dynamic observation of the posterior aspect of the shoulder may help identify gross pathology with scapular positioning or retraction, indicating underlying dyskinesis (discussed later). Deformity of the acromioclavicular joint may indicate prior trauma or separation. Last, all prior surgical scars should be noted.

Selective palpation may help identify pathology in the shoulder of the throwing athlete. Tenderness at the acromioclavicular joint may be especially common in patients who have had prior sprains of this joint or who have degenerative changes. Tenderness along the biceps tendon may be present in those with biceps tendinitis or partial tear. In addition, tenderness at the coracoid may be present in those with scapular dyskinesis. Posteriorly, palpation at the inferomedial aspect of the scapula (Figure 1), as with palpation along the medial border of the scapula, may elicit tenderness in those with scapulothoracic bursitis.

Strength testing in the shoulder is performed to elicit any deficiencies of the rotator cuff/musculature or surrounding structures. Weakness in forward elevation may indicate pathology in the supraspinatus, whereas weakness in external rotation may reflect deficiency in the infraspinatus or teres minor. Teres minor deficiency may be more isolated with weakness in a position of shoulder abduction to 90°. Last, weakness in internal rotation may indicate subscapularis deficiency. Lag signs and other provocative maneuvers are similarly elicited but typically are positive only in the event of large tears of the rotator cuff. These signs and maneuvers include the internal rotation lag sign or belly press test for subscapularis integrity, the drop-arm sign for supraspinatus function, the external rotation lag sign for infraspinatus function, and the hornblower sign for teres minor integrity. Supporting muscles of the shoulder may also be tested. Latissimus strength may be tested with resisted downward rotation of the arm with the shoulder in abduction and the elbow flexed to 90°.

2. ROM and GIRD assessment

After inspection and palpation, the shoulder should be ranged in all relevant planes of motion. Our standard examination includes forward elevation in the frontal and scapular planes, along with external rotation at the side and at 90° of abduction, as well as internal rotation behind the back with documentation of the highest spinal level that the patient can reach. This examination may be performed with the patient upright, but supine positioning can help stabilize the scapula and provide more accurate views of motion. Deficits of internal rotation may be a common finding in overhead athletes, and the degree of this deficit should be quantitatively noted.

Bony and soft-tissue remodeling of the shoulder (and associated structures) in the overhead athlete can lead to contracture of the posterior capsule. This contracture can cause excessive external rotation and subsequent decrease in internal rotation, leading to pain and anterior instability in the throwing shoulder.² For precise measurements of the internal and external rotation arc, the scapula must be stabilized. This can be done with the patient supine on the examining table or seated upright with manual stabilization of the scapula by the examiner. Once the scapula is stabilized, the arc of internal and external rotation (with the arm in about 90° of abduction) can be measured with a goniometer, with maximum values obtained as the scapula begins to move along the posterior chest wall.² The difference in internal rotation between the dominant and nondominant arms defines the extent of the athlete’s GIRD. Internal rotation can also be qualitatively assessed by having the athlete internally rotate each arm and reach up the spine while the examiner notes the difference in level achieved. However, this does not provide a quantitative assessment of the patient’s GIRD.

In general, the sum of the internal and external rotation arcs on the 2 sides should be symmetric. Consequently, in GIRD, excessive external rotation is balanced by decreased internal rotation. Symptomatic GIRD may be present when there is more than 25° of discrepancy in internal rotation between the athlete’s dominant and nondominant arms.² The goal is to reduce this discrepancy to less than 20°.

3. Internal impingement: rotator cuff and labrum

In overhead athletes, an intricate relationship involving rotator cuff, labrum, and biceps tendon allows for efficient, pain-free force delivery at the shoulder. However, because of the significant external rotation and abduction required in the overhead motion, there may be internal impingement of the posterosuperior rotator cuff (infraspinatus and posterior aspect of supraspinatus) between the posterior labrum and the greater tuberosity. Detailed examination of these structures must be performed in any assessment of an overhead athlete. Symptomatic patients may complain of pain during the throwing cycle, particularly in late cocking and early acceleration.

The modified relocation examination is a common maneuver to detect internal impingement.³ In this examination, the patient’s arm is brought into a position of maximal external rotation and abduction mimicking that found in late cocking or early acceleration. In this position, a patient with internal impingement complains of pain in the posterior shoulder. A posteriorly directed force on the humerus relieves this pain.

There are also many examinations for detecting labral pathology, specifically a SLAP (superior labrum, anterior to posterior) lesion, which is commonly found in patients with internal impingement. One commonly tested maneuver is the O’Brien active compression test (Figures 2A, 2B), which has excellent sensitivity and specificity in detecting type II SLAP lesions.⁴ In this examination, the patient holds the arm in about 15° of adduction and 90° of forward elevation. A downward force is applied with the forearm pronated and subsequently supinated. If pain is noted on the force applied to the pronated arm, and if this pain decreases in the supinated examination, the test is positive for labral pathology.

Anterior instability is routinely found in these patients. Translation is measured with the anterior load and shift test. Anterior translation is tested with the patient supine, with the arm in abduction and external rotation, and with the examiner placing an anteriorly directed force on the humeral head. Translation is compared with the contralateral side and graded on a 3-point scale (1+ is translation to glenoid rim, 2+ is translation over glenoid rim but reduces, 3+ is translation over glenoid and locking). We also use the anterior release test, in which the patient is supine, the arm is brought into abduction and external rotation, and the examiner places a posteriorly directed force on the humeral head. When the examiner removes this force, the patient notices symptoms of instability caused by subluxation (Figures 3A, 3B).

Biceps tendon testing should also be performed to help elicit signs of labral pathology. The Speed test is performed by placing a downward force on the patient’s arm, which is held in 90° forward elevation, and with elbows in extension and forearm in supination. Pain in the long head of the biceps tendon is considered a positive sign and suggestive of SLAP lesion. Although not commonly found in these athletes, external impingement should also be elicited through both the Neer test and the Hawkins test. In the Neer test, the patient’s arm is brought to maximal forward elevation with the forearm supinated and elbow extended, while the scapula is stabilized by the examiner. Pain in the shoulder indicates a positive examination. In the Hawkins test, the patient’s arm is brought into a position of forward elevation, internal rotation, and elbow flexion. The arm is then further internally rotated, and shoulder pain defines a positive examination.

Any of these findings can be concomitant with scapular dyskinesis. Moreover, symptoms related to internal impingement may be exacerbated by concomitant scapular pathology, and therefore proper assessment of scapulothoracic motion must also be performed.

4. Scapulothoracic examination

Motion coupled between the scapula and the rest of the arm (scapular rhythm) allows for efficient use of the shoulder girdle. The scapula helps transfer the force generated by the core so that the hand can efficiently deliver it. Therefore, scapular pathology (or dyskinesis) results in inefficient functioning of the arm, which can be especially debilitating in an overhead athlete.

Scapular assessment begins with visual inspection of the patient, typically from the posterior view, which allows for assessment of the resting position of the scapula. Evidence of prominence of the medial or inferomedial border, coracoid malposition (or pain on palpation), or general scapular malposition should be noted. On active ROM, as the patient forward-elevates the arm, any asymmetric prominence of the inferomedial border of the scapula should be noted. Such asymmetry may indicate underlying scapular dyskinesis. In another important test, the lateral scapular slide test (described by Kibler⁵), the distance from the inferomedial angle of the scapula to the thoracic spine should be measured for both sides and in 3 difference positions, noting any asymmetry between the affected and nonaffected sides. These 3 positions (Figures 4A–4C) are with arms at side, with hands on hips (internal rotation of humerus in 45° abduction), and in 90° of shoulder abduction. Last, medial and lateral scapular winging—caused by long thoracic nerve and spinal accessory nerve pathology, respectively—can be detected by asking the patient to do a “push-up” against the wall while the examiner views from posterior.

After assessment of scapular position at rest and through motion, a series of provocative maneuvers⁶ may aid in the diagnosis of scapular dyskinesis. The first maneuver is the scapular assistance test, in which the examiner provides a gentle force at the inferomedial angle of the scapula, promoting upward rotation and posterior tilt as the patient elevates the arm (Figures 5A, 5B). If the patient experiences a decrease or absence of symptoms through this arc, the test is considered positive. The second maneuver is the scapular retraction test, in which strength testing of the supraspinatus is performed before and after retraction stabilization of the scapula. In the baseline state, the strength of the supraspinatus is tested in standard fashion, with resisted elevation of the internally rotated and abducted arm. The strength is then tested with the scapula stabilized in retraction (the examiner medially stabilizes the scapula). With scapular stabilization, an increase in strength or a decrease in symptoms is considered a positive test.

5. Neurovascular examination

It is essential to perform a comprehensive neurovascular examination in all overhead athletes. This includes basic cervical spine testing for any motor or sensory deficits, along with assessment of scapular winging to detect long thoracic or spinal accessory nerve palsy for medial and lateral winging, respectively. Although neurovascular injury may be a rare finding in the overhead athlete, a detailed examination must still be performed to rule it out.

Thoracic outlet syndrome

Thoracic syndrome is a compressive neuropathy of nerves and vasculature exiting the thorax and entering the upper extremity. Common symptoms include pain and tingling (sometimes vague) in the neck and upper extremity. These symptoms may be positional as well.

Diagnosis of thoracic outlet syndrome begins with visual inspection of the involved upper extremity, noting atrophy or asymmetry. Weakness may also be present. Additional provocative maneuvers can be used to detect decrease or loss of pulses, along with reproduction of symptoms, during a provocative maneuver with subsequent return of pulses and resolution of symptoms after the maneuver is completed.

One examination that can be used to detect thoracic outlet syndrome is the Adson test.⁷ During this maneuver, the radial pulse is palpated with the arm at rest on the patient’s side. The patient then turns to the symptomatic side, hyperextends the arm, and holds inspiration. A positive test coincides with both decreased pulse and reproduction of symptoms, indicating compression within the scalene triangle. In the Wright test,⁷ the pulse is again palpated at rest with the arm at the side. The patient then holds inspiration and places the arm in a position of abduction and external rotation. If the pulses decrease with this maneuver, the test is considered positive, indicating compression in the sub–pectoralis minor region deep to the coracoid. In a third test, the costoclavicular test, again pulses are measured before and during the provocative maneuver, which is with the shoulders thrust backward and depressed downward. A positive test indicates compression between the clavicle and the first rib. In our practice, we use a modified Wright test in which the arm is held in abduction and external rotation while radial pulses are palpated. The fist is then opened and clenched rapidly, and diminution of radial pulses is considered a positive examination (Figures 6A, 6B).

Effort thrombosis

Overhead athletes are at increased risk for developing effort thrombosis⁸ (Paget-Schroetter syndrome). This thrombosis, which results from repetitive motion involving the upper extremity, is not limited to overhead sports; it may be caused by underlying compression of or microtrauma to the venous infrastructure. On physical examination, there may be swelling of the affected limb, along with diffuse pain and fatigue, as well as dermatologic changes. Positive findings warrant further testing, such as coagulation profile testing and advanced imaging or venography.

Arterial aneurysm

Although rare, arterial aneurysms, especially of the axillary artery, must be ruled out in the overhead athlete with vague upper extremity pain (especially distally) and without clear diagnosis.⁹ Aneurysm of the axillary artery can result from repetitive microtrauma related to repetitive overhead motion of the upper extremity. This condition may cause showering of emboli distally to the vasculature of the hand and fingers (Figure 7). Patients may complain of pain in the fingers, difficulty with grip, cyanosis, or cold sensation. On examination, the sufficiency of the radial and ulnar arteries should be assessed, as with detailed sensorimotor examination of the fingers. The fingernails should be examined for splinter hemorrhages.

Conclusion

Overhead athletes place extreme stress on the shoulder during the throwing motion and are at high risk for injury because of repetitive stress on the shoulder girdle. When examining overhead athletes with shoulder pain, surgeons must consider the entire kinetic chain, as inefficiencies anywhere along the chain can lead to altered mechanics and pathology in the shoulder.

The overhead athlete’s shoulder is exposed to extremes of stress and range of motion (ROM), predisposing this joint to unique injury patterns. Prompt diagnosis and management begin with a comprehensive history and a physical examination, supplemented by imaging studies as needed. Furthermore, the throwing shoulder undergoes adaptive changes, such as partial undersurface rotator cuff tears and capsular laxity. Imaging studies typically demonstrate abnormalities in asymptomatic throwers. Therefore, clinicians must be skilled in history taking and physical examination in throwing athletes to accurately determine the cause of symptoms and provide optimal treatment. This primer provides orthopedic surgeons with the key points in performing a thorough physical examination of the shoulder in overhead athletes.

When working with overhead athletes, surgeons must elicit the precise nature of symptoms. For example, it is important to distinguish pain from fatigue, as well as complaints related purely to decline in performance. Often, collaboration with the player’s parent or coach may help clarify the chief complaint. In addition, surgeons must have an intricate knowledge of the various stages of the overhead motion, as symptoms in specific stages (late cocking/early acceleration) may raise suspicion for distinctive pathology (labral/biceps complex). Last, it is imperative to understand that the shoulder represents only one part of the kinetic chain in overhead athletes. Successful throwing relies on integrity of the entire kinetic chain, starting with the lower extremity and trunk, extending through the spine, scapula, and shoulder, and terminating with the hand and fingers. Pathology anywhere in the chain must be evaluated and addressed.

When examining the shoulder in overhead athletes, surgeons must address several anatomical structures, both bony and soft tissue. Proper examination begins with comprehensive assessment of the ROM and strength of the various muscles around the shoulder, along with visual inspection to identify any asymmetry of these structures. In addition, the scapulothoracic structures must be examined in detail to rule out underlying dyskinesis. The capsular and ligamentous components of the shoulder joint must be further assessed to note any capsular contracture causing glenohumeral internal rotation deficit (GIRD) or any pathology with the rotator cuff or labral/biceps complex. Last, a comprehensive neurovascular examination should be performed to rule out any compression or neuropathy affecting the shoulder and overhead motion. Findings from the physical examination may then require further imaging to correlate the history and physical examination findings.

1. Inspection, palpation, strength testing

Every examination of the shoulder must begin with visual inspection, along with assessment of basic ROM and strength. The patient must be positioned and exposed adequately to promote visualization of the entire shoulder and scapular girdle, from both anterior and posterior. Visual inspection focuses on identifying any areas of asymmetry, such as position of the bony prominences or bulk of the muscular fossae. Asymmetry of the bony architecture may indicate prior trauma, and atrophy of the muscular fossae may indicate nerve compression. For example, atrophy of the infraspinatus fossa may be caused by compression of the suprascapular nerve at the spinoglenoid notch (likely by a cyst, often associated with labral pathology, but infraspinatus atrophy can result even without the presence of a compressive cyst¹). Alternatively, atrophy of both the supraspinatus and infraspinatus fossae may indicate underlying compression of the suprascapular nerve at the suprascapular notch (either by a cyst or by the transverse scapular ligament). Static and dynamic observation of the posterior aspect of the shoulder may help identify gross pathology with scapular positioning or retraction, indicating underlying dyskinesis (discussed later). Deformity of the acromioclavicular joint may indicate prior trauma or separation. Last, all prior surgical scars should be noted.

Selective palpation may help identify pathology in the shoulder of the throwing athlete. Tenderness at the acromioclavicular joint may be especially common in patients who have had prior sprains of this joint or who have degenerative changes. Tenderness along the biceps tendon may be present in those with biceps tendinitis or partial tear. In addition, tenderness at the coracoid may be present in those with scapular dyskinesis. Posteriorly, palpation at the inferomedial aspect of the scapula (Figure 1), as with palpation along the medial border of the scapula, may elicit tenderness in those with scapulothoracic bursitis.

Strength testing in the shoulder is performed to elicit any deficiencies of the rotator cuff/musculature or surrounding structures. Weakness in forward elevation may indicate pathology in the supraspinatus, whereas weakness in external rotation may reflect deficiency in the infraspinatus or teres minor. Teres minor deficiency may be more isolated with weakness in a position of shoulder abduction to 90°. Last, weakness in internal rotation may indicate subscapularis deficiency. Lag signs and other provocative maneuvers are similarly elicited but typically are positive only in the event of large tears of the rotator cuff. These signs and maneuvers include the internal rotation lag sign or belly press test for subscapularis integrity, the drop-arm sign for supraspinatus function, the external rotation lag sign for infraspinatus function, and the hornblower sign for teres minor integrity. Supporting muscles of the shoulder may also be tested. Latissimus strength may be tested with resisted downward rotation of the arm with the shoulder in abduction and the elbow flexed to 90°.

2. ROM and GIRD assessment

After inspection and palpation, the shoulder should be ranged in all relevant planes of motion. Our standard examination includes forward elevation in the frontal and scapular planes, along with external rotation at the side and at 90° of abduction, as well as internal rotation behind the back with documentation of the highest spinal level that the patient can reach. This examination may be performed with the patient upright, but supine positioning can help stabilize the scapula and provide more accurate views of motion. Deficits of internal rotation may be a common finding in overhead athletes, and the degree of this deficit should be quantitatively noted.

Bony and soft-tissue remodeling of the shoulder (and associated structures) in the overhead athlete can lead to contracture of the posterior capsule. This contracture can cause excessive external rotation and subsequent decrease in internal rotation, leading to pain and anterior instability in the throwing shoulder.² For precise measurements of the internal and external rotation arc, the scapula must be stabilized. This can be done with the patient supine on the examining table or seated upright with manual stabilization of the scapula by the examiner. Once the scapula is stabilized, the arc of internal and external rotation (with the arm in about 90° of abduction) can be measured with a goniometer, with maximum values obtained as the scapula begins to move along the posterior chest wall.² The difference in internal rotation between the dominant and nondominant arms defines the extent of the athlete’s GIRD. Internal rotation can also be qualitatively assessed by having the athlete internally rotate each arm and reach up the spine while the examiner notes the difference in level achieved. However, this does not provide a quantitative assessment of the patient’s GIRD.

In general, the sum of the internal and external rotation arcs on the 2 sides should be symmetric. Consequently, in GIRD, excessive external rotation is balanced by decreased internal rotation. Symptomatic GIRD may be present when there is more than 25° of discrepancy in internal rotation between the athlete’s dominant and nondominant arms.² The goal is to reduce this discrepancy to less than 20°.

3. Internal impingement: rotator cuff and labrum

In overhead athletes, an intricate relationship involving rotator cuff, labrum, and biceps tendon allows for efficient, pain-free force delivery at the shoulder. However, because of the significant external rotation and abduction required in the overhead motion, there may be internal impingement of the posterosuperior rotator cuff (infraspinatus and posterior aspect of supraspinatus) between the posterior labrum and the greater tuberosity. Detailed examination of these structures must be performed in any assessment of an overhead athlete. Symptomatic patients may complain of pain during the throwing cycle, particularly in late cocking and early acceleration.

The modified relocation examination is a common maneuver to detect internal impingement.³ In this examination, the patient’s arm is brought into a position of maximal external rotation and abduction mimicking that found in late cocking or early acceleration. In this position, a patient with internal impingement complains of pain in the posterior shoulder. A posteriorly directed force on the humerus relieves this pain.

There are also many examinations for detecting labral pathology, specifically a SLAP (superior labrum, anterior to posterior) lesion, which is commonly found in patients with internal impingement. One commonly tested maneuver is the O’Brien active compression test (Figures 2A, 2B), which has excellent sensitivity and specificity in detecting type II SLAP lesions.⁴ In this examination, the patient holds the arm in about 15° of adduction and 90° of forward elevation. A downward force is applied with the forearm pronated and subsequently supinated. If pain is noted on the force applied to the pronated arm, and if this pain decreases in the supinated examination, the test is positive for labral pathology.

Anterior instability is routinely found in these patients. Translation is measured with the anterior load and shift test. Anterior translation is tested with the patient supine, with the arm in abduction and external rotation, and with the examiner placing an anteriorly directed force on the humeral head. Translation is compared with the contralateral side and graded on a 3-point scale (1+ is translation to glenoid rim, 2+ is translation over glenoid rim but reduces, 3+ is translation over glenoid and locking). We also use the anterior release test, in which the patient is supine, the arm is brought into abduction and external rotation, and the examiner places a posteriorly directed force on the humeral head. When the examiner removes this force, the patient notices symptoms of instability caused by subluxation (Figures 3A, 3B).

Biceps tendon testing should also be performed to help elicit signs of labral pathology. The Speed test is performed by placing a downward force on the patient’s arm, which is held in 90° forward elevation, and with elbows in extension and forearm in supination. Pain in the long head of the biceps tendon is considered a positive sign and suggestive of SLAP lesion. Although not commonly found in these athletes, external impingement should also be elicited through both the Neer test and the Hawkins test. In the Neer test, the patient’s arm is brought to maximal forward elevation with the forearm supinated and elbow extended, while the scapula is stabilized by the examiner. Pain in the shoulder indicates a positive examination. In the Hawkins test, the patient’s arm is brought into a position of forward elevation, internal rotation, and elbow flexion. The arm is then further internally rotated, and shoulder pain defines a positive examination.

Any of these findings can be concomitant with scapular dyskinesis. Moreover, symptoms related to internal impingement may be exacerbated by concomitant scapular pathology, and therefore proper assessment of scapulothoracic motion must also be performed.

4. Scapulothoracic examination

Motion coupled between the scapula and the rest of the arm (scapular rhythm) allows for efficient use of the shoulder girdle. The scapula helps transfer the force generated by the core so that the hand can efficiently deliver it. Therefore, scapular pathology (or dyskinesis) results in inefficient functioning of the arm, which can be especially debilitating in an overhead athlete.

Scapular assessment begins with visual inspection of the patient, typically from the posterior view, which allows for assessment of the resting position of the scapula. Evidence of prominence of the medial or inferomedial border, coracoid malposition (or pain on palpation), or general scapular malposition should be noted. On active ROM, as the patient forward-elevates the arm, any asymmetric prominence of the inferomedial border of the scapula should be noted. Such asymmetry may indicate underlying scapular dyskinesis. In another important test, the lateral scapular slide test (described by Kibler⁵), the distance from the inferomedial angle of the scapula to the thoracic spine should be measured for both sides and in 3 difference positions, noting any asymmetry between the affected and nonaffected sides. These 3 positions (Figures 4A–4C) are with arms at side, with hands on hips (internal rotation of humerus in 45° abduction), and in 90° of shoulder abduction. Last, medial and lateral scapular winging—caused by long thoracic nerve and spinal accessory nerve pathology, respectively—can be detected by asking the patient to do a “push-up” against the wall while the examiner views from posterior.

After assessment of scapular position at rest and through motion, a series of provocative maneuvers⁶ may aid in the diagnosis of scapular dyskinesis. The first maneuver is the scapular assistance test, in which the examiner provides a gentle force at the inferomedial angle of the scapula, promoting upward rotation and posterior tilt as the patient elevates the arm (Figures 5A, 5B). If the patient experiences a decrease or absence of symptoms through this arc, the test is considered positive. The second maneuver is the scapular retraction test, in which strength testing of the supraspinatus is performed before and after retraction stabilization of the scapula. In the baseline state, the strength of the supraspinatus is tested in standard fashion, with resisted elevation of the internally rotated and abducted arm. The strength is then tested with the scapula stabilized in retraction (the examiner medially stabilizes the scapula). With scapular stabilization, an increase in strength or a decrease in symptoms is considered a positive test.

5. Neurovascular examination

It is essential to perform a comprehensive neurovascular examination in all overhead athletes. This includes basic cervical spine testing for any motor or sensory deficits, along with assessment of scapular winging to detect long thoracic or spinal accessory nerve palsy for medial and lateral winging, respectively. Although neurovascular injury may be a rare finding in the overhead athlete, a detailed examination must still be performed to rule it out.

Thoracic outlet syndrome

Thoracic syndrome is a compressive neuropathy of nerves and vasculature exiting the thorax and entering the upper extremity. Common symptoms include pain and tingling (sometimes vague) in the neck and upper extremity. These symptoms may be positional as well.

Diagnosis of thoracic outlet syndrome begins with visual inspection of the involved upper extremity, noting atrophy or asymmetry. Weakness may also be present. Additional provocative maneuvers can be used to detect decrease or loss of pulses, along with reproduction of symptoms, during a provocative maneuver with subsequent return of pulses and resolution of symptoms after the maneuver is completed.

One examination that can be used to detect thoracic outlet syndrome is the Adson test.⁷ During this maneuver, the radial pulse is palpated with the arm at rest on the patient’s side. The patient then turns to the symptomatic side, hyperextends the arm, and holds inspiration. A positive test coincides with both decreased pulse and reproduction of symptoms, indicating compression within the scalene triangle. In the Wright test,⁷ the pulse is again palpated at rest with the arm at the side. The patient then holds inspiration and places the arm in a position of abduction and external rotation. If the pulses decrease with this maneuver, the test is considered positive, indicating compression in the sub–pectoralis minor region deep to the coracoid. In a third test, the costoclavicular test, again pulses are measured before and during the provocative maneuver, which is with the shoulders thrust backward and depressed downward. A positive test indicates compression between the clavicle and the first rib. In our practice, we use a modified Wright test in which the arm is held in abduction and external rotation while radial pulses are palpated. The fist is then opened and clenched rapidly, and diminution of radial pulses is considered a positive examination (Figures 6A, 6B).

Effort thrombosis

Overhead athletes are at increased risk for developing effort thrombosis⁸ (Paget-Schroetter syndrome). This thrombosis, which results from repetitive motion involving the upper extremity, is not limited to overhead sports; it may be caused by underlying compression of or microtrauma to the venous infrastructure. On physical examination, there may be swelling of the affected limb, along with diffuse pain and fatigue, as well as dermatologic changes. Positive findings warrant further testing, such as coagulation profile testing and advanced imaging or venography.

Arterial aneurysm

Although rare, arterial aneurysms, especially of the axillary artery, must be ruled out in the overhead athlete with vague upper extremity pain (especially distally) and without clear diagnosis.⁹ Aneurysm of the axillary artery can result from repetitive microtrauma related to repetitive overhead motion of the upper extremity. This condition may cause showering of emboli distally to the vasculature of the hand and fingers (Figure 7). Patients may complain of pain in the fingers, difficulty with grip, cyanosis, or cold sensation. On examination, the sufficiency of the radial and ulnar arteries should be assessed, as with detailed sensorimotor examination of the fingers. The fingernails should be examined for splinter hemorrhages.

Conclusion

Overhead athletes place extreme stress on the shoulder during the throwing motion and are at high risk for injury because of repetitive stress on the shoulder girdle. When examining overhead athletes with shoulder pain, surgeons must consider the entire kinetic chain, as inefficiencies anywhere along the chain can lead to altered mechanics and pathology in the shoulder.

The overhead athlete’s shoulder is exposed to extremes of stress and range of motion (ROM), predisposing this joint to unique injury patterns. Prompt diagnosis and management begin with a comprehensive history and a physical examination, supplemented by imaging studies as needed. Furthermore, the throwing shoulder undergoes adaptive changes, such as partial undersurface rotator cuff tears and capsular laxity. Imaging studies typically demonstrate abnormalities in asymptomatic throwers. Therefore, clinicians must be skilled in history taking and physical examination in throwing athletes to accurately determine the cause of symptoms and provide optimal treatment. This primer provides orthopedic surgeons with the key points in performing a thorough physical examination of the shoulder in overhead athletes.

When working with overhead athletes, surgeons must elicit the precise nature of symptoms. For example, it is important to distinguish pain from fatigue, as well as complaints related purely to decline in performance. Often, collaboration with the player’s parent or coach may help clarify the chief complaint. In addition, surgeons must have an intricate knowledge of the various stages of the overhead motion, as symptoms in specific stages (late cocking/early acceleration) may raise suspicion for distinctive pathology (labral/biceps complex). Last, it is imperative to understand that the shoulder represents only one part of the kinetic chain in overhead athletes. Successful throwing relies on integrity of the entire kinetic chain, starting with the lower extremity and trunk, extending through the spine, scapula, and shoulder, and terminating with the hand and fingers. Pathology anywhere in the chain must be evaluated and addressed.

When examining the shoulder in overhead athletes, surgeons must address several anatomical structures, both bony and soft tissue. Proper examination begins with comprehensive assessment of the ROM and strength of the various muscles around the shoulder, along with visual inspection to identify any asymmetry of these structures. In addition, the scapulothoracic structures must be examined in detail to rule out underlying dyskinesis. The capsular and ligamentous components of the shoulder joint must be further assessed to note any capsular contracture causing glenohumeral internal rotation deficit (GIRD) or any pathology with the rotator cuff or labral/biceps complex. Last, a comprehensive neurovascular examination should be performed to rule out any compression or neuropathy affecting the shoulder and overhead motion. Findings from the physical examination may then require further imaging to correlate the history and physical examination findings.

1. Inspection, palpation, strength testing

Every examination of the shoulder must begin with visual inspection, along with assessment of basic ROM and strength. The patient must be positioned and exposed adequately to promote visualization of the entire shoulder and scapular girdle, from both anterior and posterior. Visual inspection focuses on identifying any areas of asymmetry, such as position of the bony prominences or bulk of the muscular fossae. Asymmetry of the bony architecture may indicate prior trauma, and atrophy of the muscular fossae may indicate nerve compression. For example, atrophy of the infraspinatus fossa may be caused by compression of the suprascapular nerve at the spinoglenoid notch (likely by a cyst, often associated with labral pathology, but infraspinatus atrophy can result even without the presence of a compressive cyst¹). Alternatively, atrophy of both the supraspinatus and infraspinatus fossae may indicate underlying compression of the suprascapular nerve at the suprascapular notch (either by a cyst or by the transverse scapular ligament). Static and dynamic observation of the posterior aspect of the shoulder may help identify gross pathology with scapular positioning or retraction, indicating underlying dyskinesis (discussed later). Deformity of the acromioclavicular joint may indicate prior trauma or separation. Last, all prior surgical scars should be noted.

Selective palpation may help identify pathology in the shoulder of the throwing athlete. Tenderness at the acromioclavicular joint may be especially common in patients who have had prior sprains of this joint or who have degenerative changes. Tenderness along the biceps tendon may be present in those with biceps tendinitis or partial tear. In addition, tenderness at the coracoid may be present in those with scapular dyskinesis. Posteriorly, palpation at the inferomedial aspect of the scapula (Figure 1), as with palpation along the medial border of the scapula, may elicit tenderness in those with scapulothoracic bursitis.

Strength testing in the shoulder is performed to elicit any deficiencies of the rotator cuff/musculature or surrounding structures. Weakness in forward elevation may indicate pathology in the supraspinatus, whereas weakness in external rotation may reflect deficiency in the infraspinatus or teres minor. Teres minor deficiency may be more isolated with weakness in a position of shoulder abduction to 90°. Last, weakness in internal rotation may indicate subscapularis deficiency. Lag signs and other provocative maneuvers are similarly elicited but typically are positive only in the event of large tears of the rotator cuff. These signs and maneuvers include the internal rotation lag sign or belly press test for subscapularis integrity, the drop-arm sign for supraspinatus function, the external rotation lag sign for infraspinatus function, and the hornblower sign for teres minor integrity. Supporting muscles of the shoulder may also be tested. Latissimus strength may be tested with resisted downward rotation of the arm with the shoulder in abduction and the elbow flexed to 90°.

2. ROM and GIRD assessment

After inspection and palpation, the shoulder should be ranged in all relevant planes of motion. Our standard examination includes forward elevation in the frontal and scapular planes, along with external rotation at the side and at 90° of abduction, as well as internal rotation behind the back with documentation of the highest spinal level that the patient can reach. This examination may be performed with the patient upright, but supine positioning can help stabilize the scapula and provide more accurate views of motion. Deficits of internal rotation may be a common finding in overhead athletes, and the degree of this deficit should be quantitatively noted.

Bony and soft-tissue remodeling of the shoulder (and associated structures) in the overhead athlete can lead to contracture of the posterior capsule. This contracture can cause excessive external rotation and subsequent decrease in internal rotation, leading to pain and anterior instability in the throwing shoulder.² For precise measurements of the internal and external rotation arc, the scapula must be stabilized. This can be done with the patient supine on the examining table or seated upright with manual stabilization of the scapula by the examiner. Once the scapula is stabilized, the arc of internal and external rotation (with the arm in about 90° of abduction) can be measured with a goniometer, with maximum values obtained as the scapula begins to move along the posterior chest wall.² The difference in internal rotation between the dominant and nondominant arms defines the extent of the athlete’s GIRD. Internal rotation can also be qualitatively assessed by having the athlete internally rotate each arm and reach up the spine while the examiner notes the difference in level achieved. However, this does not provide a quantitative assessment of the patient’s GIRD.

In general, the sum of the internal and external rotation arcs on the 2 sides should be symmetric. Consequently, in GIRD, excessive external rotation is balanced by decreased internal rotation. Symptomatic GIRD may be present when there is more than 25° of discrepancy in internal rotation between the athlete’s dominant and nondominant arms.² The goal is to reduce this discrepancy to less than 20°.

3. Internal impingement: rotator cuff and labrum

In overhead athletes, an intricate relationship involving rotator cuff, labrum, and biceps tendon allows for efficient, pain-free force delivery at the shoulder. However, because of the significant external rotation and abduction required in the overhead motion, there may be internal impingement of the posterosuperior rotator cuff (infraspinatus and posterior aspect of supraspinatus) between the posterior labrum and the greater tuberosity. Detailed examination of these structures must be performed in any assessment of an overhead athlete. Symptomatic patients may complain of pain during the throwing cycle, particularly in late cocking and early acceleration.

The modified relocation examination is a common maneuver to detect internal impingement.³ In this examination, the patient’s arm is brought into a position of maximal external rotation and abduction mimicking that found in late cocking or early acceleration. In this position, a patient with internal impingement complains of pain in the posterior shoulder. A posteriorly directed force on the humerus relieves this pain.

There are also many examinations for detecting labral pathology, specifically a SLAP (superior labrum, anterior to posterior) lesion, which is commonly found in patients with internal impingement. One commonly tested maneuver is the O’Brien active compression test (Figures 2A, 2B), which has excellent sensitivity and specificity in detecting type II SLAP lesions.⁴ In this examination, the patient holds the arm in about 15° of adduction and 90° of forward elevation. A downward force is applied with the forearm pronated and subsequently supinated. If pain is noted on the force applied to the pronated arm, and if this pain decreases in the supinated examination, the test is positive for labral pathology.

Anterior instability is routinely found in these patients. Translation is measured with the anterior load and shift test. Anterior translation is tested with the patient supine, with the arm in abduction and external rotation, and with the examiner placing an anteriorly directed force on the humeral head. Translation is compared with the contralateral side and graded on a 3-point scale (1+ is translation to glenoid rim, 2+ is translation over glenoid rim but reduces, 3+ is translation over glenoid and locking). We also use the anterior release test, in which the patient is supine, the arm is brought into abduction and external rotation, and the examiner places a posteriorly directed force on the humeral head. When the examiner removes this force, the patient notices symptoms of instability caused by subluxation (Figures 3A, 3B).

Biceps tendon testing should also be performed to help elicit signs of labral pathology. The Speed test is performed by placing a downward force on the patient’s arm, which is held in 90° forward elevation, and with elbows in extension and forearm in supination. Pain in the long head of the biceps tendon is considered a positive sign and suggestive of SLAP lesion. Although not commonly found in these athletes, external impingement should also be elicited through both the Neer test and the Hawkins test. In the Neer test, the patient’s arm is brought to maximal forward elevation with the forearm supinated and elbow extended, while the scapula is stabilized by the examiner. Pain in the shoulder indicates a positive examination. In the Hawkins test, the patient’s arm is brought into a position of forward elevation, internal rotation, and elbow flexion. The arm is then further internally rotated, and shoulder pain defines a positive examination.

Any of these findings can be concomitant with scapular dyskinesis. Moreover, symptoms related to internal impingement may be exacerbated by concomitant scapular pathology, and therefore proper assessment of scapulothoracic motion must also be performed.

4. Scapulothoracic examination

Motion coupled between the scapula and the rest of the arm (scapular rhythm) allows for efficient use of the shoulder girdle. The scapula helps transfer the force generated by the core so that the hand can efficiently deliver it. Therefore, scapular pathology (or dyskinesis) results in inefficient functioning of the arm, which can be especially debilitating in an overhead athlete.

Scapular assessment begins with visual inspection of the patient, typically from the posterior view, which allows for assessment of the resting position of the scapula. Evidence of prominence of the medial or inferomedial border, coracoid malposition (or pain on palpation), or general scapular malposition should be noted. On active ROM, as the patient forward-elevates the arm, any asymmetric prominence of the inferomedial border of the scapula should be noted. Such asymmetry may indicate underlying scapular dyskinesis. In another important test, the lateral scapular slide test (described by Kibler⁵), the distance from the inferomedial angle of the scapula to the thoracic spine should be measured for both sides and in 3 difference positions, noting any asymmetry between the affected and nonaffected sides. These 3 positions (Figures 4A–4C) are with arms at side, with hands on hips (internal rotation of humerus in 45° abduction), and in 90° of shoulder abduction. Last, medial and lateral scapular winging—caused by long thoracic nerve and spinal accessory nerve pathology, respectively—can be detected by asking the patient to do a “push-up” against the wall while the examiner views from posterior.

After assessment of scapular position at rest and through motion, a series of provocative maneuvers⁶ may aid in the diagnosis of scapular dyskinesis. The first maneuver is the scapular assistance test, in which the examiner provides a gentle force at the inferomedial angle of the scapula, promoting upward rotation and posterior tilt as the patient elevates the arm (Figures 5A, 5B). If the patient experiences a decrease or absence of symptoms through this arc, the test is considered positive. The second maneuver is the scapular retraction test, in which strength testing of the supraspinatus is performed before and after retraction stabilization of the scapula. In the baseline state, the strength of the supraspinatus is tested in standard fashion, with resisted elevation of the internally rotated and abducted arm. The strength is then tested with the scapula stabilized in retraction (the examiner medially stabilizes the scapula). With scapular stabilization, an increase in strength or a decrease in symptoms is considered a positive test.

5. Neurovascular examination

It is essential to perform a comprehensive neurovascular examination in all overhead athletes. This includes basic cervical spine testing for any motor or sensory deficits, along with assessment of scapular winging to detect long thoracic or spinal accessory nerve palsy for medial and lateral winging, respectively. Although neurovascular injury may be a rare finding in the overhead athlete, a detailed examination must still be performed to rule it out.

Thoracic outlet syndrome

Thoracic syndrome is a compressive neuropathy of nerves and vasculature exiting the thorax and entering the upper extremity. Common symptoms include pain and tingling (sometimes vague) in the neck and upper extremity. These symptoms may be positional as well.

Diagnosis of thoracic outlet syndrome begins with visual inspection of the involved upper extremity, noting atrophy or asymmetry. Weakness may also be present. Additional provocative maneuvers can be used to detect decrease or loss of pulses, along with reproduction of symptoms, during a provocative maneuver with subsequent return of pulses and resolution of symptoms after the maneuver is completed.

One examination that can be used to detect thoracic outlet syndrome is the Adson test.⁷ During this maneuver, the radial pulse is palpated with the arm at rest on the patient’s side. The patient then turns to the symptomatic side, hyperextends the arm, and holds inspiration. A positive test coincides with both decreased pulse and reproduction of symptoms, indicating compression within the scalene triangle. In the Wright test,⁷ the pulse is again palpated at rest with the arm at the side. The patient then holds inspiration and places the arm in a position of abduction and external rotation. If the pulses decrease with this maneuver, the test is considered positive, indicating compression in the sub–pectoralis minor region deep to the coracoid. In a third test, the costoclavicular test, again pulses are measured before and during the provocative maneuver, which is with the shoulders thrust backward and depressed downward. A positive test indicates compression between the clavicle and the first rib. In our practice, we use a modified Wright test in which the arm is held in abduction and external rotation while radial pulses are palpated. The fist is then opened and clenched rapidly, and diminution of radial pulses is considered a positive examination (Figures 6A, 6B).

Effort thrombosis

Overhead athletes are at increased risk for developing effort thrombosis⁸ (Paget-Schroetter syndrome). This thrombosis, which results from repetitive motion involving the upper extremity, is not limited to overhead sports; it may be caused by underlying compression of or microtrauma to the venous infrastructure. On physical examination, there may be swelling of the affected limb, along with diffuse pain and fatigue, as well as dermatologic changes. Positive findings warrant further testing, such as coagulation profile testing and advanced imaging or venography.

Arterial aneurysm

Although rare, arterial aneurysms, especially of the axillary artery, must be ruled out in the overhead athlete with vague upper extremity pain (especially distally) and without clear diagnosis.⁹ Aneurysm of the axillary artery can result from repetitive microtrauma related to repetitive overhead motion of the upper extremity. This condition may cause showering of emboli distally to the vasculature of the hand and fingers (Figure 7). Patients may complain of pain in the fingers, difficulty with grip, cyanosis, or cold sensation. On examination, the sufficiency of the radial and ulnar arteries should be assessed, as with detailed sensorimotor examination of the fingers. The fingernails should be examined for splinter hemorrhages.

Conclusion

Overhead athletes place extreme stress on the shoulder during the throwing motion and are at high risk for injury because of repetitive stress on the shoulder girdle. When examining overhead athletes with shoulder pain, surgeons must consider the entire kinetic chain, as inefficiencies anywhere along the chain can lead to altered mechanics and pathology in the shoulder.

Knotless suture anchor fixation techniques continue to evolve as efficient, low-profile options for arthroscopic rotator cuff repair (RCR).^1,2 Excellent outcomes have been reported for constructs that use knotless fixation laterally, typically in suture bridge-type configurations.^2-4 Early comparative biomechanical and clinical studies have also demonstrated equivalent results for all-knotless versus conventional constructs for arthroscopic RCR.^5-10 Given the increased use and availability of multiple implant designs, it is important to supplement our clinical knowledge of these devices with laboratory studies delineating the biomechanical properties of the anchors that are used to help guide appropriate clinical use of the implants in specific patient populations.

Several biomechanical studies have shown suture slippage to be the weak but crucial link in the design of knotless anchors and the most likely mode of in vivo failure.^11,12 Other studies have demonstrated frequent anchor dislodgement from bone, but these analyses involved use of elderly cadaveric specimens and relatively high-force testing protocols.^12,13 Because suture-retention force may have exceeded anchor resistance to pullout (imparted by weak cadaveric bone in such biomechanical settings), the focus on suture-retention properties was limited.¹¹ It is thought that, in clinical practice, the majority of patients who undergo RCR tend not to generate the high forces (relative to resistance to bone pullout) used to cause the anchor pullouts observed in biomechanical studies, particularly in the early postoperative setting.^11-15 Cadaveric testing, however, often involves use of specimens with diminished bone mineral density (BMD), relative to age, because of the illness and other factors leading to death and donation.

Using a novel testing apparatus, we isolated, analyzed, and compared suture slippage in 2 anchor designs, one with entirely press-fit suture clamping and the other reliant on an intrinsic suture-locking mechanism.

Materials and Methods

Six human cadaveric proximal humeri specimens were used for this biomechanical study. Mean (SD) age was 53.3 (5.7) years (range, 46-59 years). Middle-aged specimens were used in order to best represent the quality of bone typically encountered in RCR surgery. To approximate tissue in clinical use, we used fresh-frozen cadaver tissue. Specimens were maintained at –20°C until about 24 hours before use and then were thawed to room temperature for testing. Specimens were included only if they had a completely intact humeral head and no prior surgery or hardware placement. Before instrumentation, dual-energy x-ray absorptiometry with a QDR-1000 scanner (Hologic) was used to determine BMD of all proximal humeri.

Two knotless suture anchors were compared: PushLock (4.5×18.5 mm; Arthrex) and ReelX STT (5.5×19.4 mm; Stryker). These anchors have multiple surgical indications (including RCR), allow patient-specific tissue tensioning, and use polyetheretherketone eyelets. The clamping force for PushLock depends entirely on the interference fit achieved for the suture between the outside of the anchor and the surrounding trabecular/cortical bone after device insertion, whereas the suture in ReelX is secured within the anchor shaft entirely by an internal ratchet-locking mechanism.

For anchor insertion, shoulders were dissected down to the greater tuberosity of the proximal humerus, and all implants were inserted (by a fellowship-trained surgeon in accordance with manufacturer guidelines) at a 25° insertion angle with manufacturer-supplied instruments. One anchor of each type (Figure 1) was inserted into the center of the rotator cuff footprint on the greater tuberosity of each specimen. Anterior and posterior positions were randomized, and an anchor from the other group was inserted into the matching location on the contralateral matched-pair specimen. In all instances, distance between the anterior and posterior anchors was 2 cm, and anchors were placed midway between the articular margin and the lateral edge of the greater tuberosity (Figure 2). Two strands of size 2 ultrahigh-molecular-weight–polyethylene Force Fiber (Stryker) were loaded into all anchors.

A custom urethane fixture was secured over the center of each anchor to allow testing to focus on suture slippage by minimizing anchor migration (Figure 3). The small aperture of this device allowed suture tails to pass freely through the center of the fixture but prevented disengagement and proximal migration of the suture anchor from the underlying bone through contact of the urethane fixture with the anchor perimeter. Any system deformation observed during testing was restricted to the suture and/or the anchor’s suture-locking mechanism. Testing fixtures also oriented the suture anchor coaxial with the axis of tension, creating a worst-case loading scenario (Figure 3).

PushLock implants were inserted with 5 pounds of tension, as indicated, using a manufacturer-supplied suture tensioner, and ReelX devices were inserted and locked with 2 full rotations, as specified by the manufacturer. After one end of each suture was cut, as would be done in vivo, the 2 other suture ends, which would have been part of the RCR in vivo, were tied together to form an 8-cm circumference loop that was brought through the urethane fixture. Humeri were then mounted in a materials testing system (MTS 810; MTS Systems) servohydraulic load frame, and the suture loop was passed around a cross-bar on the actuator of the testing device. A mechanical testing protocol consisting of modest repetitive forces was carefully chosen to simulate expected activity during rehabilitation after RCR.¹⁵ In this protocol, a 60-second preload of 10 N was followed by tensile loading between 10 N and 90 N at a frequency of 0.5 Hz for 500 cycles.¹⁵ Cycle duration at 3 mm and 5 mm of suture slippage (threshold for clinical failure) was recorded.^12,16,17 In addition, suture slippage was measured after 1, 10, 50, 100, 200, 300, 400, and 500 cycles. The first 5 test cycles were not counted in the analysis to control for initial knot slippage. Finally, after completion of dynamic testing, samples were loaded at a displacement rate of 0.5 mm/s for tension-to-failure testing in the custom fixtures. Maximum failure load, stiffness, and failure mode were recorded. Ultimate failure was defined as suture breakage or gross suture slippage.

Paired Student t test was used to determine significant differences in suture slippage distance between the 2 groups at various cycle durations. In addition, Kaplan-Meier survival test was used to determine statistical differences in sample survival during the dynamic loading test.

Results

Mean (SD) BMD of the cadaveric shoulder specimens was 0.55 (0.13) g/cm² (range, 0.29-0.68 g/cm²). The testing fixtures isolated suture slippage from anchor–bone disengagement. All 6 PushLock implants demonstrated slippage of more than 3 mm, and 5 of the 6 demonstrated slippage of more than 5 mm. All 6 ReelX devices exhibited slippage of less than 3 mm. In addition, PushLock demonstrated more suture slippage at cycles 1, 10, and 100 (P < .05) and more maximum slippage after 500 cycles (mean, 11.2 mm; SD, 4.7 mm) compared with ReelX (mean, 1.9 mm; SD, 0.5 mm) (P = .004). Figure 4 shows mean suture slippage at each cycle.

 Kaplan-Meier analysis revealed significantly (λ² = 8.170; P = .0043) decreased survival after dynamic testing for PushLock versus ReelX (Figure 5). Survival was defined as suture slippage of less than 5 mm after completion of dynamic testing. Only 1 of the 6 PushLock anchors completed dynamic testing; the other 5 failed via complete suture slippage from the anchor before testing could be completed. All 6 ReelX devices survived dynamic testing.

Therefore, 1 PushLock implant and all 6 ReelX devices were available for subsequent load-to-failure testing. Failure in this setting was defined as suture slippage of more than 10 mm or suture breakage. The PushLock implant failed at a maximum force of 171.8 N with a stiffness of 74.4 N/mm and eventually exhibited gross suture slippage. All 6 ReelX devices failed at a mean (SD) maximum of 273.5 (20.2) N, with a mean (SD) stiffness of 74.1 (17) N/mm. Mechanism of failure for all ReelX devices was suture breakage during the tensile load-to-failure test.

Discussion

We evaluated a new technique designed to isolate suture slippage in knotless anchors used for RCR. The impetus for developing this new method was to provide a means for better analyzing the ability of a knotless anchor to resist suture slippage in the cadaveric biomechanical testing setting. Suture slippage is an important mode of failure during such analyses.^11,12 Significant slippage occurred in a range of implants before half the anchor–bone pullout strength was reached in a study using young bovine femoral heads.¹¹ In another study, using young, high-BMD cadaveric humeral heads, initial slippage and maximum failure loads were equivalent among numerous devices using various suture-retention mechanisms, and suture slippage was the most common failure mode.¹² Nevertheless, other biomechanical studies have demonstrated frequent failure caused by anchor pullout in elderly human cadaveric specimens with diminished BMD, often with high-force testing protocols.^12,13 In the more modest-force, in vivo rehabilitative environment, suture slippage rather than anchor dislodgement may be the main failure mode.^11-15

We compared the PushLock implant and its entirely press-fit suture clamping design with the ReelX device, which relies on an intrinsic suture-locking mechanism. Middle-aged (mean, 53.3 years; SD, 5.7 years) cadaveric humeri were tested under physiologically relevant biomechanical conditions to begin to help identify how relatively osteopenic bone may affect suture-retention properties for a given implant. The results showed that the study methodology prevented implant failure via anchor–bone pullout. To our knowledge, this was the first study to exclusively analyze suture slippage in knotless anchors. The findings indicated that implants that rely heavily on a tight interference fit of the suture between the anchor and the surrounding bone may exhibit early slippage and failure after RCR in middle-aged patients with relative osteopenia.^11,12 However, this study also demonstrated that devices with intrinsic clamping mechanisms that do not depend on the quality of surrounding bone may better resist suture slippage. It is not clear that all knotless anchors with intrinsic locking mechanisms function equivalently. For instance, Pietschmann and colleagues¹² found that 2 of 10 implants with a different internal clamping device were unable to resist failure via suture slippage, even in healthy bone. Similarly, in a study comparing ReelX devices with implants having a different internal suture-retention mechanism, ReelX failed at higher ultimate loads, and typically via anchor dislodgement, versus suture slippage in the other implants.¹⁸

It is important to note that, in the present study, the loads at which sutures broke in the intrinsic clamping anchors approached the maximum contractile force of the supraspinatus muscle (302 N).^19,20 In addition, these loads were above the resistance of the rotator cuff tendon to cut out with modern suture material.²¹

This study’s limitations include use of an in vitro human cadaveric model that precluded analysis of the effects of postoperative healing. Biomechanical testing was also performed in a single row-type suture configuration with the rotator cuff tendon removed. Fixtures used during testing oriented the load coaxially with the axis of tension, creating a worst-case loading scenario. Although this form of testing may limit its clinical applicability, its purpose was to critically isolate how well a knotless anchor could resist suture slippage. The methods we used were also limited because the stability of the bone–anchor interface was not assessed. For patients with osteopenia, anchor pullout rather than suture slippage could be the most limiting factor for knotless anchor construct failure, and therefore further testing of both failure modes is needed. Future biomechanical studies should compare various knotless anchors’ suture-slippage characteristics in other constructs in physiologic testing orientations, including double-row and suture-bridge configurations, as well as with intact rotator cuff tendons. In addition, use of labral tape as a substitute for polyblend suture has been suggested to limit suture slippage, and this technique theoretically could have changed the results of this study.²²

Conclusion

An implant with an internal ratcheting mechanism for suture retention demonstrated significantly less suture slippage in an axial tension evaluation protocol than a device reliant on interference fit of the suture between the anchor and surrounding bone. In the clinical setting, this may allow for less gap formation during the healing phase following RCR with a knotless anchor. There was also increased maximum load to failure, demonstrating an increased load until catastrophic failure using a device with a ratcheting internal locking mechanism.

Knotless suture anchor fixation techniques continue to evolve as efficient, low-profile options for arthroscopic rotator cuff repair (RCR).^1,2 Excellent outcomes have been reported for constructs that use knotless fixation laterally, typically in suture bridge-type configurations.^2-4 Early comparative biomechanical and clinical studies have also demonstrated equivalent results for all-knotless versus conventional constructs for arthroscopic RCR.^5-10 Given the increased use and availability of multiple implant designs, it is important to supplement our clinical knowledge of these devices with laboratory studies delineating the biomechanical properties of the anchors that are used to help guide appropriate clinical use of the implants in specific patient populations.

Several biomechanical studies have shown suture slippage to be the weak but crucial link in the design of knotless anchors and the most likely mode of in vivo failure.^11,12 Other studies have demonstrated frequent anchor dislodgement from bone, but these analyses involved use of elderly cadaveric specimens and relatively high-force testing protocols.^12,13 Because suture-retention force may have exceeded anchor resistance to pullout (imparted by weak cadaveric bone in such biomechanical settings), the focus on suture-retention properties was limited.¹¹ It is thought that, in clinical practice, the majority of patients who undergo RCR tend not to generate the high forces (relative to resistance to bone pullout) used to cause the anchor pullouts observed in biomechanical studies, particularly in the early postoperative setting.^11-15 Cadaveric testing, however, often involves use of specimens with diminished bone mineral density (BMD), relative to age, because of the illness and other factors leading to death and donation.

Using a novel testing apparatus, we isolated, analyzed, and compared suture slippage in 2 anchor designs, one with entirely press-fit suture clamping and the other reliant on an intrinsic suture-locking mechanism.

Materials and Methods

Six human cadaveric proximal humeri specimens were used for this biomechanical study. Mean (SD) age was 53.3 (5.7) years (range, 46-59 years). Middle-aged specimens were used in order to best represent the quality of bone typically encountered in RCR surgery. To approximate tissue in clinical use, we used fresh-frozen cadaver tissue. Specimens were maintained at –20°C until about 24 hours before use and then were thawed to room temperature for testing. Specimens were included only if they had a completely intact humeral head and no prior surgery or hardware placement. Before instrumentation, dual-energy x-ray absorptiometry with a QDR-1000 scanner (Hologic) was used to determine BMD of all proximal humeri.

Two knotless suture anchors were compared: PushLock (4.5×18.5 mm; Arthrex) and ReelX STT (5.5×19.4 mm; Stryker). These anchors have multiple surgical indications (including RCR), allow patient-specific tissue tensioning, and use polyetheretherketone eyelets. The clamping force for PushLock depends entirely on the interference fit achieved for the suture between the outside of the anchor and the surrounding trabecular/cortical bone after device insertion, whereas the suture in ReelX is secured within the anchor shaft entirely by an internal ratchet-locking mechanism.

For anchor insertion, shoulders were dissected down to the greater tuberosity of the proximal humerus, and all implants were inserted (by a fellowship-trained surgeon in accordance with manufacturer guidelines) at a 25° insertion angle with manufacturer-supplied instruments. One anchor of each type (Figure 1) was inserted into the center of the rotator cuff footprint on the greater tuberosity of each specimen. Anterior and posterior positions were randomized, and an anchor from the other group was inserted into the matching location on the contralateral matched-pair specimen. In all instances, distance between the anterior and posterior anchors was 2 cm, and anchors were placed midway between the articular margin and the lateral edge of the greater tuberosity (Figure 2). Two strands of size 2 ultrahigh-molecular-weight–polyethylene Force Fiber (Stryker) were loaded into all anchors.

A custom urethane fixture was secured over the center of each anchor to allow testing to focus on suture slippage by minimizing anchor migration (Figure 3). The small aperture of this device allowed suture tails to pass freely through the center of the fixture but prevented disengagement and proximal migration of the suture anchor from the underlying bone through contact of the urethane fixture with the anchor perimeter. Any system deformation observed during testing was restricted to the suture and/or the anchor’s suture-locking mechanism. Testing fixtures also oriented the suture anchor coaxial with the axis of tension, creating a worst-case loading scenario (Figure 3).

PushLock implants were inserted with 5 pounds of tension, as indicated, using a manufacturer-supplied suture tensioner, and ReelX devices were inserted and locked with 2 full rotations, as specified by the manufacturer. After one end of each suture was cut, as would be done in vivo, the 2 other suture ends, which would have been part of the RCR in vivo, were tied together to form an 8-cm circumference loop that was brought through the urethane fixture. Humeri were then mounted in a materials testing system (MTS 810; MTS Systems) servohydraulic load frame, and the suture loop was passed around a cross-bar on the actuator of the testing device. A mechanical testing protocol consisting of modest repetitive forces was carefully chosen to simulate expected activity during rehabilitation after RCR.¹⁵ In this protocol, a 60-second preload of 10 N was followed by tensile loading between 10 N and 90 N at a frequency of 0.5 Hz for 500 cycles.¹⁵ Cycle duration at 3 mm and 5 mm of suture slippage (threshold for clinical failure) was recorded.^12,16,17 In addition, suture slippage was measured after 1, 10, 50, 100, 200, 300, 400, and 500 cycles. The first 5 test cycles were not counted in the analysis to control for initial knot slippage. Finally, after completion of dynamic testing, samples were loaded at a displacement rate of 0.5 mm/s for tension-to-failure testing in the custom fixtures. Maximum failure load, stiffness, and failure mode were recorded. Ultimate failure was defined as suture breakage or gross suture slippage.

Paired Student t test was used to determine significant differences in suture slippage distance between the 2 groups at various cycle durations. In addition, Kaplan-Meier survival test was used to determine statistical differences in sample survival during the dynamic loading test.

Results

Mean (SD) BMD of the cadaveric shoulder specimens was 0.55 (0.13) g/cm² (range, 0.29-0.68 g/cm²). The testing fixtures isolated suture slippage from anchor–bone disengagement. All 6 PushLock implants demonstrated slippage of more than 3 mm, and 5 of the 6 demonstrated slippage of more than 5 mm. All 6 ReelX devices exhibited slippage of less than 3 mm. In addition, PushLock demonstrated more suture slippage at cycles 1, 10, and 100 (P < .05) and more maximum slippage after 500 cycles (mean, 11.2 mm; SD, 4.7 mm) compared with ReelX (mean, 1.9 mm; SD, 0.5 mm) (P = .004). Figure 4 shows mean suture slippage at each cycle.

 Kaplan-Meier analysis revealed significantly (λ² = 8.170; P = .0043) decreased survival after dynamic testing for PushLock versus ReelX (Figure 5). Survival was defined as suture slippage of less than 5 mm after completion of dynamic testing. Only 1 of the 6 PushLock anchors completed dynamic testing; the other 5 failed via complete suture slippage from the anchor before testing could be completed. All 6 ReelX devices survived dynamic testing.

Therefore, 1 PushLock implant and all 6 ReelX devices were available for subsequent load-to-failure testing. Failure in this setting was defined as suture slippage of more than 10 mm or suture breakage. The PushLock implant failed at a maximum force of 171.8 N with a stiffness of 74.4 N/mm and eventually exhibited gross suture slippage. All 6 ReelX devices failed at a mean (SD) maximum of 273.5 (20.2) N, with a mean (SD) stiffness of 74.1 (17) N/mm. Mechanism of failure for all ReelX devices was suture breakage during the tensile load-to-failure test.

Discussion

We evaluated a new technique designed to isolate suture slippage in knotless anchors used for RCR. The impetus for developing this new method was to provide a means for better analyzing the ability of a knotless anchor to resist suture slippage in the cadaveric biomechanical testing setting. Suture slippage is an important mode of failure during such analyses.^11,12 Significant slippage occurred in a range of implants before half the anchor–bone pullout strength was reached in a study using young bovine femoral heads.¹¹ In another study, using young, high-BMD cadaveric humeral heads, initial slippage and maximum failure loads were equivalent among numerous devices using various suture-retention mechanisms, and suture slippage was the most common failure mode.¹² Nevertheless, other biomechanical studies have demonstrated frequent failure caused by anchor pullout in elderly human cadaveric specimens with diminished BMD, often with high-force testing protocols.^12,13 In the more modest-force, in vivo rehabilitative environment, suture slippage rather than anchor dislodgement may be the main failure mode.^11-15

We compared the PushLock implant and its entirely press-fit suture clamping design with the ReelX device, which relies on an intrinsic suture-locking mechanism. Middle-aged (mean, 53.3 years; SD, 5.7 years) cadaveric humeri were tested under physiologically relevant biomechanical conditions to begin to help identify how relatively osteopenic bone may affect suture-retention properties for a given implant. The results showed that the study methodology prevented implant failure via anchor–bone pullout. To our knowledge, this was the first study to exclusively analyze suture slippage in knotless anchors. The findings indicated that implants that rely heavily on a tight interference fit of the suture between the anchor and the surrounding bone may exhibit early slippage and failure after RCR in middle-aged patients with relative osteopenia.^11,12 However, this study also demonstrated that devices with intrinsic clamping mechanisms that do not depend on the quality of surrounding bone may better resist suture slippage. It is not clear that all knotless anchors with intrinsic locking mechanisms function equivalently. For instance, Pietschmann and colleagues¹² found that 2 of 10 implants with a different internal clamping device were unable to resist failure via suture slippage, even in healthy bone. Similarly, in a study comparing ReelX devices with implants having a different internal suture-retention mechanism, ReelX failed at higher ultimate loads, and typically via anchor dislodgement, versus suture slippage in the other implants.¹⁸

It is important to note that, in the present study, the loads at which sutures broke in the intrinsic clamping anchors approached the maximum contractile force of the supraspinatus muscle (302 N).^19,20 In addition, these loads were above the resistance of the rotator cuff tendon to cut out with modern suture material.²¹

This study’s limitations include use of an in vitro human cadaveric model that precluded analysis of the effects of postoperative healing. Biomechanical testing was also performed in a single row-type suture configuration with the rotator cuff tendon removed. Fixtures used during testing oriented the load coaxially with the axis of tension, creating a worst-case loading scenario. Although this form of testing may limit its clinical applicability, its purpose was to critically isolate how well a knotless anchor could resist suture slippage. The methods we used were also limited because the stability of the bone–anchor interface was not assessed. For patients with osteopenia, anchor pullout rather than suture slippage could be the most limiting factor for knotless anchor construct failure, and therefore further testing of both failure modes is needed. Future biomechanical studies should compare various knotless anchors’ suture-slippage characteristics in other constructs in physiologic testing orientations, including double-row and suture-bridge configurations, as well as with intact rotator cuff tendons. In addition, use of labral tape as a substitute for polyblend suture has been suggested to limit suture slippage, and this technique theoretically could have changed the results of this study.²²

Conclusion

An implant with an internal ratcheting mechanism for suture retention demonstrated significantly less suture slippage in an axial tension evaluation protocol than a device reliant on interference fit of the suture between the anchor and surrounding bone. In the clinical setting, this may allow for less gap formation during the healing phase following RCR with a knotless anchor. There was also increased maximum load to failure, demonstrating an increased load until catastrophic failure using a device with a ratcheting internal locking mechanism.

Knotless suture anchor fixation techniques continue to evolve as efficient, low-profile options for arthroscopic rotator cuff repair (RCR).^1,2 Excellent outcomes have been reported for constructs that use knotless fixation laterally, typically in suture bridge-type configurations.^2-4 Early comparative biomechanical and clinical studies have also demonstrated equivalent results for all-knotless versus conventional constructs for arthroscopic RCR.^5-10 Given the increased use and availability of multiple implant designs, it is important to supplement our clinical knowledge of these devices with laboratory studies delineating the biomechanical properties of the anchors that are used to help guide appropriate clinical use of the implants in specific patient populations.

Several biomechanical studies have shown suture slippage to be the weak but crucial link in the design of knotless anchors and the most likely mode of in vivo failure.^11,12 Other studies have demonstrated frequent anchor dislodgement from bone, but these analyses involved use of elderly cadaveric specimens and relatively high-force testing protocols.^12,13 Because suture-retention force may have exceeded anchor resistance to pullout (imparted by weak cadaveric bone in such biomechanical settings), the focus on suture-retention properties was limited.¹¹ It is thought that, in clinical practice, the majority of patients who undergo RCR tend not to generate the high forces (relative to resistance to bone pullout) used to cause the anchor pullouts observed in biomechanical studies, particularly in the early postoperative setting.^11-15 Cadaveric testing, however, often involves use of specimens with diminished bone mineral density (BMD), relative to age, because of the illness and other factors leading to death and donation.

Using a novel testing apparatus, we isolated, analyzed, and compared suture slippage in 2 anchor designs, one with entirely press-fit suture clamping and the other reliant on an intrinsic suture-locking mechanism.

Materials and Methods

Six human cadaveric proximal humeri specimens were used for this biomechanical study. Mean (SD) age was 53.3 (5.7) years (range, 46-59 years). Middle-aged specimens were used in order to best represent the quality of bone typically encountered in RCR surgery. To approximate tissue in clinical use, we used fresh-frozen cadaver tissue. Specimens were maintained at –20°C until about 24 hours before use and then were thawed to room temperature for testing. Specimens were included only if they had a completely intact humeral head and no prior surgery or hardware placement. Before instrumentation, dual-energy x-ray absorptiometry with a QDR-1000 scanner (Hologic) was used to determine BMD of all proximal humeri.

Two knotless suture anchors were compared: PushLock (4.5×18.5 mm; Arthrex) and ReelX STT (5.5×19.4 mm; Stryker). These anchors have multiple surgical indications (including RCR), allow patient-specific tissue tensioning, and use polyetheretherketone eyelets. The clamping force for PushLock depends entirely on the interference fit achieved for the suture between the outside of the anchor and the surrounding trabecular/cortical bone after device insertion, whereas the suture in ReelX is secured within the anchor shaft entirely by an internal ratchet-locking mechanism.

For anchor insertion, shoulders were dissected down to the greater tuberosity of the proximal humerus, and all implants were inserted (by a fellowship-trained surgeon in accordance with manufacturer guidelines) at a 25° insertion angle with manufacturer-supplied instruments. One anchor of each type (Figure 1) was inserted into the center of the rotator cuff footprint on the greater tuberosity of each specimen. Anterior and posterior positions were randomized, and an anchor from the other group was inserted into the matching location on the contralateral matched-pair specimen. In all instances, distance between the anterior and posterior anchors was 2 cm, and anchors were placed midway between the articular margin and the lateral edge of the greater tuberosity (Figure 2). Two strands of size 2 ultrahigh-molecular-weight–polyethylene Force Fiber (Stryker) were loaded into all anchors.

A custom urethane fixture was secured over the center of each anchor to allow testing to focus on suture slippage by minimizing anchor migration (Figure 3). The small aperture of this device allowed suture tails to pass freely through the center of the fixture but prevented disengagement and proximal migration of the suture anchor from the underlying bone through contact of the urethane fixture with the anchor perimeter. Any system deformation observed during testing was restricted to the suture and/or the anchor’s suture-locking mechanism. Testing fixtures also oriented the suture anchor coaxial with the axis of tension, creating a worst-case loading scenario (Figure 3).

PushLock implants were inserted with 5 pounds of tension, as indicated, using a manufacturer-supplied suture tensioner, and ReelX devices were inserted and locked with 2 full rotations, as specified by the manufacturer. After one end of each suture was cut, as would be done in vivo, the 2 other suture ends, which would have been part of the RCR in vivo, were tied together to form an 8-cm circumference loop that was brought through the urethane fixture. Humeri were then mounted in a materials testing system (MTS 810; MTS Systems) servohydraulic load frame, and the suture loop was passed around a cross-bar on the actuator of the testing device. A mechanical testing protocol consisting of modest repetitive forces was carefully chosen to simulate expected activity during rehabilitation after RCR.¹⁵ In this protocol, a 60-second preload of 10 N was followed by tensile loading between 10 N and 90 N at a frequency of 0.5 Hz for 500 cycles.¹⁵ Cycle duration at 3 mm and 5 mm of suture slippage (threshold for clinical failure) was recorded.^12,16,17 In addition, suture slippage was measured after 1, 10, 50, 100, 200, 300, 400, and 500 cycles. The first 5 test cycles were not counted in the analysis to control for initial knot slippage. Finally, after completion of dynamic testing, samples were loaded at a displacement rate of 0.5 mm/s for tension-to-failure testing in the custom fixtures. Maximum failure load, stiffness, and failure mode were recorded. Ultimate failure was defined as suture breakage or gross suture slippage.

Paired Student t test was used to determine significant differences in suture slippage distance between the 2 groups at various cycle durations. In addition, Kaplan-Meier survival test was used to determine statistical differences in sample survival during the dynamic loading test.

Results

Mean (SD) BMD of the cadaveric shoulder specimens was 0.55 (0.13) g/cm² (range, 0.29-0.68 g/cm²). The testing fixtures isolated suture slippage from anchor–bone disengagement. All 6 PushLock implants demonstrated slippage of more than 3 mm, and 5 of the 6 demonstrated slippage of more than 5 mm. All 6 ReelX devices exhibited slippage of less than 3 mm. In addition, PushLock demonstrated more suture slippage at cycles 1, 10, and 100 (P < .05) and more maximum slippage after 500 cycles (mean, 11.2 mm; SD, 4.7 mm) compared with ReelX (mean, 1.9 mm; SD, 0.5 mm) (P = .004). Figure 4 shows mean suture slippage at each cycle.

 Kaplan-Meier analysis revealed significantly (λ² = 8.170; P = .0043) decreased survival after dynamic testing for PushLock versus ReelX (Figure 5). Survival was defined as suture slippage of less than 5 mm after completion of dynamic testing. Only 1 of the 6 PushLock anchors completed dynamic testing; the other 5 failed via complete suture slippage from the anchor before testing could be completed. All 6 ReelX devices survived dynamic testing.

Therefore, 1 PushLock implant and all 6 ReelX devices were available for subsequent load-to-failure testing. Failure in this setting was defined as suture slippage of more than 10 mm or suture breakage. The PushLock implant failed at a maximum force of 171.8 N with a stiffness of 74.4 N/mm and eventually exhibited gross suture slippage. All 6 ReelX devices failed at a mean (SD) maximum of 273.5 (20.2) N, with a mean (SD) stiffness of 74.1 (17) N/mm. Mechanism of failure for all ReelX devices was suture breakage during the tensile load-to-failure test.

Discussion

We evaluated a new technique designed to isolate suture slippage in knotless anchors used for RCR. The impetus for developing this new method was to provide a means for better analyzing the ability of a knotless anchor to resist suture slippage in the cadaveric biomechanical testing setting. Suture slippage is an important mode of failure during such analyses.^11,12 Significant slippage occurred in a range of implants before half the anchor–bone pullout strength was reached in a study using young bovine femoral heads.¹¹ In another study, using young, high-BMD cadaveric humeral heads, initial slippage and maximum failure loads were equivalent among numerous devices using various suture-retention mechanisms, and suture slippage was the most common failure mode.¹² Nevertheless, other biomechanical studies have demonstrated frequent failure caused by anchor pullout in elderly human cadaveric specimens with diminished BMD, often with high-force testing protocols.^12,13 In the more modest-force, in vivo rehabilitative environment, suture slippage rather than anchor dislodgement may be the main failure mode.^11-15

We compared the PushLock implant and its entirely press-fit suture clamping design with the ReelX device, which relies on an intrinsic suture-locking mechanism. Middle-aged (mean, 53.3 years; SD, 5.7 years) cadaveric humeri were tested under physiologically relevant biomechanical conditions to begin to help identify how relatively osteopenic bone may affect suture-retention properties for a given implant. The results showed that the study methodology prevented implant failure via anchor–bone pullout. To our knowledge, this was the first study to exclusively analyze suture slippage in knotless anchors. The findings indicated that implants that rely heavily on a tight interference fit of the suture between the anchor and the surrounding bone may exhibit early slippage and failure after RCR in middle-aged patients with relative osteopenia.^11,12 However, this study also demonstrated that devices with intrinsic clamping mechanisms that do not depend on the quality of surrounding bone may better resist suture slippage. It is not clear that all knotless anchors with intrinsic locking mechanisms function equivalently. For instance, Pietschmann and colleagues¹² found that 2 of 10 implants with a different internal clamping device were unable to resist failure via suture slippage, even in healthy bone. Similarly, in a study comparing ReelX devices with implants having a different internal suture-retention mechanism, ReelX failed at higher ultimate loads, and typically via anchor dislodgement, versus suture slippage in the other implants.¹⁸

It is important to note that, in the present study, the loads at which sutures broke in the intrinsic clamping anchors approached the maximum contractile force of the supraspinatus muscle (302 N).^19,20 In addition, these loads were above the resistance of the rotator cuff tendon to cut out with modern suture material.²¹

This study’s limitations include use of an in vitro human cadaveric model that precluded analysis of the effects of postoperative healing. Biomechanical testing was also performed in a single row-type suture configuration with the rotator cuff tendon removed. Fixtures used during testing oriented the load coaxially with the axis of tension, creating a worst-case loading scenario. Although this form of testing may limit its clinical applicability, its purpose was to critically isolate how well a knotless anchor could resist suture slippage. The methods we used were also limited because the stability of the bone–anchor interface was not assessed. For patients with osteopenia, anchor pullout rather than suture slippage could be the most limiting factor for knotless anchor construct failure, and therefore further testing of both failure modes is needed. Future biomechanical studies should compare various knotless anchors’ suture-slippage characteristics in other constructs in physiologic testing orientations, including double-row and suture-bridge configurations, as well as with intact rotator cuff tendons. In addition, use of labral tape as a substitute for polyblend suture has been suggested to limit suture slippage, and this technique theoretically could have changed the results of this study.²²

Conclusion

An implant with an internal ratcheting mechanism for suture retention demonstrated significantly less suture slippage in an axial tension evaluation protocol than a device reliant on interference fit of the suture between the anchor and surrounding bone. In the clinical setting, this may allow for less gap formation during the healing phase following RCR with a knotless anchor. There was also increased maximum load to failure, demonstrating an increased load until catastrophic failure using a device with a ratcheting internal locking mechanism.

Since Neer described the rotator interval in 1970, its closure, often used in conjunction with capsulorrhaphy, has become an important surgical technique in managing shoulder instability.^1-11 Numerous studies have sought to define the function of the rotator interval.^1-3,6-20 The etiology of lesions of the rotator interval has been debated, and there is evidence that such lesions may be in part congenital.²¹ Increased rotator interval depth and width, along with increased size of the distended inferior and posteroinferior joint capsule on magnetic resonance arthrography, have been reported in cases of multidirectional shoulder instability.²² However, confusion remains about the role of the rotator interval in shoulder instability and about the effect its closure has on shoulder function. No one knows the degree of volume reduction that results from closure of the rotator interval and whether medial and lateral sutures differ in the volume reduction achieved.

Cadaveric studies have shown that the rotator interval has an important role in shoulder motion.^{6,13-16,19,20,23} Harryman and colleagues¹³ found that sectioning the coracohumeral ligament (CHL) increased shoulder range of motion (ROM), and medial-to-lateral closure of the rotator interval restricted motion in all planes. Most notably, interval closure limited inferior translation in the adducted shoulder, posterior translation in the flexed adducted shoulder, and external rotation in the neutral position. Subsequent studies,^17,18 using rotator interval closure combined with thermal capsulorrhaphy, confirmed the results reported by Harryman and colleagues.¹³

More recent cadaveric studies using superior-to-inferior rotator interval closures have shown a decrease in anterior translation but not posterior translation.^14-16,19-21 A superior-to-inferior interval closure technique limited external rotation less than a medial-to-lateral closure did.^13-16,19-21 The majority of arthroscopically described rotator interval closures involve a superior-to-inferior technique and use 2 or 3 sutures.^1,3,9-11

Plausinis and colleagues¹⁵ examined the effects of an isolated medial, an isolated lateral, and a medial combined with a lateral closure of the rotator interval. They noted that all 3 methods limited anterior translation and motion by means of 6° flexion and 10° external rotation; however, there was no statistical difference between methods. They also found that occasionally the medial interval closure resulted in massive loss of external rotation. Earlier, Jost and colleagues¹⁴ noted that a medial rotator interval could cause this massive loss by tethering the CHL, resulting in a medial-to-lateral imbrication of the CHL.

Arthroscopic rotator interval closure has clinically demonstrated an additive effect on shoulder stability. The recurrence rate was lower for arthroscopic Bankart repair combined with arthroscopic rotator interval closure (8%) than for arthroscopic Bankart repair alone (13%).²⁴ In addition, time to recurrent dislocation was longer (42 vs 13 months) for the group that underwent the combination of Bankart repair and rotator interval closure. Regarding the concern about loss of motion after arthroscopic rotator interval closure, Chiang and colleagues²⁵ recently noted no significant loss of motion 5 years after arthroscopic Bankart repair with rotator interval closure.

What effect rotator interval closure has on intra-articular glenohumeral volume (GHV) remains unknown. Using a cadaveric model, Yamamoto and colleagues²⁰ showed that decreasing GHV can increase the responsiveness of the glenohumeral joint to the intra-articular pressure. Thus, reducing the volume can improve stability in vitro by increasing the magnitude of negative pressure stabilizing the glenohumeral joint.

We conducted a study to quantify the effects of arthroscopic rotator interval closure on capsular volume and to determine whether medial and lateral interval closures resulted in different degrees of volume reduction. Our hypothesis was that shoulder volume would be significantly reduced by closing the rotator interval.

Materials and Methods

Previous studies have not specifically evaluated GHV after rotator interval closure. Our power analysis was performed with data from a study by Karas and colleagues,²⁶ who evaluated GHV after capsular plication. To detect a capsular volume reduction of 20% per stitch, with a 2-sided 5% significance level and a power of 80%, we needed a sample size of 5 specimens per group.

After receiving institutional review board approval for this study, we obtained 10 cadaveric shoulders (5 matched pairs). Exclusion criteria included arthroscopic evaluation revealing a full-thickness rotator cuff tear or significant osteoarthritis. Two shoulders had full-thickness cuff tears, leaving 8 shoulders to be tested; 6 of these were matched pairs. The shoulders were from 1 man (matched pair) and 4 women (2 matched pairs). Age ranged from 38 to 70 years (mean, 59.6 years). Differences in material properties between the specimens were accounted for by using primarily matched pairs.

The 2 study groups consisted of 4 shoulders each. After specimens were thawed, the skin, subcutaneous tissues, and periscapular muscles were removed from the shoulder. Only the capsule, biceps, and rotator cuff remained. For measurement purposes, the shoulders were mounted in a vice clamp in a beach-chair orientation. We placed a total of 2 portals with fully threaded 8.25-mm cannulas (Arthrex, Naples, Florida). A standard posterior portal was placed in the soft spot. A low anterior portal was then placed just superior to the subscapularis tendon. For arthroscopic examination and instrumentation in a saline environment, the shoulders were rotated into the lateral decubitus position, with suspension in 30° abduction and 20° forward flexion, by a rope attached to a pin in the distal shaft of the humerus.

In both groups, medial and lateral stitches with No. 2 FiberWire (Arthrex) were used to close the interval. The medial interval closure stitch was placed more than 10 mm away from the glenoid to prevent unpredictable CHL tethering; the lateral closure stitch was placed 10 mm lateral to the medial stitch (Figure 1).¹⁴ All sutures were placed intra-articularly under direct arthroscopic visualization, similar to the methods described in the literature.^1,3,9-11 Sutures were passed through the superior glenohumeral ligament (SGHL) and through the upper subscapularis using a suture shuttle (SutureLasso; Arthrex) and Penetrator II Suture Retriever (Arthrex). The upper subscapularis was incorporated because of the unpredictable nature of the middle glenohumeral ligament (MGHL). Both rotator interval sutures were placed before tying either. In the medial group, the medial stitch was tied first, using alternating half-hitches, followed by the lateral stitch. In the lateral group, the lateral stitch was tied first, followed by the medial stitch. GHV was measured at baseline and after tying each stitch. Dr. Ponce instrumented all shoulders.

Modifying a beach-chair technique described by Miller and colleagues,²⁷ we used a viscous fatty-acid sulfate solution, liquid soap, to measure GHV.^27-29 A small slit in line with the fibers was made in the supraspinatus tendon just lateral to the musculotendinous junction. A 3-way stop-cock was placed into the joint though this defect. A 20-mL syringe with a 16-gauge needle was used to inject the soap. The needle was inserted into the rotator cuff interval, and the viscous solution was injected in 5-mL increments until there was active extravasation through the supraspinatus cannula (Figure 2). This technique, the “volcano method,” marked the maximum capacity of the joint. The joint was then copiously irrigated with normal saline and suctioned until all normal saline was evacuated. Dr. Rosenzweig took 2 measurements on each shoulder, and their mean was used for analysis.

The baseline measurement was taken with the 2 working cannulas in the shoulder joint. Measurements were obtained with cannulas to simulate normal clinical conditions. Subsequent measurements were done with the cannulas in place and inserted up to the same thread each time so as not to change the volume. The capsule and the rotator cuff were then dissected from the humerus so the size of the capsulolabral plication could be directly evaluated. Methylene blue was used to mark the capsular suture holes before removing the sutures. With use of a caliper, the size of the plication bite was measured (in millimeters).

Statistical Analysis

The primary outcome was percent reduction in GHV as a function of number of plications and size of plication. When only the first plication was tightened, the effect of position (medial or lateral) was also of interest. Percent volume reduction was calculated as (original – new) / original × 100. SAS 8.02 (SAS Institute, Cary, North Carolina) was used to fit a repeated random-intercept regression model for each outcome. This technique properly accounts for the paired nature of the specimens and the repeated measures (baseline plus 2 plications). Model fit was assessed by the method of difference in log likelihood.

Results

In the medial group, GHV was reduced by a mean of 24.2% with a single medial stitch; in the lateral group, GHV was reduced by a mean of 35.1% (Figure 3). The difference was significant (P < .02). In the medial group, when a second lateral stitch was used, GHV was reduced by another 18.7%; in the lateral group, when a medial stitch was added, GHV was reduced by another 11.4%. Final GHV for the medial and lateral groups was 42.9% and 46.5%, respectively. There was no statistical difference in final GHV, regardless of which stitch was placed first. When the 2 groups were combined, GHV was reduced by 44.9% with use of medial and lateral rotator interval closure stitches.

Mean amount of tissue purchased, or “bite size,” was 18 mm with a lateral suture and 15 mm with a medial suture (P < .05). In addition, an increase in bite size to GHV reduction was essentially linear, where an increase in bite size of 1 mm reduced GHV by about 1% (Figure 4).

Discussion

Although there have been numerous clinical series and biomechanical studies focused on isolated rotator interval closure (or its use as an adjunct) in shoulder stabilization, the precise function of the rotator interval remains poorly understood.^1-3,6-11,19 Consequently, the in vivo effects of interval closure are unknown.

Initial studies proposed that rotator interval closure limited inferior and posterior translation.³⁰ More recent studies have demonstrated that rotator interval closure confers little effect on posterior instability but increases anterior stability in cadaveric models.^15,16 Clinical series have provided evidence that rotator interval closure can increase anterior stability.^1,3,7,9,12 In a series of isolated rotator interval closures for multidirectional instability, Field and colleagues¹² found that preoperative anterior and inferior symptoms predominated over posterior symptoms. Isolated closure of the rotator interval resulted in 100% excellent results with no cases of recurrent instability. Moon and colleagues³¹ reported that arthroscopic rotator interval closure with or without inferior capsular plication in multidirectional instability and predominant symptomatic inferior instability has shown benefit by improving function and stability. Other clinical reports of rotator interval closure in conjunction with arthroscopic Bankart repair have suggested it has an additive effect on anterior shoulder stability without limiting motion.^24,25

In our study, arthroscopic closure of the rotator interval with 2 superior-to-inferior stitches reduced intracapsular volume by 45%. Even though open capsular shifts use different surgical techniques, similar technique volume reduction studies have reported reductions between 34% and 54% with open shifts.^27,30 It is unknown if the stability resulting from decreased GHV is primarily from increasing intra-articular pressures or from restricting ROM, or from a combination of both. In shoulders with multidirectional instability, the joint volume may be increased, the joint capsule may be enlarged, or the glenohumeral ligaments may be lax and thin.^4,6,32,33 Yamamoto and colleagues¹⁹ stated that intra-articular pressure is determined by 3 factors: load, joint volume, and material properties of the capsule. Load is a constant; joint volume and material properties can be changed.¹⁹ In our study, material properties were controlled by using a majority of matched specimens. Regardless of the stabilizing mechanism, our study results demonstrated that arthroscopic rotator interval closure may be a powerful tool in reducing shoulder volume, a consistent principle of surgical techniques used in reestablishing shoulder stability.^19,20

When a single rotator interval closure stitch was used, volume reduction with a lateral stitch was superior to that with a medial stitch. This finding is logical, as anatomically the dimensions of the rotator interval are larger laterally as the CHL fans out to insert on the greater and lesser tuberosities.¹⁴ This finding has also been reported in open capsular shifts for multidirectional instability, with a lateral humeral shift having a larger volume reduction than a medial glenoid shift.²⁷ Miller and colleagues²⁷ used the image of a cone, with its larger opening facing the humerus and narrower side facing the glenoid, to illustrate this difference in open capsular shifts.

Our study also showed a larger volume reduction with 2 rotator interval closure stitches than with a single interval stitch. As ROM testing has not shown a difference between results with 1 and 2 sutures, we recommend a minimum of 2 sutures for arthroscopic rotator interval closure.¹⁵ If a single plication stitch is preferred, a lateral stitch (vs a medial stitch) can be used for a significantly larger reduction in shoulder volume. We think this is because of a larger amount of capsule being purchased with lateral closure (Figure 5). However, if a medial stitch is used, it is important to not place it too near the glenoid to avoid CHL tethering and subsequent excessive loss of external rotation.¹⁵

This study had several weaknesses. First, it was a cadaveric study, and use of specimens not known to have instability or specific rotator interval injury may make generalization to a clinical situation difficult. Second, although our power analysis called for 5 shoulders in each group, full-thickness rotator cuff tears rendered 2 shoulders unusable. This reduced our sample sizes and potentially decreased the power of the study, though the data demonstrated statistically significant differences. Third, we did not compare the effects of an open medial-to-lateral imbrication of the rotator interval on intracapsular volume with the effects of our arthroscopic method. We also did not assess our specimens’ ROM, effects of interval closure stitches on shoulder stability, or glenohumeral contact surface pressures, as these factors have already been studied.^13-19 Instead, we focused on the effects of rotator interval closure on intracapsular volume, which had not been quantified until now. The clinical significance of such a volume reduction is unknown, especially with respect to influence on ROM, but the degree of volume reduction was larger than with previously reported arthroscopic instability repairs and smaller than with open capsular shifts, demonstrating that it may be a powerful tool in restoring stability in an unstable shoulder.^26-30,34 Fourth, the role of isolated rotator interval closure is poorly defined, as only 1 clinical series of isolated rotator interval closure has been reported thus far.¹² It has been far more common for rotator interval closure to be used with Bankart repair or capsulorrhaphy.^1-3,7-9

In a cadaveric study by Provencher and colleagues,¹⁶ open rotator interval closure with medial-to-lateral imbrication of the interval altered shoulder kinematics differently from what occurred with arthroscopic closure of the MGHL to the SGHL, resulting in superior-to-inferior shift. Comparing the 2 methods may therefore be inappropriate. Currently we reserve rotator interval closure for infrequent cases of revision instability and cases in which glenoid bone loss is marginal (5%-15%) and there is a willingness to potentially sacrifice ROM to restore stability and avoid an open stabilization procedure. Continued investigation into the clinical role of rotator interval closure in shoulder stability is needed. We should identify the pathology in a patient with instability and use this technique as an adjuvant to other stabilization procedures. 

Conclusion

Arthroscopic rotator interval closure with 2 plication stitches is a powerful tool in reducing the intracapsular volume of the shoulder. If a single plication stitch is preferred, a lateral rotator interval closure stitch (vs a medial stitch) can be used for a larger reduction in shoulder volume.

Since Neer described the rotator interval in 1970, its closure, often used in conjunction with capsulorrhaphy, has become an important surgical technique in managing shoulder instability.^1-11 Numerous studies have sought to define the function of the rotator interval.^1-3,6-20 The etiology of lesions of the rotator interval has been debated, and there is evidence that such lesions may be in part congenital.²¹ Increased rotator interval depth and width, along with increased size of the distended inferior and posteroinferior joint capsule on magnetic resonance arthrography, have been reported in cases of multidirectional shoulder instability.²² However, confusion remains about the role of the rotator interval in shoulder instability and about the effect its closure has on shoulder function. No one knows the degree of volume reduction that results from closure of the rotator interval and whether medial and lateral sutures differ in the volume reduction achieved.

Cadaveric studies have shown that the rotator interval has an important role in shoulder motion.^{6,13-16,19,20,23} Harryman and colleagues¹³ found that sectioning the coracohumeral ligament (CHL) increased shoulder range of motion (ROM), and medial-to-lateral closure of the rotator interval restricted motion in all planes. Most notably, interval closure limited inferior translation in the adducted shoulder, posterior translation in the flexed adducted shoulder, and external rotation in the neutral position. Subsequent studies,^17,18 using rotator interval closure combined with thermal capsulorrhaphy, confirmed the results reported by Harryman and colleagues.¹³

More recent cadaveric studies using superior-to-inferior rotator interval closures have shown a decrease in anterior translation but not posterior translation.^14-16,19-21 A superior-to-inferior interval closure technique limited external rotation less than a medial-to-lateral closure did.^13-16,19-21 The majority of arthroscopically described rotator interval closures involve a superior-to-inferior technique and use 2 or 3 sutures.^1,3,9-11

Plausinis and colleagues¹⁵ examined the effects of an isolated medial, an isolated lateral, and a medial combined with a lateral closure of the rotator interval. They noted that all 3 methods limited anterior translation and motion by means of 6° flexion and 10° external rotation; however, there was no statistical difference between methods. They also found that occasionally the medial interval closure resulted in massive loss of external rotation. Earlier, Jost and colleagues¹⁴ noted that a medial rotator interval could cause this massive loss by tethering the CHL, resulting in a medial-to-lateral imbrication of the CHL.

Arthroscopic rotator interval closure has clinically demonstrated an additive effect on shoulder stability. The recurrence rate was lower for arthroscopic Bankart repair combined with arthroscopic rotator interval closure (8%) than for arthroscopic Bankart repair alone (13%).²⁴ In addition, time to recurrent dislocation was longer (42 vs 13 months) for the group that underwent the combination of Bankart repair and rotator interval closure. Regarding the concern about loss of motion after arthroscopic rotator interval closure, Chiang and colleagues²⁵ recently noted no significant loss of motion 5 years after arthroscopic Bankart repair with rotator interval closure.

What effect rotator interval closure has on intra-articular glenohumeral volume (GHV) remains unknown. Using a cadaveric model, Yamamoto and colleagues²⁰ showed that decreasing GHV can increase the responsiveness of the glenohumeral joint to the intra-articular pressure. Thus, reducing the volume can improve stability in vitro by increasing the magnitude of negative pressure stabilizing the glenohumeral joint.

We conducted a study to quantify the effects of arthroscopic rotator interval closure on capsular volume and to determine whether medial and lateral interval closures resulted in different degrees of volume reduction. Our hypothesis was that shoulder volume would be significantly reduced by closing the rotator interval.

Materials and Methods

Previous studies have not specifically evaluated GHV after rotator interval closure. Our power analysis was performed with data from a study by Karas and colleagues,²⁶ who evaluated GHV after capsular plication. To detect a capsular volume reduction of 20% per stitch, with a 2-sided 5% significance level and a power of 80%, we needed a sample size of 5 specimens per group.

After receiving institutional review board approval for this study, we obtained 10 cadaveric shoulders (5 matched pairs). Exclusion criteria included arthroscopic evaluation revealing a full-thickness rotator cuff tear or significant osteoarthritis. Two shoulders had full-thickness cuff tears, leaving 8 shoulders to be tested; 6 of these were matched pairs. The shoulders were from 1 man (matched pair) and 4 women (2 matched pairs). Age ranged from 38 to 70 years (mean, 59.6 years). Differences in material properties between the specimens were accounted for by using primarily matched pairs.

The 2 study groups consisted of 4 shoulders each. After specimens were thawed, the skin, subcutaneous tissues, and periscapular muscles were removed from the shoulder. Only the capsule, biceps, and rotator cuff remained. For measurement purposes, the shoulders were mounted in a vice clamp in a beach-chair orientation. We placed a total of 2 portals with fully threaded 8.25-mm cannulas (Arthrex, Naples, Florida). A standard posterior portal was placed in the soft spot. A low anterior portal was then placed just superior to the subscapularis tendon. For arthroscopic examination and instrumentation in a saline environment, the shoulders were rotated into the lateral decubitus position, with suspension in 30° abduction and 20° forward flexion, by a rope attached to a pin in the distal shaft of the humerus.

In both groups, medial and lateral stitches with No. 2 FiberWire (Arthrex) were used to close the interval. The medial interval closure stitch was placed more than 10 mm away from the glenoid to prevent unpredictable CHL tethering; the lateral closure stitch was placed 10 mm lateral to the medial stitch (Figure 1).¹⁴ All sutures were placed intra-articularly under direct arthroscopic visualization, similar to the methods described in the literature.^1,3,9-11 Sutures were passed through the superior glenohumeral ligament (SGHL) and through the upper subscapularis using a suture shuttle (SutureLasso; Arthrex) and Penetrator II Suture Retriever (Arthrex). The upper subscapularis was incorporated because of the unpredictable nature of the middle glenohumeral ligament (MGHL). Both rotator interval sutures were placed before tying either. In the medial group, the medial stitch was tied first, using alternating half-hitches, followed by the lateral stitch. In the lateral group, the lateral stitch was tied first, followed by the medial stitch. GHV was measured at baseline and after tying each stitch. Dr. Ponce instrumented all shoulders.

Modifying a beach-chair technique described by Miller and colleagues,²⁷ we used a viscous fatty-acid sulfate solution, liquid soap, to measure GHV.^27-29 A small slit in line with the fibers was made in the supraspinatus tendon just lateral to the musculotendinous junction. A 3-way stop-cock was placed into the joint though this defect. A 20-mL syringe with a 16-gauge needle was used to inject the soap. The needle was inserted into the rotator cuff interval, and the viscous solution was injected in 5-mL increments until there was active extravasation through the supraspinatus cannula (Figure 2). This technique, the “volcano method,” marked the maximum capacity of the joint. The joint was then copiously irrigated with normal saline and suctioned until all normal saline was evacuated. Dr. Rosenzweig took 2 measurements on each shoulder, and their mean was used for analysis.

The baseline measurement was taken with the 2 working cannulas in the shoulder joint. Measurements were obtained with cannulas to simulate normal clinical conditions. Subsequent measurements were done with the cannulas in place and inserted up to the same thread each time so as not to change the volume. The capsule and the rotator cuff were then dissected from the humerus so the size of the capsulolabral plication could be directly evaluated. Methylene blue was used to mark the capsular suture holes before removing the sutures. With use of a caliper, the size of the plication bite was measured (in millimeters).

Statistical Analysis

The primary outcome was percent reduction in GHV as a function of number of plications and size of plication. When only the first plication was tightened, the effect of position (medial or lateral) was also of interest. Percent volume reduction was calculated as (original – new) / original × 100. SAS 8.02 (SAS Institute, Cary, North Carolina) was used to fit a repeated random-intercept regression model for each outcome. This technique properly accounts for the paired nature of the specimens and the repeated measures (baseline plus 2 plications). Model fit was assessed by the method of difference in log likelihood.

Results

In the medial group, GHV was reduced by a mean of 24.2% with a single medial stitch; in the lateral group, GHV was reduced by a mean of 35.1% (Figure 3). The difference was significant (P < .02). In the medial group, when a second lateral stitch was used, GHV was reduced by another 18.7%; in the lateral group, when a medial stitch was added, GHV was reduced by another 11.4%. Final GHV for the medial and lateral groups was 42.9% and 46.5%, respectively. There was no statistical difference in final GHV, regardless of which stitch was placed first. When the 2 groups were combined, GHV was reduced by 44.9% with use of medial and lateral rotator interval closure stitches.

Mean amount of tissue purchased, or “bite size,” was 18 mm with a lateral suture and 15 mm with a medial suture (P < .05). In addition, an increase in bite size to GHV reduction was essentially linear, where an increase in bite size of 1 mm reduced GHV by about 1% (Figure 4).

Discussion

Although there have been numerous clinical series and biomechanical studies focused on isolated rotator interval closure (or its use as an adjunct) in shoulder stabilization, the precise function of the rotator interval remains poorly understood.^1-3,6-11,19 Consequently, the in vivo effects of interval closure are unknown.

Initial studies proposed that rotator interval closure limited inferior and posterior translation.³⁰ More recent studies have demonstrated that rotator interval closure confers little effect on posterior instability but increases anterior stability in cadaveric models.^15,16 Clinical series have provided evidence that rotator interval closure can increase anterior stability.^1,3,7,9,12 In a series of isolated rotator interval closures for multidirectional instability, Field and colleagues¹² found that preoperative anterior and inferior symptoms predominated over posterior symptoms. Isolated closure of the rotator interval resulted in 100% excellent results with no cases of recurrent instability. Moon and colleagues³¹ reported that arthroscopic rotator interval closure with or without inferior capsular plication in multidirectional instability and predominant symptomatic inferior instability has shown benefit by improving function and stability. Other clinical reports of rotator interval closure in conjunction with arthroscopic Bankart repair have suggested it has an additive effect on anterior shoulder stability without limiting motion.^24,25

In our study, arthroscopic closure of the rotator interval with 2 superior-to-inferior stitches reduced intracapsular volume by 45%. Even though open capsular shifts use different surgical techniques, similar technique volume reduction studies have reported reductions between 34% and 54% with open shifts.^27,30 It is unknown if the stability resulting from decreased GHV is primarily from increasing intra-articular pressures or from restricting ROM, or from a combination of both. In shoulders with multidirectional instability, the joint volume may be increased, the joint capsule may be enlarged, or the glenohumeral ligaments may be lax and thin.^4,6,32,33 Yamamoto and colleagues¹⁹ stated that intra-articular pressure is determined by 3 factors: load, joint volume, and material properties of the capsule. Load is a constant; joint volume and material properties can be changed.¹⁹ In our study, material properties were controlled by using a majority of matched specimens. Regardless of the stabilizing mechanism, our study results demonstrated that arthroscopic rotator interval closure may be a powerful tool in reducing shoulder volume, a consistent principle of surgical techniques used in reestablishing shoulder stability.^19,20

When a single rotator interval closure stitch was used, volume reduction with a lateral stitch was superior to that with a medial stitch. This finding is logical, as anatomically the dimensions of the rotator interval are larger laterally as the CHL fans out to insert on the greater and lesser tuberosities.¹⁴ This finding has also been reported in open capsular shifts for multidirectional instability, with a lateral humeral shift having a larger volume reduction than a medial glenoid shift.²⁷ Miller and colleagues²⁷ used the image of a cone, with its larger opening facing the humerus and narrower side facing the glenoid, to illustrate this difference in open capsular shifts.

Our study also showed a larger volume reduction with 2 rotator interval closure stitches than with a single interval stitch. As ROM testing has not shown a difference between results with 1 and 2 sutures, we recommend a minimum of 2 sutures for arthroscopic rotator interval closure.¹⁵ If a single plication stitch is preferred, a lateral stitch (vs a medial stitch) can be used for a significantly larger reduction in shoulder volume. We think this is because of a larger amount of capsule being purchased with lateral closure (Figure 5). However, if a medial stitch is used, it is important to not place it too near the glenoid to avoid CHL tethering and subsequent excessive loss of external rotation.¹⁵

This study had several weaknesses. First, it was a cadaveric study, and use of specimens not known to have instability or specific rotator interval injury may make generalization to a clinical situation difficult. Second, although our power analysis called for 5 shoulders in each group, full-thickness rotator cuff tears rendered 2 shoulders unusable. This reduced our sample sizes and potentially decreased the power of the study, though the data demonstrated statistically significant differences. Third, we did not compare the effects of an open medial-to-lateral imbrication of the rotator interval on intracapsular volume with the effects of our arthroscopic method. We also did not assess our specimens’ ROM, effects of interval closure stitches on shoulder stability, or glenohumeral contact surface pressures, as these factors have already been studied.^13-19 Instead, we focused on the effects of rotator interval closure on intracapsular volume, which had not been quantified until now. The clinical significance of such a volume reduction is unknown, especially with respect to influence on ROM, but the degree of volume reduction was larger than with previously reported arthroscopic instability repairs and smaller than with open capsular shifts, demonstrating that it may be a powerful tool in restoring stability in an unstable shoulder.^26-30,34 Fourth, the role of isolated rotator interval closure is poorly defined, as only 1 clinical series of isolated rotator interval closure has been reported thus far.¹² It has been far more common for rotator interval closure to be used with Bankart repair or capsulorrhaphy.^1-3,7-9

In a cadaveric study by Provencher and colleagues,¹⁶ open rotator interval closure with medial-to-lateral imbrication of the interval altered shoulder kinematics differently from what occurred with arthroscopic closure of the MGHL to the SGHL, resulting in superior-to-inferior shift. Comparing the 2 methods may therefore be inappropriate. Currently we reserve rotator interval closure for infrequent cases of revision instability and cases in which glenoid bone loss is marginal (5%-15%) and there is a willingness to potentially sacrifice ROM to restore stability and avoid an open stabilization procedure. Continued investigation into the clinical role of rotator interval closure in shoulder stability is needed. We should identify the pathology in a patient with instability and use this technique as an adjuvant to other stabilization procedures. 

Conclusion

Arthroscopic rotator interval closure with 2 plication stitches is a powerful tool in reducing the intracapsular volume of the shoulder. If a single plication stitch is preferred, a lateral rotator interval closure stitch (vs a medial stitch) can be used for a larger reduction in shoulder volume.

Since Neer described the rotator interval in 1970, its closure, often used in conjunction with capsulorrhaphy, has become an important surgical technique in managing shoulder instability.^1-11 Numerous studies have sought to define the function of the rotator interval.^1-3,6-20 The etiology of lesions of the rotator interval has been debated, and there is evidence that such lesions may be in part congenital.²¹ Increased rotator interval depth and width, along with increased size of the distended inferior and posteroinferior joint capsule on magnetic resonance arthrography, have been reported in cases of multidirectional shoulder instability.²² However, confusion remains about the role of the rotator interval in shoulder instability and about the effect its closure has on shoulder function. No one knows the degree of volume reduction that results from closure of the rotator interval and whether medial and lateral sutures differ in the volume reduction achieved.

Cadaveric studies have shown that the rotator interval has an important role in shoulder motion.^{6,13-16,19,20,23} Harryman and colleagues¹³ found that sectioning the coracohumeral ligament (CHL) increased shoulder range of motion (ROM), and medial-to-lateral closure of the rotator interval restricted motion in all planes. Most notably, interval closure limited inferior translation in the adducted shoulder, posterior translation in the flexed adducted shoulder, and external rotation in the neutral position. Subsequent studies,^17,18 using rotator interval closure combined with thermal capsulorrhaphy, confirmed the results reported by Harryman and colleagues.¹³

More recent cadaveric studies using superior-to-inferior rotator interval closures have shown a decrease in anterior translation but not posterior translation.^14-16,19-21 A superior-to-inferior interval closure technique limited external rotation less than a medial-to-lateral closure did.^13-16,19-21 The majority of arthroscopically described rotator interval closures involve a superior-to-inferior technique and use 2 or 3 sutures.^1,3,9-11

Plausinis and colleagues¹⁵ examined the effects of an isolated medial, an isolated lateral, and a medial combined with a lateral closure of the rotator interval. They noted that all 3 methods limited anterior translation and motion by means of 6° flexion and 10° external rotation; however, there was no statistical difference between methods. They also found that occasionally the medial interval closure resulted in massive loss of external rotation. Earlier, Jost and colleagues¹⁴ noted that a medial rotator interval could cause this massive loss by tethering the CHL, resulting in a medial-to-lateral imbrication of the CHL.

Arthroscopic rotator interval closure has clinically demonstrated an additive effect on shoulder stability. The recurrence rate was lower for arthroscopic Bankart repair combined with arthroscopic rotator interval closure (8%) than for arthroscopic Bankart repair alone (13%).²⁴ In addition, time to recurrent dislocation was longer (42 vs 13 months) for the group that underwent the combination of Bankart repair and rotator interval closure. Regarding the concern about loss of motion after arthroscopic rotator interval closure, Chiang and colleagues²⁵ recently noted no significant loss of motion 5 years after arthroscopic Bankart repair with rotator interval closure.

What effect rotator interval closure has on intra-articular glenohumeral volume (GHV) remains unknown. Using a cadaveric model, Yamamoto and colleagues²⁰ showed that decreasing GHV can increase the responsiveness of the glenohumeral joint to the intra-articular pressure. Thus, reducing the volume can improve stability in vitro by increasing the magnitude of negative pressure stabilizing the glenohumeral joint.

We conducted a study to quantify the effects of arthroscopic rotator interval closure on capsular volume and to determine whether medial and lateral interval closures resulted in different degrees of volume reduction. Our hypothesis was that shoulder volume would be significantly reduced by closing the rotator interval.

Materials and Methods

Previous studies have not specifically evaluated GHV after rotator interval closure. Our power analysis was performed with data from a study by Karas and colleagues,²⁶ who evaluated GHV after capsular plication. To detect a capsular volume reduction of 20% per stitch, with a 2-sided 5% significance level and a power of 80%, we needed a sample size of 5 specimens per group.

After receiving institutional review board approval for this study, we obtained 10 cadaveric shoulders (5 matched pairs). Exclusion criteria included arthroscopic evaluation revealing a full-thickness rotator cuff tear or significant osteoarthritis. Two shoulders had full-thickness cuff tears, leaving 8 shoulders to be tested; 6 of these were matched pairs. The shoulders were from 1 man (matched pair) and 4 women (2 matched pairs). Age ranged from 38 to 70 years (mean, 59.6 years). Differences in material properties between the specimens were accounted for by using primarily matched pairs.

The 2 study groups consisted of 4 shoulders each. After specimens were thawed, the skin, subcutaneous tissues, and periscapular muscles were removed from the shoulder. Only the capsule, biceps, and rotator cuff remained. For measurement purposes, the shoulders were mounted in a vice clamp in a beach-chair orientation. We placed a total of 2 portals with fully threaded 8.25-mm cannulas (Arthrex, Naples, Florida). A standard posterior portal was placed in the soft spot. A low anterior portal was then placed just superior to the subscapularis tendon. For arthroscopic examination and instrumentation in a saline environment, the shoulders were rotated into the lateral decubitus position, with suspension in 30° abduction and 20° forward flexion, by a rope attached to a pin in the distal shaft of the humerus.

In both groups, medial and lateral stitches with No. 2 FiberWire (Arthrex) were used to close the interval. The medial interval closure stitch was placed more than 10 mm away from the glenoid to prevent unpredictable CHL tethering; the lateral closure stitch was placed 10 mm lateral to the medial stitch (Figure 1).¹⁴ All sutures were placed intra-articularly under direct arthroscopic visualization, similar to the methods described in the literature.^1,3,9-11 Sutures were passed through the superior glenohumeral ligament (SGHL) and through the upper subscapularis using a suture shuttle (SutureLasso; Arthrex) and Penetrator II Suture Retriever (Arthrex). The upper subscapularis was incorporated because of the unpredictable nature of the middle glenohumeral ligament (MGHL). Both rotator interval sutures were placed before tying either. In the medial group, the medial stitch was tied first, using alternating half-hitches, followed by the lateral stitch. In the lateral group, the lateral stitch was tied first, followed by the medial stitch. GHV was measured at baseline and after tying each stitch. Dr. Ponce instrumented all shoulders.

Modifying a beach-chair technique described by Miller and colleagues,²⁷ we used a viscous fatty-acid sulfate solution, liquid soap, to measure GHV.^27-29 A small slit in line with the fibers was made in the supraspinatus tendon just lateral to the musculotendinous junction. A 3-way stop-cock was placed into the joint though this defect. A 20-mL syringe with a 16-gauge needle was used to inject the soap. The needle was inserted into the rotator cuff interval, and the viscous solution was injected in 5-mL increments until there was active extravasation through the supraspinatus cannula (Figure 2). This technique, the “volcano method,” marked the maximum capacity of the joint. The joint was then copiously irrigated with normal saline and suctioned until all normal saline was evacuated. Dr. Rosenzweig took 2 measurements on each shoulder, and their mean was used for analysis.

The baseline measurement was taken with the 2 working cannulas in the shoulder joint. Measurements were obtained with cannulas to simulate normal clinical conditions. Subsequent measurements were done with the cannulas in place and inserted up to the same thread each time so as not to change the volume. The capsule and the rotator cuff were then dissected from the humerus so the size of the capsulolabral plication could be directly evaluated. Methylene blue was used to mark the capsular suture holes before removing the sutures. With use of a caliper, the size of the plication bite was measured (in millimeters).

Statistical Analysis

The primary outcome was percent reduction in GHV as a function of number of plications and size of plication. When only the first plication was tightened, the effect of position (medial or lateral) was also of interest. Percent volume reduction was calculated as (original – new) / original × 100. SAS 8.02 (SAS Institute, Cary, North Carolina) was used to fit a repeated random-intercept regression model for each outcome. This technique properly accounts for the paired nature of the specimens and the repeated measures (baseline plus 2 plications). Model fit was assessed by the method of difference in log likelihood.

Results

In the medial group, GHV was reduced by a mean of 24.2% with a single medial stitch; in the lateral group, GHV was reduced by a mean of 35.1% (Figure 3). The difference was significant (P < .02). In the medial group, when a second lateral stitch was used, GHV was reduced by another 18.7%; in the lateral group, when a medial stitch was added, GHV was reduced by another 11.4%. Final GHV for the medial and lateral groups was 42.9% and 46.5%, respectively. There was no statistical difference in final GHV, regardless of which stitch was placed first. When the 2 groups were combined, GHV was reduced by 44.9% with use of medial and lateral rotator interval closure stitches.

Mean amount of tissue purchased, or “bite size,” was 18 mm with a lateral suture and 15 mm with a medial suture (P < .05). In addition, an increase in bite size to GHV reduction was essentially linear, where an increase in bite size of 1 mm reduced GHV by about 1% (Figure 4).

Discussion

Although there have been numerous clinical series and biomechanical studies focused on isolated rotator interval closure (or its use as an adjunct) in shoulder stabilization, the precise function of the rotator interval remains poorly understood.^1-3,6-11,19 Consequently, the in vivo effects of interval closure are unknown.

Initial studies proposed that rotator interval closure limited inferior and posterior translation.³⁰ More recent studies have demonstrated that rotator interval closure confers little effect on posterior instability but increases anterior stability in cadaveric models.^15,16 Clinical series have provided evidence that rotator interval closure can increase anterior stability.^1,3,7,9,12 In a series of isolated rotator interval closures for multidirectional instability, Field and colleagues¹² found that preoperative anterior and inferior symptoms predominated over posterior symptoms. Isolated closure of the rotator interval resulted in 100% excellent results with no cases of recurrent instability. Moon and colleagues³¹ reported that arthroscopic rotator interval closure with or without inferior capsular plication in multidirectional instability and predominant symptomatic inferior instability has shown benefit by improving function and stability. Other clinical reports of rotator interval closure in conjunction with arthroscopic Bankart repair have suggested it has an additive effect on anterior shoulder stability without limiting motion.^24,25

In our study, arthroscopic closure of the rotator interval with 2 superior-to-inferior stitches reduced intracapsular volume by 45%. Even though open capsular shifts use different surgical techniques, similar technique volume reduction studies have reported reductions between 34% and 54% with open shifts.^27,30 It is unknown if the stability resulting from decreased GHV is primarily from increasing intra-articular pressures or from restricting ROM, or from a combination of both. In shoulders with multidirectional instability, the joint volume may be increased, the joint capsule may be enlarged, or the glenohumeral ligaments may be lax and thin.^4,6,32,33 Yamamoto and colleagues¹⁹ stated that intra-articular pressure is determined by 3 factors: load, joint volume, and material properties of the capsule. Load is a constant; joint volume and material properties can be changed.¹⁹ In our study, material properties were controlled by using a majority of matched specimens. Regardless of the stabilizing mechanism, our study results demonstrated that arthroscopic rotator interval closure may be a powerful tool in reducing shoulder volume, a consistent principle of surgical techniques used in reestablishing shoulder stability.^19,20

When a single rotator interval closure stitch was used, volume reduction with a lateral stitch was superior to that with a medial stitch. This finding is logical, as anatomically the dimensions of the rotator interval are larger laterally as the CHL fans out to insert on the greater and lesser tuberosities.¹⁴ This finding has also been reported in open capsular shifts for multidirectional instability, with a lateral humeral shift having a larger volume reduction than a medial glenoid shift.²⁷ Miller and colleagues²⁷ used the image of a cone, with its larger opening facing the humerus and narrower side facing the glenoid, to illustrate this difference in open capsular shifts.

Our study also showed a larger volume reduction with 2 rotator interval closure stitches than with a single interval stitch. As ROM testing has not shown a difference between results with 1 and 2 sutures, we recommend a minimum of 2 sutures for arthroscopic rotator interval closure.¹⁵ If a single plication stitch is preferred, a lateral stitch (vs a medial stitch) can be used for a significantly larger reduction in shoulder volume. We think this is because of a larger amount of capsule being purchased with lateral closure (Figure 5). However, if a medial stitch is used, it is important to not place it too near the glenoid to avoid CHL tethering and subsequent excessive loss of external rotation.¹⁵

This study had several weaknesses. First, it was a cadaveric study, and use of specimens not known to have instability or specific rotator interval injury may make generalization to a clinical situation difficult. Second, although our power analysis called for 5 shoulders in each group, full-thickness rotator cuff tears rendered 2 shoulders unusable. This reduced our sample sizes and potentially decreased the power of the study, though the data demonstrated statistically significant differences. Third, we did not compare the effects of an open medial-to-lateral imbrication of the rotator interval on intracapsular volume with the effects of our arthroscopic method. We also did not assess our specimens’ ROM, effects of interval closure stitches on shoulder stability, or glenohumeral contact surface pressures, as these factors have already been studied.^13-19 Instead, we focused on the effects of rotator interval closure on intracapsular volume, which had not been quantified until now. The clinical significance of such a volume reduction is unknown, especially with respect to influence on ROM, but the degree of volume reduction was larger than with previously reported arthroscopic instability repairs and smaller than with open capsular shifts, demonstrating that it may be a powerful tool in restoring stability in an unstable shoulder.^26-30,34 Fourth, the role of isolated rotator interval closure is poorly defined, as only 1 clinical series of isolated rotator interval closure has been reported thus far.¹² It has been far more common for rotator interval closure to be used with Bankart repair or capsulorrhaphy.^1-3,7-9

In a cadaveric study by Provencher and colleagues,¹⁶ open rotator interval closure with medial-to-lateral imbrication of the interval altered shoulder kinematics differently from what occurred with arthroscopic closure of the MGHL to the SGHL, resulting in superior-to-inferior shift. Comparing the 2 methods may therefore be inappropriate. Currently we reserve rotator interval closure for infrequent cases of revision instability and cases in which glenoid bone loss is marginal (5%-15%) and there is a willingness to potentially sacrifice ROM to restore stability and avoid an open stabilization procedure. Continued investigation into the clinical role of rotator interval closure in shoulder stability is needed. We should identify the pathology in a patient with instability and use this technique as an adjuvant to other stabilization procedures. 

Conclusion

Arthroscopic rotator interval closure with 2 plication stitches is a powerful tool in reducing the intracapsular volume of the shoulder. If a single plication stitch is preferred, a lateral rotator interval closure stitch (vs a medial stitch) can be used for a larger reduction in shoulder volume.