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Clinical Faceoff: What is the Role of Acromioplasty in the Treatment of Rotator Cuff Disease?

McFarland, Edward G. MD; Matsen, Frederick A. III MD; Sanchez-Sotelo, Joaquin MD, PhD, FEBOT

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Clinical Orthopaedics and Related Research: September 2018 - Volume 476 - Issue 9 - p 1707-1712
doi: 10.1097/01.blo.0000533630.65994.e2
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The debate over the cause of rotator cuff disease and its treatment has been around since the late 19th century [11], with the disagreement centering around whether the pathology seen in rotator cuff tears is caused by inherent degeneration of the tendons, contact of the tendons with some structures, or both. Charles S. Neer II MD was the first to coin the term “impingement lesions,” which he described as tears of the rotator cuff caused by contact of the rotator cuff with the anterior acromion and the coracoacromial ligament [43, 44]. For symptomatic rotator cuff disease, he recommended a partial anterior acromioplasty with release of the coracoacromial ligament. These procedures subsequently became the go-to treatment for rotator cuff disease. However, there has been continued controversy regarding the role of the acromion and coracoacromial ligament in rotator cuff disease [7, 38, 45, 47]. Some studies suggest that acromial morphology is not reliable or reproducible [8, 27], that partial acromioplasty does not make a difference in surgical result [1, 16, 19, 34, 39], and that it does not change the natural history of rotator cuff disease [26].

Because there is disagreement in the orthopaedic community about the role of partial acromioplasty in the treatment of rotator cuff disease, I have asked two shoulder experts to discuss this important topic: Frederick A. Matsen III MD the Douglas T. Harryman II Endowed Chair in Shoulder and Elbow Research in the Department of Orthopaedics at the University of Washington; and Joaquin Sanchez-Sotelo MD, PhD, FEBOT, a Consultant and Professor in the Department of Orthopaedic Surgery at the Mayo Clinic. Dr. Matsen questioned the role of partial acromioplasty based on his own experience [36] and extensive review of the literature [45]. Dr. Sanchez-Sotelo has similarly extensive clinical experience with the use of partial acromioplasty in the arthroscopic treatment of rotator cuff disease.

Edward G. McFarland MD:How have your thoughts about rotator cuff disease (including the concept of “impingement”) changed since Dr. Charles S. Neer II’s original articles?

Frederick A. Matsen III MD: Since my time studying with Dr. Neer in 1975, I’ve been trying to put the published evidence on the rotator cuff (more than 10,000 articles at this writing) together along with what I’ve personally seen work and fail during the last 43 years of shoulder practice. I’ve come to several conclusions. First, most rotator cuff defects are the result of age-related degeneration in the quality of the tendon. In many patients, the gradual progression of cuff pathology is well accommodated by the shoulder, allowing them to continue to lead functional lives without surgical intervention (I am one of these). A small percentage of individuals with cuff tears (I am not one of these) come to see shoulder surgeons. Most of our knowledge about cuff tears comes from the study of thousands of individuals who seek surgical care instead of the millions of patients living with minimally symptomatic cuff defects. Second, while some surgeons have tried to associate various morphologic features of the acromion with cuff disease, evidence is lacking that surgical modification of the acromion changes the natural history of cuff disease or improves the likelihood that a rotator cuff repair will remain intact. Third, it is evident that acromioplasty increases the risk of pseudoparalysis and anterosuperior escape in patients with cuff deficiency. Fourth, for individuals with reparable cuff tears, there is no evident difference among the different repair approaches. Last, for individuals with chronic cuff pathology, there is no rush to intervene surgically; for many of these patients, gentle ROM and strengthening exercises can decrease pain and improve function without the risks, cost, and inconvenience of surgery [30]. Patients with persistently symptomatic large degenerative cuff defects without arthritis or pseudoparalysis usually achieve durable improvement in comfort and function from the conservative surgical smoothing of the humeroscapular motion interface without attempting rotator cuff reconstruction [25].

Joaquin Sanchez-Sotelo MD: Dr. Neer formulated a number of concepts regarding rotator cuff disease that remain relevant today. However, I believe our understanding of cuff disease has improved substantially during the last 20 years. From a surgical management perspective, we know more about the risk factors for irreparability and healing compared to when Dr. Neer conducted his research. I believe we pay much more attention to the condition of the muscles (atrophy and fatty infiltration), the length of the remaining tendon after tear, and involvement of the upper subscapularis, among others. The long head of the biceps is addressed more commonly in patients undergoing surgery. I also believe progress is being made in revisiting tendon transfers for patients with irreparable cuff tears. Finally, in Dr. Neer’s time, modern reverse arthroplasty had not yet been developed, and this procedure has filled a gap for patients with no good surgical solution—although success for these patients is not universal.

I like using the word cuff “wear” (instead of “tear”) when referring to chronic cuff disease, which was suggested by Pascal Boileau MD [4]. Failure of tendon fibers leading to progressive cuff disruption is likely multifactorial and probably different among individuals. As pointed out by Dr. Matsen, age plays a major role in many shoulder injuries [48], but genetic predisposition [13] and repetitive use must be implicated in some. Genetic predisposition may facilitate cuff wear through a more fragile connective tissue structure or by determining an overall macroscopic skeletal architecture that overloads the rotator cuff, as suggested by Moor and colleagues with his studies on the critical shoulder angle [40]. Also, when Dr. Neer published his articles, we had less information regarding patterns of progression as assessed with ultrasound imaging [28].

Dr. McFarland:What is the current role of partial acromioplasty during surgery for rotator cuff disease?

Dr. Sanchez-Sotelo: Comparative studies have investigated the effects of adding an acromioplasty at the time of rotator cuff repair [5, 10, 16, 34]. The majority have reported no differences in pain, function, or healing rates when compared to cuff repair with or without acromioplasty, with only one study reporting a slightly higher risk of reoperation when acromioplasty was not performed [34]. Obviously, research comes with limitations, and several of the studies either have no randomization, small sample size, short followup, or inconsistent methods to assess healing [10, 16].

Still, acromioplasty offers some benefits, such as (1) increasing the acromiohumeral space to hopefully decrease impingement and wear on the repaired cuff [43], (2) modifying the anatomy to potentially change the vector of deltoid action and decrease strain on the repaired cuff, (3) increasing delivery of bone-marrow derived cells and mediators that might improve the healing response [18, 46], and (4) creating more working space at the time of surgery [17].

The potential theoretical disadvantages of acromioplasty include (1) prolonged surgical time, (2) worse visualization in the presence of bleeding from the acromial surface when cuff repair is performed arthroscopically [21], (3) increased risk of anterosuperior escape if the cuff repair were to fail and the coracoacromial ligament and anterior acromion have been compromised [9, 15, 33], and (4) possibly an increased risk of heterotopic ossification, although this complication has been rarely reported after acromioplasty without cuff repair [6].

Although there is no added benefit from acromioplasty as an adjunct to cuff repair [5, 10, 16, 34], failure to prove a difference does not mean that there is no difference. I perform an acromioplasty selectively when the thickness of the acromion prevents me from achieving an ideal cuff repair; when I perceive the presence of impingement in the shoulder; or when the critical shoulder angle is excessive. I avoid acromioplasty in large cuff tears that are unlikely to heal and could become complicated by escape. However, I do not think that those who avoid acromioplasty at the time of cuff repair are wrong.

Dr. Matsen: There is a tendency to confuse the association of cuff pathology and acromial changes with causation of the cuff changes by the acromion. Today, many hold the belief that “subacromial impingement” causes cuff lesions. In 1972, Dr. Neer reported a “characteristic ridge of proliferative spurs and excrescences on the undersurface of the anterior process (of the acromion) apparently caused by repeated impingement of the rotator cuff and the humeral head, with traction of the coracoacromial ligament” [43]. Stated otherwise, Dr. Neer was suggesting that the changes in the acromion were caused by the cuff pathology, rather than the other way around. Rigorously establishing causation requires the application of criteria used by Hill and colleagues [24] to demonstrate the causation of scrotal cancer in chimney sweeps, and recently used to demonstrate the causation of chondrolysis by pain pumps [35]. When we see a certain acromial configuration in patients with cuff lesions, we must ask, “which is the chicken and which is the egg or are they both products of genetics and aging?” A recent review [45] could not find good evidence to support the causation of cuff disease by contact with the coracoacromial arch or a benefit of acromioplasty in the treatment of cuff disease.

Dr. McFarland:What do you think is the relationship between acromial shape or “critical shoulder angle (CSA)” and rotator cuff disease?

Dr. Sanchez-Sotelo: Dr. Gerber’s group has published several interesting studies [20, 41, 49] that associate a relationship between the acromial length laterally (called “the critical angle” or CSA) and both cuff disease and osteoarthritis. His observations suggest potential factors other than anterior acromial morphology that contribute to the genesis of cuff disease. However, even if surgically decreasing the critical shoulder angle with a “lateral” acromioplasty could change the biomechanics of the shoulder after cuff repair, I believe it will be extremely difficult to prove that acromial reshaping translates in either a higher likelihood of healing or better overall clinical result. This is related to the multifactorial nature of “success” after cuff repair, as well as the need for studies with large numbers of patients to properly isolate this variable.

Dr. Matsen: I agree with our colleague, Dr. Sanchez-Sotelo. The studies by Gerber and colleagues [40, 41] suggest that a high CSA (> 35°) is associated with rotator cuff tears, whereas a low CSA is associated with glenohumeral arthritis. The hypothesis is that lateral acromioplasty can change the CSA and perhaps prevent or alter the history of rotator cuff disease [40, 41]. But a number of questions remain: Is the relationship between CSA and rotator cuff disease one of cause and effect or just one of association? Does cuff disease change the CSA, or does the CSA determine cuff disease, or are they both due to other factors? Is there clinical evidence that modifying the CSA changes the natural history of rotator cuff disease? If the CSA is lowered, will this predispose the shoulder to arthritis? Lastly, what is the effect on deltoid function of removing enough bone to change the CSA?

Dr. McFarland:Where surgical approaches for symptomatic pathology of the rotator cuff are concerned, what do you perceive to be the major gaps in our evidence base, and how do you make treatment decisions considering these gaps?

Dr. Sanchez-Sotelo: I find it difficult to counsel patients with a symptomatic chronic full-thickness rotator cuff tear. If nonoperative treatment is selected and initially successful, I do not know for sure how many patients will eventually experience a recurrence of symptoms, how many will require surgery, and what the effect of delay will be on the success of surgery later. On the other hand, if surgery is selected, I do not know for sure how many patients will eventually perceive that surgery was not successful because of complications, persistent symptoms, or need for further surgery.

Some of the available evidence suggests that nonoperative treatment is successful in many individuals with a chronic symptomatic full-thickness cuff tear [2, 32, 42]. But there is also evidence suggesting that both symptomatic and asymptomatic cuff tears can become larger and more symptomatic over time, and that muscular changes (atrophy and fatty infiltration) are progressive and difficult to reverse [22, 23, 28]. Dunn and colleagues [14] suggest that a patient’s preconceived opinion about the need for surgery when a tendon is torn is a major factor related to the success of surgery. What a dilemma! Why is it that despite the reported success of nonoperative treatment for cuff tears, arthroscopic rotator cuff repair is one of the most commonly performed surgical procedures in the field of orthopaedic surgery?

Despite efforts to identify factors that negatively affect tendon healing after surgery (e.g., advanced age, smoking, tear size, muscular changes), we are still lacking a comprehensive scoring system that might correlate with the probability of tendon healing. Counseling patients regarding cuff repair is a perfect area for investigation of shared decision-making processes. More work is needed to understand the value of modifying risk factors for healing around the time of surgery. We have largely ignored the bone side of the equation, yet in many individuals, poor bone quality does compromise tendon repair as perceived by the surgeon. The role of biologic enhancement of healing is in its infancy. And the relative value of dynamic tendon transfers versus static stabilization of the fulcrum with superior capsular reconstruction or an inflatable balloon is difficult to tease out, and markedly influenced by financial interests.

How do I make treatment decisions considering these gaps? At the time of counseling, I try to factor in (1) a patient’s preconceptions and expectations, (2) modifiable and nonmodifiable risk factors for incomplete healing, and (3) the structure of tendon, muscle, and bone. Most of my patients 60 years of age or younger with medium-to-large tears end up having surgery. Most of my patients 75 years of age or older with large tears are treated nonoperatively. But there are a lot of patients in the middle, and for those, it is all about shared decision making. For the nonrepairable cuff tear, I am biased in favor of tendon transfers and reverse arthroplasty, as opposed to superior capsular reconstruction or a balloon, based on opinion, not evidence.

Dr. Matsen: Once again, I agree with our colleague, Dr. Sanchez-Sotelo, that physicians do not have the information necessary to guide the treatment of patients with cuff disease. Neither the Cochrane Reviews [12] nor the American Academy of Orthopaedic Surgeons practice guidelines [3] provide evidenced-based principles for selecting the best treatment for patients with cuff failure—the most common shoulder disorder that we encounter in the practice of orthopaedics. Dunn and colleagues [14] recently noted that “a patient's decision to undergo surgery is influenced more by low expectations regarding the effectiveness of physical therapy than by patient symptoms or anatomic features of the rotator cuff tear.” These expectations are, of course, set in large part by the information they get from the healthcare provider they visit, not by their pathology. We are humbled in the knowledge that more than a quarter of a million attempted rotator cuff repairs are performed each year [14], while we have such a limited understanding of how much patients benefit from this procedure in comparison to other management approaches for cuff pathology. It is confusing for us to read that the outcomes of failed cuff repair are similar to those of successful cuff repairs [37]. Perhaps rather than asking, “Why is it that despite the reported success of nonoperative treatment for cuff tears, arthroscopic rotator cuff repair is one of the most commonly performed procedures in the field of orthopaedic surgery?” one might ask “Why is it that fewer than 5% of people with cuff tears undergo surgery each year?” [29, 31]

Until better data become available, here is my approach to cuff tears. I usually try to repair traumatic tears acutely. With degenerative tears, I take a conservative approach--if a gentle progressive passive and active range of motion program fails to effectively manage the patient’s symptoms, I consider a rotator cuff repair. When the cuff tear is irreparable, I consider a “smooth and move” procedure if the patient does not have pseudoparalysis or glenohumeral arthritis [25]. This approach gives the patient a good opportunity for durable improvement in comfort and function without the down-time of more complex procedures and doesn’t “burn bridges” for other procedures in the future should they become indicated. I am prepared to modify my practice when there is evidence that marginal convergence, biological scaffolds, superior capsular reconstruction, or tendon transfers provide more cost-effective benefits to the patient.


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