Rotator Cuff Failure: Early and Late



Rotator Cuff Failure: Early and Late


Ian R. Byram, MD

Joseph T. Labrum IV, MD



INTRODUCTION

Anatomic total shoulder arthroplasty (ATSA) has proven to be effective in alleviating pain and restoring function in the setting of severe glenohumeral osteoarthritis. Although this procedure provides reliable, positive outcomes for most patients, complications can be encountered in the early and late postoperative course. The most common complication of ATSA is rotator cuff dysfunction.1,2 The dynamic stability provided to the shoulder by the rotator cuff is pivotal for proper function of the native glenohumeral joint, and its importance is magnified in the reconstructed shoulder after removal of osteophytes and capsular releases. Unlike reverse total shoulder arthroplasty, ATSA recreates the native unconstrained glenohumeral joint and requires a functional rotator cuff for stability. Rotator cuff pathology in the setting of total shoulder arthroplasty can lead to increased pain, instability, arthroplasty component loosening or failure, need for revision surgery, and poor clinical outcomes. This chapter reviews the epidemiology, etiology, prevention, diagnosis, and management of rotator cuff failure in the setting of ATSA.


EPIDEMIOLOGY AND ETIOLOGY

Rotator cuff failure is a recognized complication following ATSA. It can present in both the early postoperative period as well as long after successful ATSA. Rotator cuff pathology can arise as a result of multiple biologic and biomechanical processes, with the majority of cases representing degenerative rotator cuff failure, traumatic rotator cuff injury, infectious etiology, and technique-related implant and soft tissue complications.


Frequency

Rotator cuff failure represents the most common complication following ATSA. Young et al observed rotator cuff dysfunction to be the most common complication in their cohort of 518 ATSAs, reporting an incidence of 16.8% at an average follow-up of 8.6 years. In addition, they found that the incidence of rotator cuff dysfunction following total shoulder arthroplasty increased with increasing postoperative follow-up.1 They estimated total shoulder arthroplasty (TSA) survivorship free of secondary rotator cuff dysfunction to be 100% at 5-year follow-up, 84% at 10-year follow-up, and 45% at 15-year follow-up.1 Chin et al similarly observed rotator cuff failure to be the most common complication following ATSA.2 They observed a total of 53 complications in a cohort of 421 ATSAs at an average follow-up of 4.2 years, with 32% (17/53) of complications resulting from rotator cuff tears.2 Chin et al noted only four cases of acute rotator cuff failure within the 90-day postoperative period, all of which were due to subscapularis repair failure.2 Deshmukh et al carried out a retrospective review of 320 consecutive ATSAs and observed instability and secondary traumatic rotator cuff injury in approximately 1% of cases.3


Biomechanical and Biologic Etiology


Degenerative

The most common etiology of rotator cuff insufficiency following ATSA is degenerative rotator cuff dysfunction. As degenerative rotator cuff disease progresses, the dynamic stability provided to the prosthetic glenohumeral articulation is compromised. This lack of stability results in altered joint reactive forces, thereby subjecting the glenoid and humeral components to abnormal stresses and loads. Mechanically, this results in humeral component translation and eccentric loading of the glenoid component, leading to the “rocking horse phenomenon.”1,4 Secondary rotator cuff dysfunction is a chronic process encountered in long-term ATSA follow-up. In a review of 596 cases, Young et al noted that secondary rotator cuff dysfunction occurred only after the 5-year follow-up interval.1 Preoperative magnetic resonance imaging (MRI) finding of fatty infiltration of the infraspinatus has been noted to be a statistically significant predictor for development of secondary rotator cuff dysfunction following ATSA.1 Fatty degeneration of the rotator cuff has been associated with poor clinical outcomes following ATSA.5


Traumatic

Traumatic rotator cuff failure can occur following injury to the shoulder that results in a sudden contracture of the rotator cuff. This complication can present with or
without concurrent glenohumeral dislocation and can occur at any point postoperatively. However, the subscapularis is most vulnerable to failure in the acute postoperative period following ATSA, because of the time required for healing of the subscapularis tenotomy (SST), lesser tuberosity osteotomy (LTO), or subscapularis tendon reattachment. Subscapularis failure commonly takes place following a sudden active internal rotation moment or forced external rotation moment in the setting of an incompletely healed subscapularis. Similar to degenerative rotator cuff pathology, traumatic rotator cuff insufficiency results in uncoupling of the balanced rotator cuff forces that function to stabilize the glenohumeral articulation, resulting in ATSA instability.


Infection-Related Rotator Cuff Failure

Periprosthetic joint infection (PJI) in the setting of ATSA is an uncommon yet devastating complication. Total shoulder replacement complicated by PJI can result in chronic inflammation and degeneration of the rotator cuff, resulting in subsequent rotator cuff failure. PJI following total shoulder arthroplasty has an estimated incidence of 0.7% to 4.0%.4,6 A retrospective review of 2588 primary ATSAs by Singh et al observed the 5-, 10-, and 20-year prosthetic infection-free rates to be 99.3%, 98.5%, and 97.2%, respectively.7 The authors found that male sex and younger age were significant risk factors for the development of PJI.7 The prevention, evaluation, diagnosis, and management of PJI following total shoulder replacement, which will be covered extensively in Chapters 32 and 49, can be challenging and should be considered in presentations of rotator cuff dysfunction following TSA.


Technique-Related Rotator Cuff Failure and Prevention in ATSA

Although rotator cuff deficiency following TSA is in many cases unavoidable, there are several iatrogenic, technique-related errors that can also result in this complication. Surgeons should be aware of these potential pitfalls in order to minimize the risk of future rotator cuff failure.

Superior inclination of the glenoid component on immediate postoperative radiographs following ATSA has been noted as a significant risk factor for the development of secondary cuff dysfunction.1 As such, surgeons should remove all inferior glenoid osteophytes and critically evaluate inclination prior to glenoid reaming and preparation.

Studies evaluating LTO, SST, and subscapularis peel have shown excellent clinical results with all techniques.8 The literature on the recovery of subscapularis strength following these techniques remains mixed.8 Lapner et al found no clinical differences at 2-year follow-up in TSA patients randomized to subscapularis peel versus LTO,9 but others have shown improved subscapularis function and healing rates with ATSA performed using a LTO.10,11,12 Scalise et al reported a prospective evaluation of 35 TSAs comparing SST and LTO, noting higher clinical outcome scores, superior subscapularis tendon retear rates, and universal osteotomy healing in the LTO cohort.10 Similarly, Jandhyala et al noted improved subscapularis function following anatomic TSA with LTO when compared with SST as assessed with the graded belly press test in a consecutive cohort of 36 TSAs.11 A recent biomechanical analysis by Terrier et al evaluating subscapularis function in the setting of ATSA observed that a dysfunctional subscapularis disrupts the mechanical force coupling of the rotator cuff, resulting in a decrease in infraspinatus force.13 This imbalance results in a compensatory increase in force on the supraspinatus and middle deltoid, inducing upward migration of the humeral head and eccentric contact and stress patterns across the glenoid component.13 Subscapularis deficiency can disrupt the mechanical equilibrium of the glenohumeral joint and may play a role in the development of secondary rotator cuff dysfunction. As such, surgeons should utilize meticulous surgical technique regardless of which technique is utilized to maintain proper subscapularis healing and function following ATSA.

Failure to restore native glenoid version during ATSA in cases with excessive pathologic glenoid retroversion (Walch B2 and B3 glenoids) may also play a role in rotator cuff-related failure. Donohue et al observed a significant and direct association between fatty infiltration of the infraspinatus, teres minor, and combined posterior rotator cuff muscles and increasing glenoid retroversion in glenohumeral arthritis.14 Given these findings, failure to address pathologic glenoid retroversion may further predispose patients to secondary rotator cuff dysfunction following ATSA.

Glenoid and humeral component size mismatch and failure to completely remove humeral neck osteophytes are theorized to contribute to suboptimal ATSA outcome by resulting in improperly tensioned soft tissues and altered joint kinematics, which may lead to secondary rotator cuff dysfunction. “Overstuffing” the joint with a large humeral head may increase stress on the rotator cuff leading to progressive dysfunction.4,15,16

Aggressive physical therapy regimens with excessive external rotation exercises have been cited as a source of acute subscapularis failure postoperatively.4 An intraoperative assessment of the subscapularis repair is necessary to establish postoperative range-of-motion parameters for the rehabilitation program. Surgeons should utilize a standardized physical therapy protocol and clearly communicate the goals of this regimen to their patients and physical therapist colleagues. Postoperative ATSA rehabilitation protocols will be reviewed in depth in Chapter 15.



Jun 23, 2022 | Posted by in ORTHOPEDIC | Comments Off on Rotator Cuff Failure: Early and Late
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