Massive tears can cause an uncoupling of forces across the glenohumeral joint and result in unstable shoulder kinematics, leading to a change in muscle activation patterns and coordination [36]. If shoulder kinematics can be maintained by the activation of other muscle groups, it is possible for the deltoid to compensate and allow continued functional overhead use of the arm [21]. This mechanism may explain asymptomatic massive rotator cuff tears [34, 37]. The preservation of teres minor is important for this compensation to occur, as teres minor is required for glenohumeral stability [38].

Due to the loss of the contribution of the supraspinatus in massive rotator cuff tears, the loss of abduction torque can only be compensated for by the use of the deltoid muscle. Relative to the supraspinatus, the deltoid can potentially generate a greater abduction torque, but the muscle force vector is more superiorly directed. With the lack of depressing and centralizing forces of the torn rotator cuff tendons, the consequence of this new deltoid muscle force vector is the superior shift of the reaction force and a dynamic upward glenohumeral subluxation [36, 38]. As a result, it becomes necessary for muscles with large adductor components, such as the pectoralis major and latissimus dorsi, to contract in order to provide glenohumeral stability. This “expensive” cocontraction is the only solution to generate net abduction torque [38]. However, it is likely that this cocontraction is also a cause for pain and the limitation in maximal arm elevation in patients with massive tears [39–41]. Steenbrink et al. [36] studied shoulder muscle activation in patients with massive rotator cuff tears, including the effects of subacromial pain suppression. They found that patients with massive rotator cuff tears were capable of arm abduction, but were actively hampered to do so due to pain [36, 41]. They also found that several depressor and adductor muscles (latissimus dorsi, pectoralis major, and teres major) shifted from generating adduction torque towards generating humeral head depression forces [36]. This increase in adductor muscle contraction was diminished to some extent after subacromial pain suppression.

Other studies have also demonstrated that massive cuff tears result in kinematic changes to multiple muscles that control scapulothoracic and scapulohumeral positions. Hawkes et al. [42] showed that in patients with massive cuff tears, EMG signal amplitudes were significantly higher in the biceps brachii, brachioradialis, upper trapezius, serratus anterior, latissimus dorsi, and teres major muscles.

Over time, patients may begin to fail to fully compensate for the destabilizing forces, and the overwhelming superiorly directed reaction force results in a static upward glenohumeral subluxation, also known as proximal migration of the humeral head [36]. This proximal migration of the humeral head is a common finding in symptomatic massive rotator cuff tears and represents a part of the natural history of tear progression [38].

The abnormal joint mechanics secondary to massive cuff tears along with the superior migration of the humeral head result in significant alterations in articular surface contact pressures on both the glenoid and the humeral head [43]. These changes primarily affect the anterosuperior and anteroinferior glenoid, as well as the anteroinferior and the posterosuperior humeral head [43]. Reuther et al. [23] studied the effect of massive rotator cuff tears on glenohumeral articular cartilage in a rat model with a unilateral massive cuff tear. They found that massive tears led to decreased glenoid cartilage thickness in the anteroinferior region of the affected shoulders. In addition, equilibrium elastic modulus significantly decreased in the center, anterosuperior, anteroinferior, and superior regions. These results suggest that altered loading after rotator cuff injury may lead to damage to the joint with significant pain and dysfunction.

It is also postulated that articular cartilage nutrition is impaired both by synovial fluid leakage and by joint immobility, with resulting articular cartilage atrophy and subchondral osteoporosis. These factors combined contribute to the development of rotator cuff tear arthropathy, a term coined by Neer in 1977, who described the entity as a distinct form of glenohumeral arthritis associated with massive tears of the rotator cuff [25]. The end result of cuff tear arthropathy is the phenomenon of acetabularization of the acromion and femoralization of the humeral head, in which the articulation of the humeral head with the acromion from superior migration of the humeral head results in degenerative wear that creates cupping of the undersurface of the acromion (acetabularization) and rounding off of the humeral head (femoralization) (Fig. 4.2).

The LHB also undergoes changes in massive rotator cuff tears. The LHB is believed to be a depressor or a dynamic stabilizer of the humeral head. Itoi et al. demonstrated that the biceps tendon contributes not only to the superior-inferior stability of the humeral head but also to the anterior-posterior stability [44]. This role becomes more important in the presence of a rotator cuff tear [19, 45]. However, other studies have suggested that this stabilizing force is too small alone to stabilize the humeral head [46].

Sakurai et al. [47] studied the morphological changes of the LHB tendon in rotator cuff dysfunction in 170 cadavers. They found that in specimens with rotator cuff tears with a diameter less than 5 cm, stenosis at the bicipital groove induced by enlargement of the LHB occurred. In contrast, specimens with massive cuff tears (the longest diameter more than 5 cm) showed degenerative changes in the LHB as well as deficiency and wear in the medial wall of the groove, a potential cause of LHB instability. They suggested that the volume of the LHB increases in small tears to compensate for insufficient cuff function, which leads to stenosis of the bicipital groove, subsequently resulting in bicipital tendinitis. However, in massive cuff tears, the volume of the LHB decreases due to progressive wear of the LHB caused by the degenerative changes. Moreover, in specimens with massive cuff tears, medial instability of the LHB was common as a result of the decrease in height of the medial wall of the bicipital groove due to the extent of wear involving the subscapularis, including the soft tissues attached to the lesser tubercle. Therefore, LHB changes and degeneration are considered an important cause of shoulder pain in the setting of massive rotator cuff tears. Although it is often difficult to differentiate pain due to LHB changes from rotator cuff tear pain, it is an important consideration as LHB tenotomy or tenodesis may provide substantial relief and improvement [19, 21, 48, 49].

Massive rotator cuff tears have been implicated as a cause of deltoid tears. Although tears of the deltoid muscle in patients without prior surgical intervention are quite rare, there have been reports that massive rotator cuff tears can lead to attritional deltoid muscle or tendon tears over time [50, 51] (Fig. 4.3). The exact etiology of these deltoid tears is not clearly known. Yet, it has been speculated that the proximal migration of the humeral head associated with massive cuff tears results in friction between the greater tuberosity and the undersurface of the myotendinous junction of the deltoid, with resultant stretching and fraying of the deltoid muscle fibers that progressively weakens the muscle and eventually causes rupture [50]. This theory is supported by the fact that reported deltoid partial thickness tears involve the undersurface of the deltoid [51]. These partial thickness tears leak bursal fluid into the deltoid muscle belly resulting in intramuscular cyst formation described by Ilaslan et al. [51].

Blazar et al. [50] reported on a series of patients with spontaneous detachment of the acromial origin of the deltoid. All patients had chronic massive rotator cuff tears and were older than 65 years of age (mean 73 years). The majority of the patients were women. All patients described a sudden onset of weakness consistent with an acute deltoid detachment, and physical examination showed involvement of the middle deltoid and a characteristic defect at the acromion, a defect that became pronounced with attempted elevation of the arm. Using MRI, Ilaslan et al. [51] also demonstrated that the anterior deltoid can be involved and stressed the importance of the coracoacromial arch in providing superior restraint to the humeral head in the setting of a massive rotator cuff tear.

Erosion or stress fracture of the acromion has also been reported in chronic massive cuff tears as a result of the superior migration of the humeral head and progressive wear along the undersurface of the acromion [52] (Fig. 4.4). The dynamic anterosuperior dislocation of the humeral head, known as anterior-superior escape, has also been implicated as a cause of erosion and fracture of the acromion and attritional changes to the anterior deltoid [51].

The management of massive rotator cuff tears is complex due to the many involved variables. The goal of the treatment is focused on pain reduction and functional improvements [23]. Unfortunately, the published literature does not contain enough data to allow establishment of an evidence-based, universally acceptable treatment algorithm for massive rotator cuff tears [19]. Furthermore, the value of nonoperative treatment is not well established, and there is no evidence that nonoperative treatment substantially alters the course or natural history of massive tears [17, 28, 31, 53–55].

Nonoperative management of massive rotator cuff tears is typically reserved for patients whose symptoms do not involve debilitating pain or in whom surgical intervention is contraindicated. It involves a combination of activity modification, nonsteroidal anti-inflammatories (NSAIDs), steroid injections, physical therapy with emphasis on training the anterior deltoid muscle, and other alternative treatment methods. Other goals of therapy include reeducation of muscle recruitment, coordination of muscle cocontraction, periscapular strengthening, maintenance of motion, and improvement of proprioception [21]. Therapy should be altered based on the specific patient complaints, as some patients may have pain primarily from loss of function and strength due to their massive rotator cuff tear, while others may have pain related to stiffness that has developed from arthritic changes or the occurrence of an adhesive capsulitis.

NSAIDs help with both pain control and reduction of inflammation and thus are thought to improve function. These medications can be taken as needed in over-the-counter or prescription doses. More extended use of NSAIDs should be closely monitored for potential side effects, including gastrointestinal discomfort or bleeding, and renal or cardiac abnormalities. Oral narcotics may also be used to reduce more severe, acute pain from massive rotator cuff tears, such as after an acute injury. However, we do not recommend the use of narcotics for pain control, as they can be associated with nausea, vomiting, and constipation, and more extended use can lead to problems with drug tolerance and dependence.

Steroid injections are also thought to be an effective nonoperative treatment modality in patients with massive rotator cuff tears because of their strong anti-inflammatory effect, with the ability to locally decrease inflammation in the shoulder caused by the rotator cuff tear and/or associated degenerative changes, resulting in decreased pain and improvement in function. This effect can be stronger and more long lasting than the anti-inflammatory response of an oral NSAID. Due to the massive size of the rotator cuff tear, a subacromial steroid injection also becomes an intra-articular injection in these patients. Therefore, the injection can be performed from any approach, including anterior, posterior, or lateral (Fig. 4.5). The desired approach should be determined based on clinician preference, bony anatomy, and patient body habitus.

A posterior injection is typically performed in the location of a standard posterior arthroscopic portal (Fig. 4.5). This point is approximately 1–2 cm medial and 2–3 cm distal to the posterolateral corner of the acromion; however, the location can vary based on patient body habitus. Aiming the needle just under the acromion will direct the injection subacromially, while pointing the needle deeper and in the direction of the coracoid process anteriorly will guide the injection more directly into the glenohumeral joint. An anterior injection may provide easier access to the glenohumeral joint in a larger patient, as the soft tissue distance the needle must traverse is less because of the deltopectoral interval and rotator interval. This injection is performed in the location of a standard anterior arthroscopic portal, at a point just lateral to the tip of the coracoid process, in the natural soft spot created by the glenohumeral joint (Fig. 4.5). Finally, a lateral injection provides access to the subacromial space. This injection is performed in the location of a standard lateral arthroscopic portal, approximately 2–3 cm distal to the lateral edge of the acromion, along the anterior aspect of the bone (Fig. 4.5). In a patient with superior migration of the humeral head and a decreased acromiohumeral interval, this point may be a more difficult approach for injection, and an anterior or posterior approach may be preferred. Regardless of the chosen injection location, confirmation of correct needle position is made by the ease with which the steroid is injected. If substantial resistance is felt while trying to perform an injection, the needle should be repositioned until fluid from the syringe can be easily injected without resistance.

The primary benefit of steroid injections is pain relief, which may also improve shoulder function due to the loss of pain inhibition and increase the ability to participate in therapy. Side effects can rarely occur, including an allergic reaction to one of the injection ingredients, skin depigmentation at the injection site, infection, bleeding, and elevation of blood sugar levels in diabetic patients (see Pearls and Pitfalls of Steroid Injections). Muscle or tendon rupture is also possible if the steroid is inadvertently injected while in an intramuscular or intratendinous position.

Viscosupplementation injections with hyaluronate, as well as platelet-rich plasma (PRP) injections, have also been described in the nonoperative treatment of rotator cuff tears, but with minimal supporting evidence to date. Finally, alternative treatment methods such as electric, shock wave, laser, and acupuncture therapies have been described.