The rotator cuff assists with glenohumeral joint compression, rotation, and dynamic stability.
Rotator cuff injuries cover a continuum of symptoms and dysfunction, from tendinitis and small tears to larger tears and irreparable cuff disease.
Rotator cuff disease is a degenerative process. The prevalence of rotator cuff tears increases with advancing age, and cuff tears may progress in size over time.
Not all rotator cuff tears require surgery.
The decision for surgery should be based on the age and activity level of the patient, the size of the cuff tear, the presence or absence of muscle atrophy, and patient expectations.
Whether the program is prescribed as the first line of treatment or initiated after surgery, the exercises are crucial to management of the disease.
Rehabilitation and physical therapy must be individualized to each patient.
Patient education regarding the disease process, arm positioning, and the goals of therapy is key to compliance.
Rehabilitation focuses on improving range of motion (ROM) and strength.
Rotator cuff disease ranks among the most prevalent of the musculoskeletal disorders and is one of the most common conditions affecting the shoulder. It is a process that most commonly affects patients in their fifth, sixth, and seventh decades of life. Dysfunction of the rotator cuff should be viewed as a disease process rather than just the presence of a tear. The spectrum of the disease can range from acute tendinosis to full-thickness tears to chronic irreparable tears.
This chapter focuses primarily on the nonoperative and postoperative rehabilitation of patients with rotator cuff problems. However, by way of background and completeness, the topics of anatomy and biomechanics of the rotator cuff, the pathophysiology and natural history of rotator cuff disease, and the various treatment options available are also briefly touched on.
The rotator cuff comprises four muscle–tendon units: the supraspinatus, infraspinatus, teres minor, and subscapularis ( Fig. 88-1 ). These four muscles take origin on the body of the scapula and insert on the tuberosities of the proximal humerus. The supraspinatus, innervated by the suprascapular nerve, originates cephalad in the supraspinatus fossa and inserts on the greater tuberosity of the proximal humerus. The infraspinatus, also innervated by the suprascapular nerve, and the teres minor, which is innervated by the axillary nerve, originate posteriorly in the infraspinatus fossa. Both also insert onto the greater tuberosity. The subscapularis originates anteriorly along the entire ventral or costal surface of the scapula and inserts on the lesser tuberosity of the proximal humerus. It has a dual innervation by both the upper and lower subscapular nerves, with the upper subscapular nerve innervating a larger portion of the muscle. The subscapularis is the largest and most powerful of the rotator cuff muscles. The rotator cuff muscles transition into tendons as they near their attachment to the proximal humerus.
The rotator cuff tendons form a continuous veil of connective tissue that envelops the humeral head. The fibers of the rotator cuff tendons interdigitate and fuse, forming a common insertion on the tuberosities of the humerus. They closely adhere to the glenohumeral joint capsule and provide circumferential reinforcement except at the rotator interval and axillary recess. The rotator interval is a triangular area that is bordered by the upper margin of the subscapularis and the anterior margin of the supraspinatus. The rotator interval contains the coracohumeral ligament, the superior glenohumeral ligament, and the biceps tendon. The coracohumeral and superior glenohumeral ligaments function to limit external rotation of the adducted arm and to prevent inferior translation of the humeral head.
The shoulder joint can be viewed as containing two ball-and-socket articulations. The first is the glenohumeral joint, with the convex humeral head articulating with the concave glenoid. The second is the coracoacromial arch. In this articulation, the convex surface comprises the rotator cuff tendons and rotator interval, while the concave surface comprises the osseous coracoid and acromion and the intervening coracoacromial ligament. Abnormalities or disruptions of the coracoacromial arch can contribute to rotator cuff disease.
Several bursae lie in close proximity to the glenohumeral joint and contribute to the function and pathology of the shoulder. The subscapularis bursa lies deep to the subscapularis, between the muscle and the neck of the glenoid. The subacromial and subdeltoid bursae are found superficial to the rotator cuff. The subacromial bursa lies between the acromion and the rotator cuff, and cephalad to the glenohumeral joint, whereas the subdeltoid bursa extends laterally from the subacromial space to the proximal humeral metaphysis. The bursae vary in size and separate the rotator cuff from the deltoid muscle. They may become inflamed following trauma or overuse conditions. This bursitis can be particularly painful and functionally limiting when present.
The primary workhorse of the shoulder joint is the deltoid muscle. The deltoid has three heads (anterior, middle, and posterior), all innervated by the axillary nerve. It has a very broad origin, arising from the distal one third of the clavicle, the acromion, and the lateral one third of the scapular spine. All three heads converge laterally to insert on the deltoid tuberosity of the humeral diaphysis. The three heads of the deltoid function to provide a wide ROM of the shoulder joint and are the primary muscles for glenohumeral abduction, elevation, and extension. The extensive origin from the mobile clavicle and scapula affords the deltoid a mechanical advantage by allowing the muscle to maintain its resting length at various arm positions.
The rotator cuff serves several functions in glenohumeral joint motion and stability. It provides joint compression and resistance to glenohumeral translation, as well as allowing some rotation in all planes of motion. A complex interaction exists between the muscles surrounding the scapula and the shoulder, providing this joint with a wide range of movement. The primary role of the rotator cuff is to provide dynamic stability throughout this range. Stability is achieved by compression of the glenohumeral joint by the rotator cuff tendons. The subscapularis, infraspinatus, and teres minor depress the humeral head, counteracting the upward pull of the deltoid. The infraspinatus becomes a very effective head depressor with the arm at 90 degrees of abduction and neutral rotation, whereas the subscapularis acts as a head depressor in external rotation. In this way, the rotator cuff provides direct joint compression and allows the humeral head to maintain a relatively constant position in relation to the glenoid. The rotator cuff keeps the humeral head centered within the glenoid during motion and allows the deltoid to function.
The rotator cuff is intricately involved in powering movement of the shoulder. The supraspinatus assists the deltoid in initiating humeral abduction, especially the first 30 degrees of abduction. Howell and coworkers found that the supraspinatus and deltoid contribute equally to measured torque in abduction. The infraspinatus and teres minor are the only cuff muscles that produce external rotation. Tears in these tendons, especially when chronic in nature, can lead to profound deficits in external rotation motion and strength. The subscapularis functions as a strong internal rotator of the arm, but also contributes to arm abduction and humeral head depression. Several powerful muscles contribute to internal rotation, but the subscapularis is most important at the extremes of internal rotation. This is exemplified in patients with a subscapularis tear, who are unable to perform an abdominal compression test or lift-off test. Thus, loss of rotator cuff function can be expected to result in loss of strength in arm elevation, early fatigability, loss of dynamic stability, and joint subluxation.
Pathogenesis of Rotator Cuff Disease
Many factors have been proposed to play a role in the cause of rotator cuff disease, and more than one is likely involved. Tendon degeneration, vascular insufficiency, subacromial impingement, glenohumeral instability, trauma, and congenital anomalies may all contribute to the development and progression of rotator cuff lesions.
Partial and complete rotator cuff tears are known to occur with increasing frequency with advancing age in asymptomatic patients. DePalma and coworkers noted that partial-thickness tears typically begin to occur between 40 and 60 years of age and are also more frequent in older persons. Yamaguchi and colleagues showed that the prevalence of rotator cuff disease increases with age. In an ultrasonographic study of 588 patients with unilateral shoulder pain, they discovered a 10-year difference between three subgroups of patients. The average age for patients with no rotator cuff tear was 48.7 years, for those with a unilateral tear was 58.7 years, and for those with a bilateral tear was 67.8 years. Logistic regression analysis showed a 50% likelihood of a bilateral tear after the age of 66 years.
Vascular insufficiency may also contribute to rotator cuff disease. The rotator cuff tendons receive blood supply from the associated muscle bellies as well as from the osseous insertion at the greater tuberosity. Approximately 1 cm from the insertion, a watershed area exists at the anastomosis between these two blood supplies. Codman proposed that vascular ischemia within this region, in association with a traumatic event, leads to rupture of the rotator cuff. Lindblom, as well as Rothman and Parke, confirmed a region of relative hypovascularity within the distal rotator cuff tendon near the insertion into the greater tuberosity. More recently, Lohr and Uhthoff also confirmed the presence of a hypovascular critical zone in cadaveric rotator cuff tendon close to the insertion on the humeral head. However, Lohr and Uhthoff discovered a discrepancy between the rich vascularity of the bursal surface and the uniformly sparse vascular distribution of the articular surface. This may contribute to the high prevalence of articular-sided tears observed in partial-thickness rotator cuff disease.
Impingement syndrome is hypothesized to contribute to rotator cuff disease. Neer popularized the idea that the anterior leading edge of the acromion was important in the pathogenesis of impingement and rotator cuff tears. Impingement may arise from a hooked (type III) acromion, a subacromial spur, or irregularities of the coracoacromial arch, such as a thickened or ossified coracoacromial ligament or an os acromiale. An os acromiale is an unfused ossification center in the acromion, which may contribute to impingement by allowing abnormal motion through the unfused bone or by the development of osteophytes in this region. These anomalies or variations can lead to areas of higher than normal compression of the rotator cuff during active arm motion. The rough undersurface of the coracoacromial arch and compression caused by these structures can contribute to degeneration and tearing of the underlying rotator cuff tendons.
Muscle imbalance and capsular tightness contribute to rotator cuff pathology by allowing excess translation at the glenohumeral joint. Weakness of the supraspinatus or subscapularis can compromise compression of the glenohumeral joint during active shoulder motion. This in turn leads to increased translation across the joint. Superior translation allows the head to migrate closer to the acromion, and an increase in the force transmitted to the rotator cuff results as the cuff is pressed between the humeral head and the overlying coracoacromial arch. A tight posterior capsule causes a similar result as the head is pushed anterior–superiorly into the coracoacromial arch during flexion. In both scenarios, the increased pressure on the cuff can lead to degradation and damage over time.
Instability can also lead to rotator cuff pathology. A single traumatic dislocation has been associated with rotator cuff tears, especially in patients older than age 40. An anterior glenohumeral dislocation places a sudden extreme stretch on the supraspinatus and posterior cuff and can avulse the rotator cuff tendons off of the insertion into the greater tuberosity. An anterior SLAP (superior labrum anterior–posterior) lesion can have a similar result. Looseness of the superior labrum allows motion upward, and the humeral head slides superiorly toward the coracoacromial arch. Recurrent instability can have a similar effect over time. Incompetence of the static stabilizers of the shoulder allows translation across the glenohumeral joint, which can place tension on the rotator cuff and contribute to rotator cuff disease.
Whereas tissue degeneration, vascular insufficiency, and impingement certainly play a role in rotator cuff disease with advancing age, trauma plays a larger role in the younger patient. Younger patients are more likely to injure their rotator cuff from a single high-energy traumatic event. Trauma may also destabilize the glenohumeral joint through labral or ligament tears, placing more tension on the rotator cuff. Finally, microtrauma from repetitive use may damage the cuff over time. The cause of rotator cuff disease is likely multifactorial, but the end result of shoulder pain and loss of function is the same for all patients.
History and Physical Examination
Rotator cuff disease is characterized by specific signs and symptoms. Clinically, patients present with predominant complaints of pain or weakness, or a combination of the two. The onset of symptoms may be acute or chronic. Patients may recall a single traumatic event; however, most describe activity-related shoulder pain that has slowly progressed over time. The pain usually is localized to the front of the shoulder or lateral acromion, but may radiate down the lateral arm along the deltoid. It is exacerbated by lifting objects in front of the body and activities overhead, as well as positioning the arm behind the back such as while dressing. Pain at night is a frequent component. The severity and duration of the patients’ symptoms are important clinical markers to guide treatment.
The physical examination of the painful shoulder should always begin with inspection. The supraspinatus fossae and infraspinatus fossae should be inspected for muscle atrophy, and compared with the contralateral side ( Fig. 88-2 ). Atrophy in these areas can be a sign of a chronic rotator cuff tear or possible neurologic deficit, such as compression of the suprascapular nerve. The deltoid should be inspected to assess for muscle bulk and to ensure that all three heads of the muscle are functioning. The biceps muscle should be examined for contour and irregularities to rule out proximal biceps tendon rupture. Finally, the posterior shoulder should be inspected during active arm elevation to assess for scapular dyskinesia or scapular winging.
Palpation may reveal reproducible tender spots. These include the greater tuberosity, supraspinatus insertion, and the acromioclavicular joint. Acromioclavicular arthritis is often present in patients with rotator cuff problems but is not necessarily symptomatic. Tenderness over the acromioclavicular joint that resolves with injection is indicative of symptomatic acromioclavicular joint arthritis.
ROM of the shoulder, both active (AROM) and passive (PROM), should be assessed and compared with the contralateral side. Painful motion of the shoulder joint is nearly always present. The American Shoulder and Elbow Surgeons have recommended that four functional ROMs be measured: (1) forward elevation, (2) internal rotation, (3) external rotation at the side, and (4) at 90 degrees abduction. It is important to note the presence of stiffness, particularly if surgery is being contemplated.
Several provocative tests are helpful in the diagnosis of rotator cuff disease. These include the classic impingement sign described by Neer and the impingement reinforcement sign as described by Hawkins. These signs have been shown to have high sensitivity and negative predictive value, but low specificity and positive predictive values. Impingement signs differ from the impingement test , which is performance of the same maneuvers following local injection of an anesthetic, such as lidocaine, into the subacromial space. Resolution of pain following injection of anesthetic into the subacromial space during an impingement test can be diagnostic of rotator cuff disease.
In patients with tears of the rotator cuff, weakness may be elicited on exam. Jobe’s test ( Fig. 88-3 ) is performed with the arm abducted 30 degrees from the side in the plane of the scapula, with the thumb turned down in full shoulder internal rotation and forearm pronation, as if pouring out a can of soda. Resistance against elevation in this position tests the integrity of the supraspinatus, and weakness indicates an injury to the tendon. External rotation with the elbow at the side tests the posterior rotator cuff, and weakness in this position suggests injury to the infraspinatus and teres minor. Seventy percent of external rotation strength in this position depends on the infraspinatus, and loss of strength correlates closely with the size of a rotator cuff tear. Finally, the integrity of the subscapularis must be assessed. The subscapularis is a powerful internal rotator of the arm. The abdominal compression test, or belly press test ( Fig. 88-4 ), examines the subscapularis by having the patient press inward on the abdomen with the elbow held in front of the body. Similarly, the lift-off test assesses the integrity of the subscapularis by asking the patient to place the hand behind the back, and then lift the hand off of the back. Inability to perform either test is an indication that the subscapularis is incompetent.
In the presence of a large chronic rotator cuff tear, lag signs may be present. To test for a lag sign, the examiner places the patient’s forearm in an externally rotated position with the elbow held at the side. The examiner then lets go of the patient’s forearm. If a patient is unable to hold the forearm in an externally rotated position, and the arm returns to a position of neutral rotation, then a lag sign is present. The hornblower’s sign also assesses for a chronic rotator cuff tear by asking the patient to externally rotate the arm while the shoulder is held in 90 degrees of abduction. If a patient is unable to hold the forearm in an externally rotated position while the shoulder is abducted 90 degrees, the hornblower’s lag sign is positive. A lag sign with the arm at the side usually indicates a chronic tear of the infraspinatus, whereas the presence of a hornblower’s lag sign indicates a chronic tear of teres minor.
Imaging studies of the shoulder should always begin with plain film radiographs. Plain films provide visualization of the bony architecture of the shoulder. It is important to obtain several radiographic views. An anteroposterior (AP) view of the shoulder taken in the plane of the scapula with the arm in neutral rotation produces a perpendicular view of the glenohumeral joint. This enables the practitioner to assess the glenohumeral joint space, the degree of loss of joint space from arthritis, and osteophyte formation on the inferior glenoid or humeral head. AP views in internal and external rotation should also be obtained. These views allow better visualization of the lesser and greater tuberosities, respectively, and identify any changes in the contour between the humeral head and the glenoid, as well as changes in the subacromial space. The subacromial space is measured as the distance between the superior border of the humeral head and the inferior border of the acromion. Normal variation should range between 7 and 14 mm. Loss of the subacromial space, with proximal migration of the humeral head, is suggestive of a large chronic rotator cuff tear.
The outlet view, or “scapula Y ” lateral radiograph, provides a lateral view of the body of the scapula. This view visualizes the supraspinatus fossa, defined as the superior border of the scapula anterior to the spine of the scapula. It can be useful to identify fractures of the scapular body as well as acromial spurs. It also allows inspection of the morphology of the acromion and can be used to classify the acromion as type I (flat), type II (curved), or type III (hooked). Finally, an axillary radiograph provides a lateral view of the glenohumeral joint with the arm fully abducted. An axillary radiograph is necessary to assess glenohumeral subluxation or dislocation. It also may reveal eccentric anterior or posterior glenoid wear that may be present in the setting of degenerative joint disease or chronic instability.
Magnetic Resonance Imaging
MRI is the modality of choice to assess the integrity of the rotator cuff. Whereas plain films provide visualization of the osseous anatomy of the shoulder, MRI is optimal for evaluation of the soft tissue structures. MRI can visualize the tendons of the rotator cuff, as well as the muscle bellies of the four cuff muscles ( Fig. 88-5 ). It can identify partial- and full-thickness cuff tears, tears of the glenoid labrum, and inflammation of the subacromial bursa. Although MRI provides the most information about the soft tissues around the shoulder, it should not be used as the initial imaging modality. MRI can be utilized to confirm a tear when one is suggested based on the physical exam and to assess the size of a tear when planning surgical repair.
MRI is exceptionally helpful for determining the size and chronicity of a rotator cuff tear. All four tendons of the rotator cuff can be assessed individually, and the amount of tendon retraction can be measured. Examination of the muscle bellies of the rotator cuff can yield valuable information to the practitioner, such as size and composition of the muscles. Acute rotator cuff tears generally are associated with a large healthy muscle belly with a small amount of tendon retraction. When a rotator cuff tear is chronic, the tendon retracts, and the muscle belly atrophies. Over time, the muscle fibers are replaced with fat. This fatty infiltration can be visualized on MRI sequences, and is an indication that the tear is chronic in nature ( Fig. 88-6 ). Chronic rotator cuff tears, with tendon retraction and fatty infiltration of the muscle bellies, are not surgically reparable and are discussed further in the following section.
Ultrasound is an additional modality that may be used to assess the integrity of the rotator cuff. Ultrasound provides the benefit of dynamic visualization and may enable inspection of the rotator cuff in different arm positions and during active movement. It may be used to assess for healing following repair or the integrity of the rotator cuff following previous surgery, where suture anchors or scar tissue may cause distorting artifact on MRI. An added benefit is its use in patients who are unable to obtain an MRI because of metal implants elsewhere in the body. The downside of ultrasound is that it is extremely technician-dependent. If an ultrasonographer is unfamiliar with the shoulder, adequate images may be difficult to obtain.
Rotator cuff disease is a degenerative process. Rather than the specific presence or absence of a tear, it represents a continuum that ranges from tendinosis to partial- and full-thickness tears to chronic irreparable tears. When considering treatment options, it is imperative to consider the structure of the cuff, the patient’s symptoms, and the function of the shoulder. Not all cuff tears cause pain, just as not all painful shoulders have a cuff tear.
Anatomic studies evaluating the prevalence of rotator cuff tears in cadavers have described rates ranging from 17% to 72%. The majority of studies describe rates between 30% and 50%. More recent studies have focused on MRI or ultrasound studies of asymptomatic patients. Sher and associates evaluated 96 asymptomatic patients with MRI. They found that the prevalence of partial and complete tears was 34% overall, 28% for patients between 40 and 60 years old, and 54% for those who were older than 60 years old. This clinical study demonstrates that the incidence of rotator cuff tears increases with age.
Frequently, the earliest changes seen in the rotator cuff occur at the microscopic level. Microscopic changes occur in the collagen fibers of the tendon, usually on the articular side. Over time, these may coalesce to become an incomplete tear. If small, these partial-thickness tears may have no effect on function. However, if painful, they may alter the mechanics of shoulder motion and result in weakness or dysfunction.
As damage continues, a small full-thickness tendon tear may result, usually in the supraspinatus. Even these full-thickness tears may or may not be symptomatic for the patient. Over time, small tears can grow into large tears that involve two or more tendons. If the tear occurs at the tendon insertion into bone, the remaining tendon will retract, and a triangular defect is created. This triangular defect is described as a crescent tear. The tendons retract away from the insertion site by the pull of the muscle belly. As the tear progresses over time, it may continue to pull away from the insertion site, or it may follow along the boundary lines of adjacent tendons. When the latter occurs, an L -shaped curve may develop, as one limb occurs at the insertion site of the tendon into bone and the other limb extends medially between two tendons of the rotator cuff.
The tear may remain static, or it may progress. Recent data about the natural history of untreated rotator cuff tears have revealed that in certain patients, unrepaired rotator cuff tears may progress and become irreparable. Progression can occur in two different ways: the tear can grow larger or the tear can degenerate. Over time, the muscle belly of the torn tendon shortens and loses its elasticity. Contracture develops of the adjacent soft tissues, such as the capsule and coracohumeral ligament, and the shortened tendon becomes scarred down in its contracted position. Chronic shortening of the tendon and lack of pull by the muscle belly lead to atrophy and fatty infiltration of the muscle. Once muscle fibers have been replaced by fat from chronic disuse, then cuff function is no longer recoverable. The muscle fibers cannot regenerate. In addition to retraction and fat replacement, the tear may extend to an adjacent tendon. Large tears of the rotator cuff are not always painful, but weakness and functional deficits almost certainly result.
At the point of retraction and fatty infiltration, the tear has become surgically irreparable. The tendon is shortened and contracted, and the muscle belly has lost its elasticity. It is no longer physically possible to pull the retracted tendon back to its insertion on the greater tuberosity. Also, because of collagen degradation at the torn end of the tendon, the tendon often cannot hold suture to allow for a repair; the suture pulls right through the degenerative tissue. Chronic rotator cuff tears that are not surgically reparable most commonly occur in patients in their seventh and eighth decades of life, although they may occur less frequently in younger patients. In these older patients with chronic cuff tears, the quality of the cuff tendon and muscle tissue is often poor, and healing may not occur. However, it is important to remember that the presence of a massive, irreparable rotator cuff tear is not incompatible with good overhead function.
Nonoperative management may not be indicated in young patients who have sustained a recent traumatic rotator cuff tear, particularly if it is retracted. Moreover, in acute or chronic tears that are large, nonoperative treatment may also not be indicated. This decision must be individualized. When nonoperative treatment is indicated, the patient’s response can be influenced by many factors, including age, health status, and the patient’s occupation or activity level. In addition, the amount of reactivity to movement and resistance can dictate response to treatment. Therefore, a time-based rehabilitation program is not practical. A criterion-based rehabilitation program based on the patient’s impairments and response to treatment is best for rotator cuff disease.
Early intervention is a critical component to nonoperative management of rotator cuff disease. However, the quantity of rehabilitation does not always equate to quality. Each patient requires a different level of intervention. Supervised therapy three times per week is not necessary for the best course for all patients. Many patients need only instruction in a home program and periodic evaluation and progression of the rehabilitation program. Others may benefit from more intensive instruction and manual therapy intervention in conjunction with a home program. As the patient improves, he or she can gradually progress to a more limited amount of supervised and hands-on care. Therefore, it is incumbent on therapists, physicians, and the patient to administer the appropriate amount of rehabilitation following the onset of a shoulder injury.
The importance of patient education cannot be emphasized enough. The patient needs to be educated about the healing process and the importance of rest from positions or activities that may contribute to the inflammatory process. He or she should also be instructed in proper positioning of the arm for comfort. Many patients report that while at rest or sleeping, the most comfortable position is with the arm supported in the plane of the scapula. From a biomechanical standpoint, this also appears to be a more advantageous position. Patients should be instructed to perform activities such as typing on a computer or driving with their affected arm supported at the elbow. Walther and colleagues compared the short-term effectiveness of conventional physical therapy, a guided self-training program, and a functional brace in patients with early-stage rotator cuff disease. All three groups showed a significant improvement in shoulder function as well as a significant reduction in pain. In addition, the group using a functional brace demonstrated significantly greater abduction strength after 12 weeks than the other two groups. This study highlights the importance of rest from activity in this patient population.
In addition to terminating or modifying aggravating activities, patients should be instructed to take nonsteroidal anti-inflammatory drugs (NSAIDs) as prescribed. It should be noted that the use of NSAIDs for the treatment of tendon injuries may help to reduce pain, although they do not facilitate quicker healing and do little to promote long-term healing. Patients who continue to have pain despite resting from painful activities and taking NSAIDs may benefit from an injection of corticosteroid into the subacromial space. Reducing pain enables the patient to perform the exercises necessary to regain ROM, strength, and function of the shoulder.
Other treatment modalities have not been shown to be very effective in the treatment of rotator cuff disease. Heat or cold (or both) may be used to help augment treatment. Therapeutic ultrasound has been shown to be no better than placebo, and it should not be used. The use of transcutaneous electrical nerve stimulation (TENS) may be beneficial as an adjunct to exercise intervention.
Several systematic reviews of interventions for rotator cuff pathology and shoulder pain suggest that exercise may be an effective treatment. Exercise is a broad term and can include PROM, active-assisted, and AROM, strengthening, and manual therapy. Variations on individual exercises have been promoted by a number of authors who offer rehabilitation protocol suggestions. Therefore, there is no consensus on an ideal exercise program to treat all patients with rotator cuff disease.
The rehabilitation approach to patients with rotator cuff disease and no tear is similar to that for patients with a partial or small tear. The impairments and clinical presentation of patients with medium, large, and massive rotator cuff tears require a slightly different rehabilitation approach. We discuss the rehabilitation of these two groups of patients separately.
Rehabilitation for Rotator Cuff Disease (No Tear or Small Tear)
Patients with rotator cuff disease and no tear or a small tear may present with limited forward elevation or internal rotation ROM (or both), decreased rotator cuff strength, and occasionally decreased scapular muscle strength and coordination. PROM or active-assisted ROM exercises are initiated in pain-free ranges to improve or maintain ROM, provide gentle stress to healing collagen tissue, and optimize the subacromial gliding mechanism. We have divided our ROM exercises into phase I and II. Phase I ROM includes supine forward elevation and external rotation ( Fig. 88-7 ). Forward elevation is performed supine with the shoulder slightly anterior to the plane of the scapula. This allows for a more functional and comfortable stretch. External rotation is typically started with the patient supine, the arm at 45 degrees in the plane of the scapula, and supported by a pillow. This position minimizes excessive tension on the superior cuff and capsuloligamentous complex and avoids the impingement position at 90 degrees abduction. If external rotation is restricted with the arm in adduction or at 90 degrees abduction, stretching can progress to these positions as long as reactivity is limited. Many individuals can also begin phase II ROM exercises. These exercises include extension, internal rotation, and cross-body adduction ( Fig. 88-8 ). The patient is asked to achieve a tolerable stretch and hold the position for at least 10 sec. Each exercise is repeated 10 times, and the patient is asked to perform the exercises two to four times per day. Internal rotation ROM should be approached with caution. This position places the supraspinatus in its most elongated state. Although, it is typically the most limited motion, it is also the most provocative in patients with rotator cuff disease.
Depending on the degree of tissue reactivity and limitation in ROM, glenohumeral joint mobilizations and manual stretching can be performed. Joint mobilization involves the translation of one joint surface relative to another. Oscillations are then performed at the end of the translation. Grade I and II glenohumeral joint mobilization may assist in pain reduction and regaining motion limited by pain. Pain relief is thought to be mediated through a neurophysiologic mechanism beginning in the joint and soft tissue mechanoreceptors and nocireceptors. The proposed effect of grades III and IV mobilizations is to mechanically stretch the soft tissue. The authors have found a combination of mobilization with stretching to be effective in improving ROM. Bang and Deyle reported that combining manual therapy with supervised exercise in a brief clinical trial was better than exercise alone for increasing strength, decreasing pain, and improving function in patients with shoulder impingement syndrome.
Phase I Strengthening
Strengthening exercises using elastic bands or free weights of 1 to 4 pounds can also be initiated in this early phase. We have found exercises with elastic bands easier to do and for the patient to reproduce at home. The patient can exercise with the bands in the erect position and better integrate the scapular muscles. These exercises include external rotation, internal rotation, and extension ( Fig. 88-9 ). Each exercise is performed with the elbow bent to 90 degrees. To ensure consistent tension with the elastic band, the patient is asked to begin in the starting position with no tension on the band. He then walks away from the anchor of the band to take up the slack in the band. The patient is asked to “set” the scapula to integrate the scapular muscles. He is then asked to perform 10 repetitions of the first exercise. If he feels a “burn” or has difficulty completing that set of 10, he moves on to the next exercise. If, however, he performs that first set without difficulty, he rests for 5 seconds and adds a second set. Again, if he has difficulty with that set, he moves to the next exercise. If he can perform the exercise without difficulty, he adds a third set. Once he can comfortably perform all three sets of an exercise without difficulty, he can progress to the next color band or add 1 pound of resistance. Isolated scapular-strengthening exercises can be performed with elastic resistance and rowing at waist level. If reactivity allows, rowing can be performed from an overhead position. If the patient is being seen in supervised therapy, manual resistance to external and internal rotation can be employed. These exercises are typically performed in supine position with the arm in the plane of the scapula, supported on a pillow at 45 degrees of abduction. Alternating isometrics can be performed allowing the clinician to assess strength and reactivity.