ROTATOR CUFF DISEASE

ROTATOR CUFF DISEASE

In 1834, Smith wrote the first description of a rupture of the rotator cuff tendon.

Since then, with the work of such authors as Duplay, Von Meyer, Codman, and Neer, degenerative changes to the rotator cuff have been better characterized; however, the exact mechanisms leading to the degeneration of the rotator cuff still are debated today.

PATHOPHYSIOLOGY

The pathophysiology of rotator cuff degeneration is a controversial topic that still is not fully understood.

Two hypotheses (ie, extrinsic, intrinsic) coexist and are supported by different authors.

EXTRINSIC HYPOTHESIS

In this theory, the lesion results mainly from repeated impingement of the rotator cuff tendon against different structures of the glenohumeral joint.

The following 3 distinct impingement syndromes have been described:

ANTEROSUPERIOR IMPINGEMENT SYNDROME

Impingement of the rotator cuff beneath the coracoacromial arch is an established cause of chronic shoulder pain.

In 1972, Neer, in a landmark article, described and popularized the term impingement syndrome. Observations from cadaver studies and

surgery gave evidence that impingement occurs against the under surface of the anterior third of the acromion, the coracoacromial ligament, and at times, the acromioclavicular joint.

Located anterior to the coracoacromial arch in the neutral position, the supraspinatus tendon insertion to the greater tuberosity and the bicipital groove must past beneath the arch with forward flexion of the shoulder, especially if internally rotated, causing an impingement.

His works showed that degenerative tendinitis and tendon ruptures were centered in the supraspinatus tendon, extending at times to the anterior part of the infraspinatus tendon and the long head of the biceps tendon.

Biglianni described 3 different shapes of acromia in cadavers, according to the anterior slope:

• Type 1 - Flat

• Type 2 - Curved

• Type 3 - Hooked

Only 3% of tears are associated with a type 1 acromion.

Although there is a strong association between cuff tears and hook acromia, it is unclear whether the shape is the cause or the result of the cuff tear or simply the result of aging; however, Ozaki et al's study on cadavers showed that the undersurface of the acromion was normal when the incomplete tear was on the articular side.

On the other hand, when the incomplete tear was on the bursal side of the cuff tendon, pathological changes of the under surface of the acromion were observed, suggesting that a hooked acromion is the result of the cuff tear on the bursal side of the tendon and not the cause.

Nevertheless, curved and hooked acromia appear to be due to a degenerative process with formation of the osteophyte-enthesophyte complex at the acromion-coracoacromial ligament junction that is increasingly prevalent with age.

Neer described impingement lesions in the following 3 progressive stages:

• In stage 1, edema and hemorrhage result from excessive overhead use and are observed in patients younger than 25 years.

• In stage 2, fibrosis and tendinitis affect the bursa and the cuff following repeated episodes of mechanical inflammation in patients aged 25-40 years.

• In stage 3, bone spurs and incomplete and complete tears of the rotator cuff and long head of the biceps tendon are found almost exclusively in patients older than 40 years.

Clinical course and treatment vary according to the stage of the disease process.

Neer's picture of the impingement syndrome may explain tears on the bursal (superficial) side of the tendon. However, partial tears most commonly involve the articular (deep) side of the tendon, as observed by many investigators.

POSTEROSUPERIOR IMPINGEMENT SYNDROME

In 1991, Walch et al described, from arthrographic observations, an impingement occurring between the articular side of the supraspinatus tendon and the posterosuperior edge of the glenoid cavity.

With the shoulder held at 120° of abduction, retropulsion, and in extreme external rotation (similar to the late cocking phase in throwers), the labrum moves away from the glenoid and the glenoid rim comes in contact with the deep surface of the tendon, producing repeated microtrauma and leading to partial tears.

This process has been confirmed by MRI studies and may explain some of the articular side tears, especially in overhead sport athletes; however, it does not account for all the tears observed in older patients.

ANTEROINTERNAL IMPINGEMENT SYNDROME

In 1985, Gerber described, from CT scan studies and from surgery observations, impingement of the cuff in the coracohumeral interval.

He demonstrated that, when the shoulder is held in flexion and internal rotation, the coracohumeral distance is reduced from 8.6 mm when the arm is at the side to 6.7 mm.

In this position, the lesser tuberosity, and also the biceps tendon and the supraspinatus tendon, become closer to the coracoid process, creating subcoracoid impingement and cuff lesions.

Subcoracoid impingement can be idiopathic (eg, large coracoid tip), iatrogenic (eg, following a Trillat procedure) or following a fracture (eg, humeral head or neck fracture).

INTRINSIC HYPOTHESIS

In this theory, the lesions result from progressive age-related degeneration of the tendon. Von Meyer was probably the first to introduce the concept that degeneration of the tendon plays a major role in the production of cuff lesions.

Many histologic studies show the age-related degeneration of the cuff tendon; however, it is not the purpose of this article to describe those numerous changes.

Observations from various sources (eg, cadaver, surgical, MRI, ultrasonographic, arthrographic studies) show that cuff tears rarely are seen in patients before age 40 years and that the number observed after the patient has reached 50 years increases progressively.

In 1934, Codman introduced the concept that most tears originate on the articular side of the tendon. Since that time, many authors have come to support that theory from cadaver, surgery, and MRI observations.

Most of the tears have been observed on the articular surface of the tendon, near its insertion on the greater tuberosity, in an area Codman called the critical zone. This zone appears to be at greater risk of developing a tear.

To explain why the critical zone is more prone to tearing, some investigators have suggested that it is a poorly vascularized area. Histologic, cadaver, and

Doppler studies show that the articular side of the tendon, near its insertion on the tuberosity, is relatively avascular when compared to the remainder of the cuff.

In all probability, the intrinsic and the extrinsic theories coexist and explain the pathophysiology of rotator cuff degeneration.

Nevertheless, this degeneration is the result of a continuum that is beautifully described by Matsen, Arntz, and Lippitt.  

The lesion starts where the load is presumably the greatest (eg, on the articular side of the anterior insertion of the supraspinatus tendon, near the tendon of the long head of the biceps muscle).

Tendon fibers fail when the load exceeds their strength. The fibers tend to retract because they are under tension, causing rupture.

Fiber failure causes at least the following 4 complications:

• Increases the load on the neighboring, yet intact, fibers

• Detaches muscle fibers from the bone, diminishing the force that the cuff muscles can deliver

• Compromises the tendon fibers' blood supply by distorting the anatomy, contributing to progressive local ischemia

• Exposes increasing amounts of the tendon to joint fluid containing lytic enzymes, which remove any hematoma that could contribute to tendon healing

The scar tissue of the healing tendon lacks the normal resilience of tendon and, therefore, is under increased risk for failure.

In the absence of repair, the degenerative process tends to continue through the substance of the supraspinatus tendon to produce a full thickness defect in the anterior supraspinatus tendon.

The full thickness tear tends to concentrate loads at its margin, facilitating additional fiber failure with smaller loads than those that produced the initial defect.

Once a supraspinatus tendon defect is established, it typically propagates posteriorly through the remainder of the supraspinatus tendon, then into the infraspinatus tendon.

With the increasing defect of the cuff tendon, the spacer effect of the cuff tendon is lost (as well as its stabilizing effect), allowing the humeral head to displace superiorly, placing increased load on the biceps tendon.

As a result, the breadth of the long head tendon of the biceps is often greater in patients with cuff tears in comparison with uninjured shoulders. In chronic cuff deficiency, the long head tendon of the biceps frequently is ruptured.

Further propagation of the cuff defect crosses the bicipital groove to involve the subscapularis tendon, starting at the top of the lesser tuberosity and extending inferiorly.

As the defect extends across the bicipital groove, it may be associated with rupture of the transverse humeral ligament and destabilization of the long head tendon of the biceps, allowing its medial displacement.

The concavity compression mechanism of glenohumeral stability is compromised by cuff disease. Beginning with the early stage of cuff fiber failure, the compression of the humeral head becomes less effective in resisting the upward pull of the deltoid.

A partial thickness cuff tear causes pain on muscle contraction. This pain produces reflex inhibition of the muscle action.

In turn, the combination of reflex inhibition and loss of strength from fiber detachment makes the muscle less effective for balance and stability; however, as long as the glenoid cavity is intact, the compressive action of the residual cuff may stabilize the humeral head.

When the weakened cuff cannot prevent the humeral head from rising under the pull of the deltoid, the residual cuff becomes squeezed between the humeral head and the coracoacromial arch, contributing to further cuff degeneration.

Degenerative traction spurs develop in the coracoacromial ligament, which is loaded by pressure from the humeral head.

Upper displacement of the humeral head also wears on the upper lip of the glenoid rim and labrum, reducing the effectiveness of the upper glenoid concavity.

Further deterioration of the cuff allows the tendon to slide down below the center of the humeral head, producing a boutonnière deformity. The cuff tendons become humeral head elevators, rather than head compressor-depressors.

Just as in the boutonnière deformity of the fingers, the shoulder with a buttonholed cuff is affected by the conversion of balancing forces into unbalancing forces.

In summary, the pathophysiology of rotator cuff degeneration may be explained by a combination of extrinsic, intrinsic, and biomechanical factors; however, it is not understood why in some individuals those pathological changes cause pain, but not in some others. This question should keep investigators busy for many years to come.

FREQUENCY

Shoulder pain is the third most common cause of musculoskeletal disorder after low back pain (LBP) and cervical pain. Estimates of the cumulative annual incidence of shoulder disorders vary from 7-25% in Western general population.

MORTALITY/MORBIDITY

As mentioned before, shoulder pain is the third most common cause of musculoskeletal disorder after low back and neck pain. Although considered a benign condition, according to a study on the long-term outcome of rotator cuff tendinitis, 61% of the patients were still symptomatic at 18 months, despite receiving what was considered sufficient conservative treatment.

Moreover, 26% of patients rated their symptoms as severe. Musculoskeletal disorders are the primary disabling conditions of working adults. The prevalence of rotator cuff tendinitis has been found to be as high as 18% in certain workers who performed heavy manual labor.

SEX

In one study, there is a predominance of male patients (66%) seeking consultation for rotator disease, but, in other studies, the male-to-female ratio is 1:1.

AGE

Rotator cuff disease is more common after age 40 years. The average age of onset is estimated at 55 years.

CLINICAL

HISTORY

Without a good knowledge of the anatomy and biomechanics of the shoulder complex, the probability that a systematic history and physical examination leads to the correct diagnosis is reduced. The following paragraphs review these topics.

FOCUSED ANATOMY

The shoulder joint is a complex structure comprising not 1, but 5 joints (ie, 3 synovial joints [sternoclavicular, acromioclavicular, glenohumeral joints] and 2 physiologic joints [scapulothoracic joint, subdeltoid joint]).

The latter are called physiologic joints because they are not true anatomic joints with the usual joint characteristics (eg, capsule, ligament).

Instead, they are gliding structures that play an important role in the biomechanics of the shoulder by positioning and stabilizing the shoulder complex.

The 5 joints fall into the following 2 groups:

Ø  First group

§  Glenohumeral joint, a true joint

§  Subdeltoid joint, a physiologic joint

Ø  Second group

§  Sternoclavicular joint, a true joint

§  Acromioclavicular joint, a true joint

§  Scapulothoracic joint, a physiologic joint

In both groups, true joints are linked mechanically to physiologic joints and work simultaneously to produce movement.

STERNOCLAVICULAR JOINT

This joint represents the only bony connection between the trunk and the upper limb.

The sternoclavicular joint is a synovial saddle-shaped joint composed of a capsule, the sternal side of the clavicle, the sternoclavicular joint surface, an articular disk, the costoclavicular ligament, the anterior and posterior sternoclavicular ligaments, and the interclavicular ligament.

The fibrous capsule surrounds the joint and is attached around the clavicular and sternochondral articular surfaces. The concave clavicular surface fits snugly on the convex sternocostal surface similar to how a rider sits on a saddle and the saddle fits on the back of a horse.

The fibrocartilaginous articular disk increases the capacity for movement, cushions forces transmitted from the shoulder, improves the congruity of the surfaces, and resists upward dislocation of the clavicle. This costoclavicular ligament is a short flat band of fibers running between the cartilage of the first rib and the costal tuberosity on the undersurface of the clavicle.

This ligament is the principal stabilizer of the sternoclavicular joint, opposing the upward pull of the sternocleidomastoid muscles, and it also resists the elevation of the clavicle.

The anterior sternoclavicular ligament is a broad anterior band linking the upper and anterior borders of the sternal end of the clavicle and the upper anterior surface of the manubrium of the sternum.

Reinforced by the tendinous origin of the sternocleidomastoid muscle, it stabilizes the joint anteriorly.

The posterior sternoclavicular ligament has similar origin and insertion and stabilizes the joint posteriorly.

The interclavicular ligament attaches on the upper border of both clavicles and the sternum, strengthening the capsule above.

ACROMIOCLAVICULAR JOINT

The acromioclavicular joint is a synovial plane joint composed of a capsule, the lateral end of the clavicle, the medial border of the acromion, an articular disk, the acromioclavicular ligaments, the coracoclavicular ligaments, and the coracoacromial ligament.

The joint stability is maintained by the surrounding ligaments rather than by the bony configuration of the joint. The plane joint surfaces slope downward and medially, favoring displacement of the acromion downward and under the clavicle.

The articular capsule encloses the joint, attaching at the articular margins. The capsule is reinforced by the fibers of the deltoid and the upper trapezius muscles and the powerful superior acromioclavicular ligament superiorly, and the anterior, inferior, and posterior acromioclavicular ligaments.

The wedge-shaped articular disk dips into the joint from the superior part of the capsule and makes the articular surfaces more congruent.

The coracoclavicular ligaments, although separated medially from the joint, are the primary joint stabilizers. Its 2 parts, named for their shape, are the posteromedial conoid ligament and the anterolaterally placed trapezoid ligament.

The 2 ligaments lie in 2 planes, more or less at right angles to each other. A third part, the medial coracoclavicular ligament, is described inconsistently in anatomy textbooks.

The coracoclavicular ligaments act to resist superior and, to a lesser extent, anterior dislocation of the acromioclavicular joint, resist axial compression at the distal clavicle, and indirectly limit excess rotation of the joint.

The conoid ligament is fan-shaped with its apex lying inferiorly. This ligament inserts on the "tip of the elbow" of the coracoid process and the undersurface of the medial third of the clavicle.

During abduction and external rotation, the angle between the scapula and the clavicle widens and the conoid ligament is stretched, transmitting the force to the clavicle and, ultimately, to the strong acromioclavicular ligaments, preventing dislocation.

The trapezoid ligament inserts on the medial border of the upper surface of the coracoid process and runs superiorly and laterally to attach on the undersurface of the clavicle.

During adduction, the angle between the scapula and the clavicle is closed and the trapezoid ligament is stretched, preventing the dislocation of the acromioclavicular joint by the same force-transmission mechanism.

In summary, the vertical stability of the acromioclavicular joint is provided mainly by the coracoclavicular ligaments, and the anteroposterior stability is provided mainly by the acromioclavicular ligament-capsule complex.

SCAPULOTHORACIC JOINT

The scapulothoracic joint is not a true anatomic joint because it lacks the usual joint characteristics.

Except for its attachment to the axial skeleton at the acromioclavicular joint and with the coracoclavicular ligaments, the scapulothoracic joint is free gliding without any ligament restraint.

Although it is not a true joint, the scapulothoracic joint plays an important role in the biomechanics of the shoulder complex.

 The scapula represents a mobile platform from which the upper limb operates.

The main role of the scapula is to orient the glenoid fossa in an optimal position to receive the humeral head and to provide a stable base of support for the controlled movement of the articular surface of the humeral head. It also allows increased shoulder mobility.

In the resting position, the scapula lies between the second and seventh rib, over the serratus anterior and the subscapularis muscles. The superomedial angle corresponds to the first thoracic vertebra; the inferior angle corresponds to the seventh thoracic vertebra. The scapula runs obliquely, mediolaterally, and posteroanteriorly, forming an angle of 30° open anterolaterally with the frontal plane.

Five muscles directly control the scapula (trapezius, rhomboids, levator scapulae, serratus anterior, and, to a lesser extent, the pectoralis minor). These muscles act in a synchronous way to position the glenoid fossa.

GLENOHUMERAL JOINT

The glenohumeral joint is a multiaxial ball and joint socket that is the most mobile and the least stable of all the joints.

This joint is composed of a capsule, the head of the humerus, the glenoid fossa, the glenoid labrum, the glenohumeral ligaments, the coracohumeral ligament, and the transverse humeral ligament.

The glenohumeral joint also is stabilized externally by the tendons of the rotator cuff muscles and the long head of the biceps tendon.

The joint capsule is a loose thin redundant sleeve that contributes to the mobility of the joint, but also to its instability. On the humeral head, the capsule attaches on the anatomic neck, immediately medial to the tuberosities, and then it extends onto the medial surface of the shaft, slightly below the articular head.

The capsule has 2 openings. The upper end opening allows the passage of the long head of the biceps tendon; the anterior opening allows a communication between the joint cavity and the subscapular bursa.

On the glenoid side, the capsule attaches to the labrum and, less frequently, to the scapular neck. Because of its laxity, the joint capsule is 2 times larger than the humeral head, and assistance is needed to stabilize the glenohumeral joint. This assistance is provided partly by the glenohumeral ligaments and the coracohumeral ligament.

Three intrinsic, yet distinct, capsular ligaments provide anterior stability to the joint.

The anterior inferior, middle, and superior glenohumeral ligaments form a Z in front of the joint capsule. These ligaments become taut and restrict certain motions of the humerus. They are the last structures that provide stability after other static and dynamic stabilizers have been involved.

The thin superior glenohumeral ligament arises from the anterosuperior edge of the glenoid and attaches to the top of the lesser tuberosity of the humerus, limiting inferior dislocation in the adducted shoulder and providing secondary restraint to posterior dislocation.

The middle glenohumeral ligament arises from the supraglenoid tubercle and the superior labrum, next to the superior ligament and attaches medially to the base of the lesser tuberosity, beneath the subscapularis tendon.

The primary role of the middle glenohumeral ligament is to limit external rotation at 45° of abduction. This ligament also provides a secondary restraint to anterior dislocation.

The inferior glenohumeral ligament complex arises from the anteroinferior labrum and the glenoid border and attaches to the lesser tuberosity, just inferior to the middle ligament. This ligament is a hammock-shaped structure that consists of 3 parts, the axillary pouch and the anterior and posterior bands.

The anterior and posterior bands reciprocally tighten as the humeral head is rotated. The anterior band is the primary restraint to anterior dislocation and external rotation at 90° of abduction.

The loss of integrity of this ligament is a major cause of anterior instability in the throwing athlete.

The coracohumeral ligament is a broad band that arises from the lateral border of the horizontal arm of the coracoid process and attaches to the top of the greater and lesser tuberosities and the transverse humeral ligament.

The primary role of this ligament is to stabilize the adducted shoulder and resist inferior subluxation of the humeral head.

The transverse humeral ligament stretches from the greater to the lesser tuberosity. The primary role of this ligament is to stabilize the long head of the biceps tendon in the bicipital groove.

HUMERAL HEAD AND GLENOID FOSSA

The large humeral head articulates with the slender and shallow glenoid fossa, only a little more than one third its size.

The axis forms an angle of 135° with the shaft and an axis of 30° with the frontal plane (retroversion angle).

The head faces superiorly, medially, and posteriorly; the glenoid points anteriorly, laterally, and slightly superiorly. The concavity of the humeral head is irregular and less marked than the convexity of the humeral head.

The irregular minimal bony contact between those 2 joint surfaces explains the lack of joint stability and the necessity for other mechanisms of stabilization.

The glenoid labrum is a rim of fibrocartilage that surrounds the glenoid fossa. This labrum serves many important functions for the glenohumeral joint, including the following:

• Provides an extension to the concavity of the glenoid fossa and deepens the glenoid by 50%

• Provides an increase in depth and, to a lesser extent in width, resulting in an increased stabilization against translating forces

• Serves as an articular surface to the humeral head

• Serves as an attachment for the capsule, the ligaments, and the long head of the biceps tendon

ROTATOR CUFF MUSCLES & LONG HEAD OF BICEPS TENDON

The rotator cuff is made up of 4 interrelated muscles arising from the scapula and attaching to the tuberosities.

Their tendons form a continuous cuff around the head that allows the cuff muscles to provide an infinite variety of moments to rotate and adjust the humeral head in the glenoid fossa, providing the optimal muscle balance for precise coordinated movements.

The supraspinatus muscle arises from the medial two thirds of the supraspinous fossa of the scapula. This muscle passes under the acromion and acromioclavicular joint and inserts onto the superior aspect of the greater tuberosity and joint capsule.

The supraspinatus muscle is innervated by the suprascapular nerve (C4-C5-C6). Its primary role is to stabilize the head of the humerus in the glenoid fossa and to abduct the shoulder.

The infraspinatus muscle arises from the medial two thirds of the infraspinous fossa of the scapula and inserts on the middle facet of the greater tuberosity and joint capsule.

This muscle is innervated by the suprascapular nerve (C4-C5-C6). Its primary role is to stabilize and externally rotate the head of the humerus.

The teres minor muscle arises from the upper two thirds of the dorsal aspect of the lateral border of the scapula and inserts onto the lower facet of the greater tuberosity and joint capsule. Its primary role is to stabilize and externally rotate the head of the humerus.

The subscapularis muscle arises from the subscapular fossa of the scapula and inserts to the lesser tuberosity and joint capsule.

This muscle is innervated by the upper and lower subscapular nerve (C5-C6-C7). Its primary role is to stabilize and externally rotate the head of the humerus.

The long head of the biceps tendon arises from the supraglenoid tubercle of the scapula, runs between the supraspinatus and subscapularis muscles, exits the shoulder through the bicipital groove under the transverse humeral ligament, and inserts onto the tuberosity of the radius.

The long head of the biceps is innervated by the musculocutaneous nerve (C5-C6). Its primary role is to stabilize and flex the humeral head and flex the elbow.

SUBDELTOID JOINT

Like the scapulothoracic joint, the subdeltoid joint is not a true anatomic joint. The subdeltoid is composed of the undersurface of the acromion, the coracoacromial ligament, the subacromiodeltoid bursa, the rotator cuff, and the long head of the biceps tendon.

Like the glenoid fossa, they form a concave structure that matches with the convex humeral head.

Many authors have stressed the importance of this joint and have described it as the fifth joint of the shoulder.

The subdeltoid joint serves the following 2 major roles:

• Provides a gliding surface for the head of the humerus, especially during abduction and flexion

• Resists the upward pull of the humeral head during abduction and flexion and provides superior stability

Degenerative changes observed on the undersurface of the acromion and coracoacromial ligament tend to confirm the involvement of this physiologic joint in shoulder motion.

HISTORY

A complete medical history should be obtained in order to direct the physical examination and make the right diagnosis.

Most of the time, the diagnosis can be made following a systematic history. Relevant past history, treatments, and test results should complement the history of the present injury. Sometimes, relevant social and family histories are necessary.

The following questions should help the physician in assessing the patient:

• What is the patient's age?

Ø  Shoulder pain in young overhead athletes suggests underlying shoulder instability.

Ø  In older patients, degenerative rotator cuff disease or frozen shoulder is suggested by shoulder pain.

• What is the patient's occupation or sport? Repetitive overhead activities and sports predispose to rotator cuff tendinitis.

• What was the mechanism of injury?

Ø  A fall on an outstretched arm could indicate a dislocation of the glenohumeral joint or a fracture of the humeral neck.

Ø  Repetitive overhead motions can cause tendinitis and, in the long run, chronic degenerative changes.

Ø  A fall or a trauma on the tip of the shoulder can result in an acromioclavicular sprain.

• What was the onset?

Ø  Insidious slow onset may suggest tendinitis or osteoarthritis.

Ø  Sudden onset usually is due to a trauma causing a fracture, dislocation, or a rotator cuff tear.

• Where is the pain located?

Ø  Pain located on the superior or lateral aspect of the shoulder suggests rotator cuff tendinitis.

Ø  Pain on the anterior aspect of the shoulder may result from bicipital tendinitis, an acromioclavicular sprain, or anterior instability.

Ø  Neck pain and radicular pain or paresthesias suggest a cervical spine disorder.

• What is the severity of the pain?

Ø  An acute burning pain could indicate an acute bursitis.

Ø  An intermittent dull pain may be due to a degenerative rotator cuff disease.

• What is the type of pain?

Ø  Sharp burning pain suggests a neurologic origin.

Ø  Bone and tendon pain is deep, boring, and localized.

Ø  Muscle pain is dull and aching, not localized, and may be referred to other areas.

Ø  Vascular pain is aching, cramp-like, poorly localized, and may be referred to other areas.

• What is the duration of the symptoms?

Ø  Frozen shoulder goes through 3 stages that can last up to 3-4 years.

Ø  Acute bursitis has a short-term evolution and responds well to nonsteroidal anti-inflammatory drugs (NSAIDs).

• What is the timing of the pain?

Ø  Predominantly night pain suggests frozen shoulder.

Ø  Morning pain and stiffness improved by activity may be caused by a synovitis.

Ø  Pain that increases with activity is usually the result of a rotator cuff tendinitis.

• Which activities/positions increase the pain?

Ø  Pain increased by overhead activities or arm-length activities suggests rotator cuff tendinitis.

Ø  Pain increased when throwing is likely to be due to anterior instability.

Ø  Pain increased by lying on the affected shoulder may be caused by an acromioclavicular sprain.

• Which activities/positions relieve the pain?

• Is there any weakness or paresthesias in the upper extremities? Neurologic symptoms are caused by a cervical radiculopathy or peripheral nerve entrapment/lesion.

• Are the symptoms constant or intermittent?

Ø  Intermittent symptoms usually result from soft tissues or joint disorders.

Ø  Constant symptoms suggest a neurologic lesion.

• Are there any joint motion restrictions?

Ø  Passive and active joint restriction in all directions of ROM is caused by a frozen shoulder or glenohumeral synovitis.

Ø  Restriction in internal rotation suggests an impingement syndrome due to rotator cuff tendinitis.

Ø  Inability to perform active abduction suggests a rotator cuff tear or a frozen shoulder.

• Is some crepitus noted?

Ø  Crepitus is the result of degenerative rotator cuff changes.

Ø  Crepitus is not a normal finding in the shoulder.

• Are there any changes in the color of the arm?

Ø  Color changes may be due to ischemia secondary to vascular insufficiency.

Ø  Reflex sympathetic dystrophy (also called complex regional pain syndrome, type 1) can cause skin color changes.

• Has the patient had any treatments like oral medication, injections, or physical therapy to date?

• Has the patient had any diagnostic tests performed to date?

• What is the evolution of the symptoms?

Ø  Has the pain changed?

Ø  Has the pain spread or moved?

Ø  Has the pain subsided or increased?

PHYSICAL

A systematic examination of the shoulder region includes a careful observation, the palpation of the bones and soft tissues, passive and active ROM, impingement and topographic tests complemented, as needed, by instability tests, labrum tests, and special tests.

The examination is completed by a cervical spine examination, along with neurologic and vascular examination.

OBSERVATION

The observation begins from the moment the patient enters the room. The smoothness and symmetry of the shoulders and the movements of the upper extremities are evaluated, as well as the patient's gait.

The examiner must be aware of any signs of painful posturing and irregularity of motion of the affected shoulder. Bilateral examination allows for comparison of the affected shoulder with the unaffected one.

The patient then must be asked to get suitably undressed so that an appropriate assessment of the bone and soft tissues can be performed. The shoulder, cervical region, and the entire upper extremity must be assessed.

The examiner should assess bones and joints for possible asymmetry or deformities, as well as soft tissue changes suggesting vasomotor abnormalities, like swelling, erythema, white shiny skin, loss of hair, or atrophy.

Scars and abrasions also must be noted. The observer should assess bony contours first and then soft tissues. Observation of the patient must be completed from the front, side, and back.

PALPATION

Like observation, palpation must be performed in an orderly manner, beginning with the anterior structures and finishing with the posterior structures.

Palpation must include bony structures and soft tissues. Irregular joint surfaces, swelling, heat, crepitus, pain, tenderness, and muscle tension and spasms must be looked for.

Palpation can be performed more conveniently with the patient standing. In this position, it is easier for the examiner to move around the patient. The examiner should stand behind the patient for the palpation.

RANGE OF MOTION

Both active and passive ROM must be evaluated.

Although some authors suggest that there is no need to assess passive ROM if the patient is able to perform a complete active ROM without pain, passive ROM must be assessed systematically. Some patients with glenohumeral ROM restrictions have learned to compensate with increased scapulothoracic mobility and seem to have near normal active range.

The following movements (with the normal ranges provided) should be assessed:

v  Abduction (70-180°)

v  Adduction (30-45°)

v  Flexion (160-180°)

v  Extension (45-50°)

v  External rotation (80-90°)

v  Internal rotation (90-110°)

Active movements are evaluated first. With the observer behind the patient who is standing, active abduction is performed.

The scapulohumeral rhythm is observed.

If a painful arc (ie, pain or inability to abduct because of pain) is observed between 45-120°, a subacromial impingement syndrome is suggested.

If the pain is greater after 120°, when full elevation is reached, an acromioclavicular joint disorder is suggested.

If a reverse scapulohumeral rhythm (ie, an abduction initiated by the scapulothoracic joint rather than by the glenohumeral joint) is observed, a frozen shoulder is suggested.

Look for a winging of the scapula caused by a trapezius or rhomboid muscle weakness. Active flexion also is evaluated. In the presence of a subacromial impingement syndrome, this movement also can be painful. Active flexion also can elicit a winging of the scapula caused by a serratus anterior weakness.

PASSIVE RANGE OF MOTION

The evaluation can be performed with the patient standing, sitting, or lying down. For practical purposes, the examination is performed with the patient standing.

Passive abduction is assessed with the observer behind the patient.

Full abduction is performed first to evaluate the combination of scapulothoracic and glenohumeral motion. Then, the scapulothoracic joint is locked by putting one hand over the scapula and the clavicle to resist any motion of this joint. This maneuver allows for a more selective evaluation of the glenohumeral joint (90-120°).

IMPINGEMENT TESTS

Positive impingement tests result from the reproduction of the impingement of the rotator cuff tendon by different provocative maneuvers.

In the case of an anterosuperior impingement syndrome, the impingement takes place underneath the coracoacromial arch; in the case of the posterosuperior impingement syndrome, the impingement is on the posterosuperior border of the glenoid cavity, whereas, in the case of the anterointernal impingement syndrome, the impingement takes place in the subcoracoid space or in the coracohumeral interval.

v  Neer impingement test

o    With the examiner standing behind the patient, the shoulder is flexed passively. Although not originally described by Neer, the shoulder is positioned in internal rotation by this author.

o    When positive, this test produces pain that is caused by the contact of the bursal side of the rotator cuff on the anterior third of the undersurface of the acromion and the coracoacromial ligament, as well as by contact of the articular side of the tendon with the anterosuperior glenoid rim.

o    A positive test suggests an anterosuperior impingement syndrome.

o    The sensitivity of this test, assessed by operatively observed anatomic lesions, is 89%

v  Hawkins-Kennedy test

o    With the examiner standing behind the patient, the shoulder is flexed passively to 90°, followed by repeated internal rotation.

o    When positive, this test produces pain that is caused by the contact of the bursal side of the rotator cuff on the coracoacromial ligament and by the contact between the articular surface of the tendon and the anterosuperior glenoid rim.

o    Contact between the subscapularis tendon and the coracoid process also is observed.

o    A positive test suggests an anterosuperior or an anterointernal impingement test.

o    This author uses a modified version of this test with the shoulder positioned initially at 90° of abduction and 30° of flexion, in the plane of the scapula. Along with repeated internal rotation motion, the shoulder is brought progressively to 90° of flexion.

o    If pain is present when the shoulder is flexed at 30°, it is caused by an anterosuperior impingement syndrome.

o    If the pain is present only when the shoulder is brought to 90° of flexion, reducing the coracohumeral interval, an anterointernal impingement syndrome is suggested.

o    The sensitivity of this test is 87%.

v  Yocum test

o    With the examiner standing behind the patient, the hand on the ipsilateral side of the examined shoulder is placed on the contralateral shoulder.

o    The elevation of the elbow is resisted by the examiner.

o    When positive, this test produces pain caused by the contact of the bursal side of the cuff tendon with the coracoacromial ligament and possibly the undersurface of the acromioclavicular joint.

o    A positive test suggests an anterosuperior or an anterointernal impingement syndrome.

o    The sensitivity of this test is only 78%; however, the sensitivity of the 3 tests together is 100%, which justifies that the 3 tests should be systematically performed together.

v  Posterior impingement test

o    With the patient lying down, the shoulder is positioned at 90-100° of abduction and maximally externally rotated.

o    When positive, this test produces pain in the posterior aspect of the shoulder that is caused by the impingement of the articular side of the cuff tendon between the greater tuberosity and the posterosuperior glenoid rim and labrum.

o    The relocation of the humeral head, performed by applying a posteriorly directed force to the humeral head, causes a reduction in pain.

o    The sensitivity of this test is 90%.

o    Impingement tests confirm an impingement syndrome; however, they do not determine the location of the rotator cuff lesion.

TOPOGRAPHIC TESTS

Using resisted isometric contraction of specific muscles of the rotator cuff, it is possible to identify the location of the tendon lesion causing the impingement.

SUPRASPINATUS TENDON

• Jobe test

  • The shoulder is placed at 90° of abduction and 30° of flexion in the plane of the scapula.

  • Shoulder elevation is resisted.

  • The test is positive if pain is noted. When compared with surgical observations, the sensitivity of this test is 86%, and its specificity is 50%.

  • The positive predictive value (the ratio of true positive tests on all the positive tests) of the Jobe test is 96%, and its negative predictive value (the ratio of all the negative tests on all the negative tests) is 22%.

• Full can test

  • The shoulder is placed at 90° of flexion and 45° of external humeral rotation (thumb pointing upward, like someone holding a full can, right-side-up).

  • Shoulder elevation is resisted.

  • The test is positive if it produces pain.

  • An electromyographic (EMG) study showed that this test results in the greatest supraspinatus activation with the least activation from the infraspinatus.

INFRASPINATUS TENDON

• Infraspinatus isolation test

  • The shoulder is positioned at 0° of elevation (elbows against the waist flexed at 90°) and 45° of internal rotation.

  • Shoulder external rotation is resisted.

  • The test is positive if it produces pain.

  • EMG shows that this is the optimal infraspinatus isolation test.

• Patte test

  • The shoulder is placed at 90° of abduction, neutral rotation, and in the plane of the scapula.

  • The examiner holds the elbow of the patient and the external rotation is resisted.

  • The test is positive if it produces pain.

  • The sensitivity of the test is 92%, but its specificity is only 30%.

  • The positive predictive value is 29%, and its negative predictive value is 93%.

A PALSY OF THE EXTERNAL ROTATOR ALSO CAN BE TESTED.

• With the elbow held against the waist, the shoulder is positioned passively in external rotation.

• The test is positive when the patient is unable to maintain the shoulder in external rotation, suggesting a full tear of the external rotators.

TERES MINOR TENDON

• No specific teres minor isolation tests exist.

• The same tests used to test the infraspinatus tendon serves for the teres minor.

SUBSCAPULAR TENDON

• The Gerber lift-off test

  • The shoulder is placed passively in internal rotation and slight extension by placing the hand 5-10 cm from the back with the palm facing outward and the elbow flexed at 90°.

  • The test is positive when the patient cannot hold this position, with the back of the hand hitting the patient's back.

  • The sensitivity and specificity of this test are 100% when there is a full tear of the subscapularis.

• The Gerber push with force test

  • The shoulder is placed in the same position as the lift-off test; however, the patient has to keep his hand away from the back and resists a push in the palm of the hand.

  • EMG shows that this is the optimal subscapularis isolation test with minimal activation of the pectoralis and latissimus dorsi muscles.

LONG HEAD OF THE BICEPS TENDON

• The Speed palm up test

  • The shoulder is placed at 90° of flexion with the elbow in extension and the forearm in supination, bringing the palm of the hand up.

  • The flexion of the shoulder is resisted.

  • The test is positive if it produces pain.

  • The sensitivity of this test is 63%, but its specificity is only 35%.

  • The positive predictive value is 43%, and its negative predictive value is 55%.

• The Yergason test: In this author's opinion, this test is technically difficult and ineffective, and, therefore, it is not described in this article.

Generally, the topographic tests are sensitive but not specific, except for the Gerber's lift-off test. The combination of the impingement and topographic tests make up the rotator cuff tests that allow determination of whether or not a patient's symptoms are caused by rotator cuff disease.

As mentioned before, the examination must be completed by instability and labrum tests, special tests (eg, thoracic outlet syndrome tests), a cervicothoracic spine examination, and a neurologic and vascular examination, but it is not the purpose of this section to describe them.

CAUSES

Rotator cuff disease may result from a variety of causes. Damage to the rotator cuff commonly is caused by degeneration associated with aging.

Other causes of injury to the rotator cuff may include tendinitis, bursitis, or arthritis. These injuries are particularly common in individuals who perform repetitive overhead activities at work or through involvement in sports.

Throwing athletes are prone to this problem secondary to the repetitive stress and trauma to the rotator cuff. Rotator cuff disease also may be the result of a traumatic injury (eg, a fall onto the shoulder, motor vehicle accident).

DIAGNOSIS

LABORATORY STUDIES

• Laboratory studies are not necessary for diagnosing rotator cuff disease.

IMAGING STUDIES

• A wide variety of radiological examinations are offered to image the rotator cuff. Each of them has advantages and limitations. To prescribe the most useful examination, one must start with a good clinical history and physical examination. Imaging should be used to confirm the anomaly, describe its extension and the associated findings. The following paragraphs briefly explain the indications, the technique, and the findings for each modality available to image the rotator cuff in radiology.

• Plain film radiography

  • Indication

    • Plain films are not very specific or sensitive to rotator cuff disease, but they remain the first examination to perform.

    • Radiographs give a gross evaluation of the mineralization of the bone, the alignment, posttraumatic changes, the normal variant of the acromion shape, the presence of degenerative changes, and the presence of fine soft tissue calcifications that could be missed otherwise by other modalities.

    • This is most useful test in trauma or chronic complete tear.

    • In the last stage of complete chronic rotator cuff tear, it could be the only imaging modality needed to confirm the diagnosis.

  • Technique: Plain films are acquired routinely in 3 planes (ie, neutral, internal, external rotation). Additional views, like the Neer profile, can be performed to better characterize the shape of the acromion.

  • Findings (see Table 1)

    • Rotator cuff tendinitis: Signs of chronic tendinitis without tear include subchondral sclerosis of humeral head, flattening and geode of the greater tuberosity, sclerosis of the acromion, calcifications located in the presumed area of rotator cuff tendon, acromion spurs, or a type 2 or 3 acromion.

    • Partial rotator cuff tear: All of the above can be present, but no specific signs can help in the diagnosis of a partial tear, as tendons are not visible on plain film.

    • Complete rotator cuff tear: In acute tears, the presence of synovial effusion or hemorrhage can subluxate the humeral head caudally. On the other hand, if the tear is chronic, the humeral head migrates superiorly as the rotator cuff loses its ability to stabilize the humeral head in the glenoid cavity. Radiographically, an acromiohumeral space less than 6 mm, with or without erosion, on the inferior aspect of the acromion is a good semiologic landmark for chronic complete tear. All the signs of tendinitis also can be found in complete chronic tears.

RADIOLOGICAL FINDINGS ON PLAIN FILM 

• Arthrography

  • Indication

    • The main indication of arthrography is to identify complete rotator cuff tears and intra-articular infiltration of corticoid.

    • As a diagnostic tool, it is combined generally with arthro-CT.

  • Technique: Arthrography is performed by injecting iodine contrast medium or air or both into the glenohumeral joint. Eight to twelve milliliters of contrast (or 3-4 mL of contrast and 10-12 mL of air) are injected to distend the joint capsule. If air and contrast are injected the term double contrast study is used. Then, plain films are taken in different positions, such as external rotation, internal rotation, and subacromial views before and after motions. The image below shows an intact capsule.

  • Findings: In the presence of a complete tear, the contrast floods from the glenohumeral joint into the subacromial-subdeltoid bursa. With a partial tear, the contrast is seen as a line or small filled cavity within the tendon but without contrast in the subacromial-subdeltoid bursa. This finding is more difficult to demonstrate than in a complete tear. Intratendon tears and tears on the superior aspect of the tendon (bursal side) are not visualized with this technique. Arthrography also can provide some information about the long portion of the biceps tendon, loose bodies, and synovial disorders, such as inflammatory synovitis, osteochondromatosis, or villonodular pigmented synovitis.

• CT-arthrography

  • Indication: This study, although very accurate (100% sensibility, 100% specificity) in depicting complete rotator cuff tears, is limited in the evaluation of tendinitis and partial tears where its sensitivity drops to 17-43%. On the other hand, this test gives more information than arthrography about the joint itself and the soft tissues around it. The ability to evaluate the labrum, the glenohumeral ligaments, the long head of the biceps tendon, and the bony structures, as well as the presence of loose bodies, makes this a useful study.

  • Technique: CT-arthrography is performed exactly like a double contrast (air and iodine contrast) arthrography but followed by tomodensitometry imaging (CT scan). For this examination, the shoulder is imaged in the axial plan in internal and external rotation. Thin slices as small as 2-3 mm are acquired throughout the entire joint. With new CT scan technology, it has become easy to reformat images in multiple planes.

  • Findings

    • The semiologic signs of rotator cuff tears are essentially the same as seen on conventional arthrography. The presence of contrast in the subacromial-subdeltoid space confirms the diagnosis of complete rotator cuff tears. The contrast also can facilitate determination of the size and location of the tear to help the surgeon plan the surgery. Degenerative findings such as osteophytes, geodes, sclerosis, and articular space narrowing also are well depicted.

    • In addition to conventional arthrography, this technique can identify labral and glenohumeral ligament tears. The presence of contrast between the labrum and the articular space indicates the presence of a tear. The axial views also permit a good visualization of the long head of the biceps tendon in its groove. Therefore, subluxation of this tendon, or rupture, also can be diagnosed. Finally, the shape of the acromion can be evaluated on the oblique sagittal reformatted study that requires a special acquisition.

• Magnetic resonance imaging

  • Indication

    • Magnetic resonance imaging (MRI) is the state-of- the-art diagnostic tool for a full evaluation of the shoulder. MRI allows a fine evaluation of the bone marrow, tendons, muscles, ligaments, capsules, bursae, and labrum. MRI combines the advantage of visualization of the bony structures, as well as all the soft tissues about the shoulder and in any plane desirable. With this imaging modality, it is now possible to diagnose the full continuum of rotator cuff disease, from simple tendinosis, to complete tear. MRI is much more powerful than the previous modalities to identify partial tears, and it also can identify intratendon tears or tears on the bursal aspect of the tendon. As with CT scan and plain film, the bone structures resulting or contributing to the impingement syndrome can be evaluated.

    • MRI also can give information about retraction of the muscle, atrophy, bursitis, and bone marrow abnormalities (such as edema or contusion), which all are associated findings in rotator cuff disease.

    • MRI is somewhat limited in the evaluation of the labrum and glenohumeral ligaments. MRI arthrography is the study of choice for the evaluation of labrum and glenohumeral ligaments.

  • Technique: This technique takes advantage of the properties of hydrogen protons submitted to a magnetic field and RF waves. Therefore, there is no radiation exposure for the patient. Multiple sequences are available to highlight different substances such as water, fat, blood, or solid structures. Mainly spin echo T1, spin echo T2, and gradient echo sequences, in axial, sagittal, and coronal oblique plans, are acquired in different combinations. Inversion recovery, fat saturation, and injection of gadolinium (IV or intra-articular) can be added if necessary.

  • Findings

    • MRI shows great detail of the anatomy in multiple plans. MRI also allows seeing the nature of a structure or an anomaly better, according to its intrinsic property. Therefore, the examiner should know some characteristics of the MRI signals for the most common structures. Fat, methemoglobin, melamine, gadolinium, and some forms of calcium all are hyperintense in T1-weighted images. On the contrary, water appears at low signal intensity. In T2-weighted images or in gradient echo, the liquids are hyperintense, as are most lesions, meaning that edema, inflammatory processes, tumors, tendinitis, and tendon tears are hyperintense in T2-weighted images and hypointense in T1-weighted images. Therefore, the presence of fluid in a bursa or articular joint is hyperintense in T2 or gradient echo, and indicates inflammatory or posttraumatic fluid. A full thickness tear of the tendon is demonstrated by a hypersignal intensity in T2 that extends throughout the tendon.

• Tendinitis is recognized as a grey signal in the tendon. Finally, calcification, as well as cortical bone, appears hypointense in all sequences.

• Arthro-MRI follows the same principle as arthro-CT. This modality can help to identify labral tears and glenohumeral tears.

RADIOLOGICAL FINDINGS ON MRI 

RADIOLOGICAL SIGNS OF SPECIFIC DISORDERS 

• Ultrasonography

  • Indication: The main purpose of ultrasonography is to study the soft tissues. In experienced hands, ultrasonography has a sensitivity of 93-100% and a respective specificity of 85-97% for complete tear and a sensitivity of 69-93% for partial tear. These results are comparable to MRI.

  • Technique

    • Ultrasonography is a technique that uses the same principles as radar. The images are created using a high- resolution transducer that first sends a sound signal and then receives the echo produced when the sound hits the different structures at different depths.

    • The advantages of this technique reside in its low cost, high availability, and high resolution. Ultrasonography is a dynamic study for demonstrating impingement syndrome.

    • The disadvantages are that it is time consuming for the radiologist and is operator-dependent. Ultrasonography cannot study bone structures, as sound does not penetrate bone very well.

  • Findings

    • With ultrasonography, the normal tendon is an echoic structure, whereas the cartilage and fluids are hypoechoic (see Table 4, below). All the tendons, bony landmarks (eg, humerus, greater tuberosity) and intra-articular or intrabursal effusion are recognized easily. Tendinitis is diagnosed when the tendon loses its echogenicity and becomes diffusely hypoechoic. Calcifications appear as bright foci within the tendon, accompanied by a posterior shadowing, as the sound cannot pass through the calcium.

    • The main, and most sensitive, sign of a complete rotator cuff tear is an interruption in the tendon that fills with fluid, producing a hypoechogenic foci extending from the cartilage surface to the subdeltoid-subacromial bursa. The secondary signs include the uncovered cartilage (cartilage appears hyperechoic at the site of the tear), bursa herniation, loss of convexity of the tendon and bursa, and effusion within the glenohumeral articulation and the subacromial-subdeltoid bursa.

    • The diagnosis of a partial rotator cuff tear is made when the hypoechoic or bursal herniation does not cross the full width of the tendon. The use of ultrasonography also allows the operator to demonstrate in real time the impingement of the supraspinatus tendon on the acromion when the arm is positioned in internal rotation and moved in abduction or flexion.

ULTRASONOGRAPHIC SIGNS OF ROTATOR CUFF DISEASE 

• Nuclear medicine imaging: Bone scintigraphy is not used routinely in the rotator cuff disease imaging.

TREATMENT

PHYSICAL THERAPY

Physical therapy can be a useful adjunct in the conservative treatment of patients with degenerative rotator cuffs.

Although there are numerous studies on the conservative treatment and surgical approach of the painful shoulder and, more specifically, the rotator cuff, the conclusions of a review of randomized controlled trials of interventions for painful shoulder were that little evidence supports or refutes the efficacy of common interventions for shoulder pain.

Lack of definition and strict diagnostic criteria for the different painful shoulder conditions, valid randomization procedures, blinding, valid scales for outcome measurement, and heterogeneous populations are among the reasons why it is difficult to draw firm conclusions about the efficacy of any of these interventions.

In his/her approach to conservative treatment, the clinician must be critical and try to use an evidence-based medicine approach as much as possible when planning the patient's treatment.

The clinician also must use a combination of experience and intuition to compensate for the lack of scientific evidence supporting the different therapeutic modalities to be prescribed.

CONSERVATIVE TREATMENT 

v  Pain relief

§  Avoidance of painful motions and activities

§  Simple analgesics

§  Nonsteroidal anti-inflammatory drugs

§  Physical modalities

§  Manual physical therapy

§  Subacromial corticosteroid injection

§  A new promising procedure called the bupivacaine suprascapular nerve block

v  Restoration of motion

§  Stretching of the glenohumeral capsule and muscles

§  Manual physical therapy of the glenohumeral, scapulothoracic, acromioclavicular, and sternoclavicular joints and the parascapular and scapula-stabilizer muscles

§  Normal scapulohumeral rhythm must be restored.

§  Manual therapy of the cervicodorsal spine, because of its close relationship with the shoulder, often is necessary. Restoration of strength and function: Restoration of strength is achieved by strengthening of the rotator cuff muscles, the scapula-stabilizer muscles and the long humeral depressor muscles (latissimus dorsi and pectoralis major).

v  Proprioception: In a young individual who has premature degenerative rotator cuff changes because of shoulder instability, proprioceptive exercises must complement strengthening exercises.

v  Sport-specific rehabilitation

§  In a young individual or athlete, sport-specific exercises must be included before resuming normal sport activities.

§  With the aging of the active population, this aspect of the rehabilitation, combined with progressive return to sport activities should not be omitted.

PHYSICAL MODALITIES FOR ROTATOR CUFF DISEASE

Physical modalities are used widely in the treatment of rotator cuff disease.

Physical therapists should be diligent in choosing the modalities and their parameters to be used for treatment.

Some excellent review articles have been published on the different therapeutic modalities for the painful shoulder. Van der Heijden, Grauer, and Green did a systematic review of randomized clinical trials on the therapeutic effects of physical modalities on painful shoulder disorders.

These authors concluded that there is insufficient evidence to prove or disprove the efficacy of most therapies for the treatment of various shoulder pain syndromes.

Based on these review studies, it appears that ultrasonographic therapy, transcutaneous electrical nerve stimulation (TENS), magnetotherapy, and different methods of thermotherapy are not effective in the treatment of shoulder disorder.

Pulsed electromagnetic field therapy and low power laser could have short-term efficacy as compared with placebo.

• Ultrasonography

  • Ebenbichler et al showed in a randomized, double-blind, placebo-controlled study that the use of pulsed ultrasonography performed 5 times a week for 15 minutes (0.89 MHz frequency, 2.5 watts per square centimeter, pulsed mode 1:4) significantly resolves calcification of the shoulder, decreases pain, and improves the short-term quality of life (QOL). Long-term follow-up did not show significant differences; however, in the long term, the symptoms of calcifying tendinitis may be self-limiting and may improve independently from the resolution of the calcium deposit.

  • This theory may explain why the use of ultrasonography is only significantly effective in the short term. The short-term efficacy of ultrasonographic therapy has been demonstrated only in calcifying tendinitis. Its efficacy in other shoulder disorders has not been shown. Extracorporeal shock wave therapy

  • Another modality that looks promising is extracorporeal shock wave therapy. Passing a strong electric current through a flat coil inducing a magnetic field generates shock waves. Shock waves were used first for the treatment of delayed and nonunion fractures by stimulating osteogenesis. In an uncontrolled study, shock wave therapy (1500 impulses of 0.28 mj/mm2) reportedly disintegrated calcium deposits partially or completely in 62% of patients, and 75% had significant improvement in pain, power, ROM, and shoulder function. The authors of the study concluded that a larger scale placebo-controlled trial should be conducted to analyze the benefits of this modality. A subsequent prospective, randomized, controlled study by Loew, using valid functional shoulder scale, showed the efficacy of extracorporeal shock wave therapy. At 3-6 months, there was a significant improvement in pain and function. At 6 months, there was radiological disappearance or disintegration of calcium deposits in up to 77% of patients. Comparing different regimens of shock waves, they concluded that the improvement in pain and function, as well as the radiological disintegration of calcification was dose-dependent. Thus, extracorporeal shock wave therapy appears to be a promising treatment for calcifying tendinitis. Like ultrasonography, its efficacy in other shoulder conditions has not been established.

• Iontophoresis

  • Some randomized controlled studies have shown the efficacy of topical steroids, NSAIDs, and acetic acid iontophoresis compared with a placebo in different musculoskeletal disorders; however, those studies were not specifically on rotator cuff disease. Moreover, a later trial did not show any difference in outcomes between no treatment and treatment with acetic acid iontophoresis followed immediately by 9 sessions of ultrasonographic therapy in a constant mode (0.8 W/cm2 at a frequency of 1 MHz for 5 minutes) over a period of 3 weeks. Some authors could not show any effect of iontophoresis on steroid migration through in vivo and in vitro studies, whereas others did. Thus, it is not possible to draw any conclusions on the efficacy of iontophoresis in the treatment of rotator cuff disease.

EXERCISES

Exercise program is the basis of the conservative treatment and no therapeutic modality will provide long-term relief of pain and increased functional status unless it is complemented by an exercise program.

The goal of this program is to restore shoulder ROM, enhance glenohumeral and scapulothoracic function to normalize the scapulohumeral motion, and improve the shoulder stability.

MANUAL THERAPY

Most of the trials on manual therapy study its efficacy in frozen shoulder.

Manual therapy has been compared with no intervention, corticosteroid injection, and cold therapy, and it has not shown any superiority over these modalities. As for exercises, trials on manual therapy in rotator cuff disease are rare.

Thus, manual therapy may be a useful adjunct to exercises and other therapeutic modalities in the treatment of rotator cuff disease.

MEDICATION

Oral medications for the treatment of degenerative rotator cuff disease include simple analgesics and nonsteroidal anti-inflammatory drugs. Because rotator cuff disease is a chronic condition, opioid analgesics are not recommended.

SIMPLE ANALGESICS

While NSAIDs are known to be effective in reducing pain and improving function and ROM, they may exert their effect through their analgesic rather than their anti-inflammatory properties.

One study with poor methodological quality did not show short-term superiority of NSAIDs as compared to acetaminophen in the treatment of painful shoulder syndrome. Long-term and short-term studies comparing the efficacy of NSAIDs with acetaminophen in osteoarthritis of the knee exist and showed similar efficacy.

Moreover, even the presence of inflammatory signs did not predict a better response to treatment with NSAIDs than acetaminophen, suggesting that improvements are not necessarily dependent on an anti-inflammatory effect.

Considering the toxicity of NSAIDs, the need for an analgesic rather than anti-inflammatory effect, the lower cost of a simple analgesic, and the chronicity of degenerative rotator cuff disease, it is indicated to prescribe acetaminophen (APAP) as an initial treatment. 

ACETAMINOPHEN (Tylenol, Feverall, Aspirin Free Anacin)

Analgesic effect of acetaminophen is mediated by prostaglandin inhibition.

Adult: 325-650 mg PO q4-6h or 1000 mg tid/qid; not to exceed 4 g/d

Pediatric:

<12 years: 10-15 mg/kg/dose PO q4-6h prn; not to exceed 2.6 g/d

>12 years: 325-650 mg PO q4h; not to exceed 5 doses in 24 h

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hepatotoxicity possible in chronic alcoholics following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; APAP is contained in many OTC products and combined use with these products may result in cumulative APAP doses exceeding recommended

NONSTEROIDAL ANTI-INFLAMMATORY DRUGS

Numerous studies on the efficacy of NSAIDs for different shoulder conditions have been published; however, because of the factors previously mentioned, most of them have poor methodological quality and, therefore, no conclusions can be drawn about the efficacy of NSAIDs.  

CELECOXIB (Celebrex)

Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme, induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus GI toxicity may be decreased. Seek lowest dose of celecoxib for each patient.

Adult: 200 mg/d PO qd; alternatively, 100 mg PO bid.