Anterior Glenohumeral Instability

Anterior Glenohumeral Instability

Background

The shoulder is the most commonly dislocated joint in the body. When shoulder dislocation occurs in adolescents and children, it has the worst natural history of any injury; the rate of recurrence in later years is at least 70%. As many as 95% of shoulder dislocations are anterior. Anterior dislocations often lead to recurrent anterior glenohumeral instability. Recurrent anterior glenohumeral instability accounts for the largest portion of the shoulder laxity spectrum. Excessive deviation of the humeral head on the glenoid occurs in all or 1 of 3 directions: anterior, posterior, or inferior. Although certainly not life threatening, recurrent subluxation or dislocation is clearly lifestyle threatening and can effectively disable an otherwise active individual.

See the images below.

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Upper - Type I superior labrum anterior posterior lesion. Lower - Type II superior labrum anterior posterior lesion.

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Upper - Type III superior labrum anterior posterior lesion. Lower - Type IV superior labrum anterior posterior lesion.

Normal shoulders have a certain degree of laxity due to minimal bony restraint of the joint, which in turn allows the widest range of motion of any joint in the body. The result is a tremendous need for competent soft-tissue balance and control. Traumatic damage leads to laxity in the soft-tissue and bony restraints; thus, recurrent subluxation and dislocation ensues. Atraumatic etiologies also exist, but this article focuses on recurrent subluxation and dislocation due to trauma.

Nonoperative and operative therapies both play a role in treatment of anterior shoulder instability. Both have been studied extensively. Surgical management has gone through an evolutionary process involving multiple methods of fixation. This evolution has led to operative fixation that achieves a stable repair with little restriction of motion.

For patient education resources, see the Breaks, Fractures, and Dislocations Center, as well as Shoulder Dislocation.

History of the Procedure

Reports of anterior glenohumeral instability and its many repair methods date back to Hippocrates' treatise, "On Joints." Hippocrates described the practice of using cautery to cause the capsule to scar and thus tighten around the joint. He wrote, "grasp the skin at the armpit between the fingers and draw it in the direction towards which the head of the humerus gets dislocated, then pass the cautery right through the skin thus drawn away."

Since Hippocrates' description of capsule repair, a multitude of new techniques have been reported, all aimed at preventing recurrent dislocation or subluxation. These repairs can be divided into anatomic and nonanatomic. Anatomic repairs focus on repairing the structure that has been disrupted. With nonanatomic repairs (eg, Putti-Platt, Magnuson-Stack, and Bristow procedures), an attempt is made to shorten or tighten certain anterior structures regardless of the specific shoulder pathology.

Early in the evolution of capsular repair, loss of motion was considered acceptable and even desired as a necessary part of stabilizing a shoulder. As new techniques followed, shoulder stability was achieved without significant loss of motion. Postoperative motion restriction is now considered a complication.

In 1923, Bankart described the lesion of traumatic shoulder dislocation in theBritish Medical Journal, as follows: "The essential lesion is the detachment of the capsule from the fibro-cartilaginous glenoid ligament." He goes on to say, "... the only rational treatment is to reattach the fibrous capsule to the glenoid ligament whence it has been torn."

In 1965, du Toit and Roux reported a similar procedure in which staples were used to attach the capsule to the anterior glenoid rim. This method had the potential to simplify the procedure, but it also added complications, such as glenoid damage from the staples and loosening.

The Magnuson-Stack procedure was described next, in 1943. This procedure involves transferring the subscapularis from its attachment on the lesser tuberosity to a point lateral to the bicipital groove. The goal was to produce a sling effect on the humeral head. Like the Putti-Platt procedure that would follow, it decreased external rotation by design.

In 1948, the Putti-Platt procedure was described. Here, the subscapularis tendon and capsule are divided longitudinally at the mid portion. The lateral free end is attached to the anterior rim of the glenoid, and the medial free end is attached over the lateral end. The Putti-Platt operation led to low dislocation recurrence rates, but it also led to decreased external rotation.

In 1954, Latarjet proposed the Bristow procedure. This procedure was later popularized by Helfet, in 1958. This involved transferring the tip of the coracoid process with its muscular attachments. A vertical slit in the subscapularis allowed the osteotomized coracoid to be attached to the anterior glenoid with sutures. This procedure thus provided a bony block to anterior glenohumeral translation.

Problem

The term anterior glenohumeral instability describes the shoulder in which soft-tissue or bony insult allows the humeral head to sublux or dislocate from the glenoid fossa. Function of these shoulders is compromised. Patients typically experience apprehension, recurrent subluxations, and frank dislocations. This pathology limits many activities, including overhead arm motions, external rotation, and, thus, physical or athletic activities.

Epidemiology

Frequency

In studies of anterior glenohumeral instability, a wide array of incidences have been proposed. Most report an average age of initial shoulder dislocation early in the third decade of life. The vast majority, 85-95%, of these are anterior dislocations. One fourth of all patients with dislocations present with a family history of the same problem. Rowe's 1956 analysis of 500 shoulder dislocations found only 8 occurred in children younger than 10 years; the largest cohort of dislocations occurred in the subsequent decade of life, in patients aged 10-20 years.

The age at the time of dislocation is the biggest determinant of future recurrence. Recurrences result from anterior glenohumeral instability and occur most commonly in patients younger than 20 years. Reported recurrence rates in patients younger than 20 years vary from 70-100%.

Etiology

The cause of anterior glenohumeral instability can be traumatic or atraumatic. Either mechanism leads to the loss of balance in the surrounding muscular and capsular structures.

Traumatic injury to any one component of the shoulder soft tissue leads to instability. This traumatic insult most commonly comes in the form of an anterior shoulder dislocation.

Atraumatic causes leading to multidirectional instability are not the focus of this article. These causes include repetitive atraumatic injury, Ehlers-Danlos syndrome, Marfan syndrome, congenital absence of the glenoid, deformities of the proximal humerus, and emotional and psychiatric instability.

Pathophysiology

In an unstable shoulder, many findings are possible. Each finding can occur alone or in combination with other lesions. These lesions include the Bankart lesion (in 85% of cases), Hill-Sachs lesion (in 77% of cases), anterior glenoid rim damage (in 73% of cases), capsular redundancy, subscapularis deficiency, and glenoid fossa deficiency. Absence of pathological findings is also possible.

In 1923, Bankart described the "essential lesion" in posttraumatic anterior glenohumeral instability as the detachment of the capsule from the fibrocartilaginous glenoid ligament. In this lesion, the humeral head translates forward, shearing the inferior glenohumeral ligament (IGHL) with the anteroinferior labrum from the glenoid rim.

Rowe's review of 28 patients in which he examined shoulder pathology after traumatic anterior dislocation disputed Bankart's claim to the essential lesion. Rowe's results showed "there was no evidence that there is a single essential lesion responsible for the recurrent dislocations of the shoulder." The Bankart lesions occurred in 27-100% of cases.

Other lesions were just as variable. Subscapularis laxity ranged from being present in every case to not being present in any cases. Hill-Sachs lesions were present in 26-100% of cases. Anterior glenoid trauma of all variations occurred in 2-52% of cases.

The next logical question is which of these lesions actually causes the recurrent instability observed after traumatic dislocations. This remains a debated topic. The most accurate conclusion is the one Rowe came to in 1978 when he declared that no single lesion is responsible for the recurrent dislocations of the traumatized shoulder.

Several lesions have been suggested. Baker et al devised a system of classification for the Perthes-Bankart lesion, as follows:

                     Type I - Pure capsular lesion

                     Type II - Partial labral detachment

                     Type III - Complete detachment of the inferior glenohumeral-labral complex

Other lesions include attenuation of capsule and capsular ligaments, Hill-Sachs lesions, attenuation of the subscapularis, and humeral avulsion of the IGHL.

Presentation

Children presenting with a dislocated shoulder may relate a couple of possible mechanisms. These mechanisms occur in a number of ways and are similar to those in adults. Most commonly, the child falls on the outstretched hand, forcing the arm into abduction and external rotation, levering the humeral head out of the glenoid cavity. Activities promoting this injury include contact sports, falls from heights, fights, and motor vehicle accidents. Other mechanisms have been described, including elevation with external rotation and direct blows.

A history of prior dislocations suggests a high likelihood of anterior glenohumeral instability. Studies have shown a 70-100% recurrence rate in various population groups of patients younger than 20 years.

As with physical examinations of any joint, beginning by observing the shoulder is important. Note any atrophy of the biceps, supraspinatus, or infraspinatus. Gross deformities can also suggest the direction of a dislocation.

Range of motion of the shoulder must be tested for restriction or hypermobility. Atraumatic instability generally manifests with hypermobility of the shoulder, whereas traumatic instability typically results in bilaterally symmetric motion. Generalized joint laxity is demonstrated by extending the elbow, wrist, metacarpal-phalangeal, and distal interphalangeal joints. External rotation can be increased as much as 28 or decreased as much as 14 after dislocation.

Next, the examiner manually assesses translation of the humeral head in the glenoid fossa. The humeral head is grasped in one hand, and the clavicle and scapula are stabilized in the other as the examiner pushes anteriorly and posteriorly. This is known as a shoulder drawer sign. Compared with the unaffected shoulder, the affected shoulder often demonstrates increased laxity. Remember that as much as 50% of posterior translation may be normal.

A sulcus sign is demonstrated by pulling inferiorly on the relaxed shoulder. A sulcus observed between the acromion and proximal humeral head is considered a positive finding. This finding indicates that the shoulder has multidirectional instability.

The key finding in anterior glenohumeral instability is a positive apprehension test. The arm is placed in abduction, extension, and external rotation while stressing it in anterior translation. If the patient becomes apprehensive and reports pain, this is considered a positive finding.

The relocation test involves placing the shoulder in the position of apprehension and applying a posteriorly directed force on the humeral head. The result is considered positive if this relieves the patient's apprehension.

Impingement signs must also be evaluated because as many as 10% of patients experience impingement after dislocation. Evaluate for the Hawkins sign and perform the Neer impingement test.

Indications

The indications for open surgical repair depend on the individual surgeon. Shoulders in which conservative therapy has failed or any shoulder rendered unstable may undergo open repair.

Frequently, classifying patients into one of two categories helps to determine treatment. Young patients with heavy physical demands may forego conservative therapy and proceed to immediate surgical repair. This recommendation is based on the high recurrence rate and the patient's desire to return to activity.

In contrast, older patients who are less physically demanding may try conservative therapy prior to assuming the risks of surgical repair. These patients have a lower likelihood of recurrence and may only require conservative therapy.

Surgery is also indicated if the patient is symptomatic with activities of daily living or if overhead stability is specifically needed. The patient must understand that overhead stability cannot be guaranteed.

Relevant Anatomy

The shoulder joint is a simple structure that provides complex function. It is the most mobile joint of the body, and it is also the joint that is most frequently dislocated. The gross anatomy consists of 3 main components: musculature, capsule/ligaments, and bone.

Capsuloligamentous structures provide the primary stabilization for the joint. The capsule of the shoulder joint extends from the periphery of the glenoid around the articular surface of the proximal humerus. Within this capsule are 3 distinct thickenings that constitute the superior glenohumeral ligament (SGHL), middle glenohumeral ligament (MGHL), and IGHL.

The SGHL and MGHL attach proximally at the anterosuperior portion of the glenoid labrum. The proximal attachment of the SGHL has 2 origins, including the one at the apex of the labrum that is joined with the long head of the biceps brachii and a second origin at the base of the coracoid process. Distally, the SGHL attaches just superior to the lesser tuberosity at the edge of the articular surface. The MGHL inserts just medial to the lesser tuberosity.

The IGHL is the key stabilizer of the shoulder, preventing anterior glenohumeral instability. The IGHL attaches proximally to the anterior, inferior, and posterior margins of the glenoid labrum. Distally, it attaches to the inferior margin of the anatomic neck of the humerus.

Together, the glenohumeral ligaments function to limit lateral rotation of the shoulder. Each of the 3 ligaments is relied upon for stability, depending on the position of the arm. In 1910, Delorme found that the MGHL tightens as the arm is externally rotated or dorsally flexed. If the arm is then abducted, the IGHL becomes the primary stabilizer, with the upper fibers tight at slight abduction and the whole ligament tightening at about 45 of abduction.

The secondary stabilizers of the shoulder joint are the surrounding musculature. This consists of the rotator cuff muscles. The supraspinatus, infraspinatus, teres minor, and subscapularis are intimately associated with the capsule. These muscles provide dynamic secondary stabilization. Conservative therapy focuses on strengthening the rotator cuff muscles to prevent recurrent dislocation.

The subscapularis is the most important contributor of the rotator cuff muscles to anterior shoulder stability. With the arm adducted, it tightens with external rotation. Cutting it results in 15-20 of increased external rotation. At 45 of abduction, the subscapularis becomes taught over the anterior joint surface and ascends so its inferior margin lies at the inferior margin of the glenoid. External rotation raises it even further and makes it more taught. Finally, at 90 of abduction, the inferior portion of the subscapularis no longer covers the inferior humeral head. It continues to provide anterior stabilization by remaining taught.

The glenoid fossa provides a shallow socket in which the humeral head articulates. It is composed of the bony glenoid and the glenoid labrum.

The labrum is comparable to the menisci of the knee. It is a fibrocartilaginous structure surrounding the periphery of the glenoid. Like the menisci of the knee, it is flexible but constant; when torn, it generally does not heal. The stability of the glenohumeral joint is greatly increased by the labrum, which provides a 50% increase in the depth of the concavity. The bony concavity measures approximately 2.5 mm and has been measured at 5.0 mm with an intact labrum.

In 1923, Bankart claimed that anterior inferior detachment of the labrum from the glenoid was the essential lesion in anterior glenohumeral instability. It has since been proven that this is true in most cases of instability but is not required for instability.

The labrum is closely related to the joint capsule and the glenohumeral ligaments. It is anchored to the bony rim of the glenoid and can be attached to the capsular structures as well.

Finally, understand the supporting musculature of the scapula that allows such a wide range of motion at the shoulder. A total of 16 muscles move and stabilize the scapula.

Contraindications

Surgical repair is relatively contraindicated in older patients with low physical demand, who have little chance of recurrence. Conservative therapy, including physical therapy to strengthen the rotator cuff, is indicated rather than exposing these patients to the risks of operation.

Patients who have been asymptomatic in their activities of daily living also need not be exposed to the risks of surgery. These patients are best monitored for any recurrent dislocations.

A certain contraindication exists in the case of multidirectional instability of the shoulder. In these atraumatic dislocations, patients are able to voluntarily dislocate and relocate their shoulder. Predisposing factors include psychiatric dislocations, laxity due to repetitive injury as occurs in competitive swimmers, and congenital collagen abnormalities such as Ehlers-Danlos syndrome and Marfan disease. The history and physical examination must be used to identify these patients.

If these patients are treated as patients with unidirectional dislocations, operative therapy will fail. The amount of inferior capsular redundancy in multidirectional instability requires an operative procedure addressing the possibility of future inferior instability.

 

Rotator Cuff Pathology

Background

The first description of rupture of the rotator cuff tendon was by Smith in 1834. With history, degenerative changes of the rotator cuff have been better characterized by Duplay, Von Meyer, Codman, and Neer. The exact mechanisms leading to the degeneration of the rotator cuff, however, are still being debated.

Frequency

Shoulder pain is the third most common cause of musculoskeletal disorders (MSDs) after low back pain and cervical pain. Estimates of the cumulative annual incidence of shoulder disorders vary from 7-25% in the Western general population. The annual incidence is estimated at 10 cases per 1000 population, peaking at 25 cases per 1000 population in persons aged 42-46 years. In persons aged 70 years or older, 21% of persons have shoulder symptoms, most of which were attributed to the rotator cuff. In cadaver studies, the rate of full thickness tears varies from 18-26%. The rate of partial thickness tears varies from 32-37% after age 40 years. Before age 40 years, tears are rare. In magnetic resonance imaging (MRI) studies, tears have been observed in 34% of asymptomatic individuals of any age. After age 60 years, 26% of patients have partial thickness tears, and 28% demonstrate full-thickness tears.

Morbidity and mortality

As mentioned, shoulder pain is the third most common cause of MSDs 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. MSDs 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.

Webster and Snook estimated that the mean compensation cost per case of upper extremity work-related MSDs was $8070 in 1993; the total US compensable cost for upper extremity, work-related MSDs was $563 million in the 1993 workforce. The compensable cost is limited to the medical expenses and indemnity costs (lost wages). When other expenses (eg, full lost wages, lost production, cost of recruiting and training replacement workers, cost of rehabilitating the affected workers) are considered, the total cost to the national economy becomes much greater.[7]

The impact of rotator cuff disease on quality of life is even more difficult to assess than its cost. Further studies using valid methods such as the Medical Outcomes Study (MOS) 36-item short-form health survey (SF-36), which measure the impact of the disorder on general health, should help assess this issue.

Race, sex, and age

No known racial variation associated with rotator cuff disease is cited in the literature. In one study, a predominance of male patients (66%) seeking consultation for rotator disease is reported, but in other studies, the male-to-female ratio is 1:1. Rotator cuff disease is more common after age 40 years. The average age of onset is estimated at 55 years.

Anatomy

The rotator cuff, as shown in the image below, is composed of 4 musclesthe subscapularis, supraspinatus, infraspinatus, and teres minorand their musculotendinous attachments. The subscapularis muscle is innervated by the subscapular nerve and originates on the scapula. It inserts on the lesser tuberosity of the humerus. The supraspinatus and infraspinatus are both innervated by the suprascapular nerve, originate in the scapula, and insert on the greater tuberosity. The teres minor is innervated by the axillary nerve, originates on the scapula, and inserts on the greater tuberosity. The subacromial space lies underneath the acromion, the coracoid process, the acromioclavicular joint, and the coracoacromial ligament. A bursa in the subacromial space provides lubrication for the rotator cuff.

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Rotator cuff anatomy.

Functional anatomy

Understanding the functional anatomy of the rotator cuff assists in understanding its disorders. The rotator cuff is the dynamic stabilizer of the glenohumeral joint. The static stabilizers are the capsule and the labrum complex, including the glenohumeral ligaments. Although the rotator cuff muscles generate torque, they also depress the humeral head. The deltoid abducts the shoulder. Without an intact rotator cuff, particularly during the first 60 of humeral elevation, the unopposed deltoid would cause cephalad migration of the humeral head, with resulting subacromial impingement.

Recent studies

Piasecki et al found that arthroscopic-revision rotator cuff repair may be a reasonable treatment option even after previous open repairs, providing improved pain relief and shoulder function. In the 54 patients, studied, the American Shoulder and Elbow Surgeons scores improved from 43.8 5.7 to 68.1 7.2, and the Simple Shoulder Test improved from 3.56 0.8 to 7.5 1.1. Visual analog pain scale scores improved from 5.17 0.8 to 2.75 0.8 (P = .03), and forward elevation increased from 121.0º 12.3º to 136º 11.8º. The authors noted that female patients and those who had undergone more than 1 ipsilateral shoulder surgery had poorer results.[10]

De Jesus et al performed a meta-analysis study to compare the diagnostic accuracy of MRI, MR arthrography, and ultrasound in diagnosing rotator cuff tears. The literature showed that MR arthrography is the most sensitive and specific technique for diagnosing both full- and partial-thickness rotator cuff tears and that ultrasound and MRI are comparable in both sensitivity and specificity. Summary ROC (receiving operating characteristic) curves for MR arthrography, MRI, and ultrasound for all tears showed the area under the ROC curve is greatest for MR arthrography (0.935), followed by ultrasound (0.889) and then MRI (0.878); however, pairwise comparisons of these curves showed no significant differences between MRI and ultrasound (P >.05).

In a systematic review of the published literature, Nho et al compared single-row (SR) with double-row (DR) suture anchor fixation in arthroscopic rotator cuff repair. The authors found no clinical differences between the SR and DR suture anchor repair techniques. They concluded that the data in the published literature do not support the use of DR suture anchor fixation to improve clinical outcome, although they noted that there are some studies reporting that DR suture anchor fixation may improve tendon healing.

A meta-analysis, including 3 randomized controlled studies and 2 controlled clinical cohort studies, compared outcomes between single-row and double-row rotator cuff repair. The results found that while the double-row technique significantly increased operative time, it provided greater external rotation, improved tendon healing, and decreased recurrence rate. However, no significant differences were found between the 2 techniques with regard to shoulder function, muscle strength, forward flexion, internal rotation, patient satisfaction, or return to work.

One study analyzed the structural and functional outcomes after arthroscopic rotator cuff repair between single-, double-, and combined double-row/suture-bridge techniques. After an average follow-up of 38.5 months, the data noted that repair with combined double-row and suture-bridge technique resulted in an overall decreased retear rate, especially for large and massive tears. This combined technique proved to be an effective option for arthroscopic rotator cuff repair.

Schofer et al, in a prospective, randomized, controlled study, compared high-energy extracorporeal shock-wave therapy (ESWT) with low-energy ESWT in the treatment of rotator cuff tendinopathy. Patients in the high-energy group received 6000 impulses of ED+ 0.78 mJ/mm2 in 3 sessions, and patients in the low-energy group received 6000 impulses of ED+ 0.33 mJ/mm2. An increase in function and a reduction of pain were found in both groups (P < .001). Although the improvement in Constant score was greater in the high-energy group, statistical analysis showed no significant difference between the 2 groups regarding Constant score, pain reduction, and subjective improvement after 12 weeks and after 1-year follow-up.

Drake et al reviewed the use of reverse total shoulder arthroplasty (RTSA) in patients with rotator cuff disease. The authors found that modern RTSA designs restore deltoid tension and a functional fulcrum to the rotator cuff-deficient shoulder, allowing recovery of active shoulder elevation and restoring function. The authors noted that contraindications to RTSA include severely impaired deltoid function, an isolated supraspinatus tear, and the presence of full active shoulder elevation with a massive rotator cuff tear and arthritis. They concluded that for properly selected patients who have symptomatic and disabling rotator cuff deficiency, RTSA can result in life-changing improvements in pain, motion, function, and patient satisfaction.

Wellmann et al concluded that for patients with symptomatic and disabling rotator cuff deficiency, RTSA can result in a significant reduction in pain and improvements in motion and function.

Using propensity-matching methods, one study compared the outcomes of patients with pseudoparalytic large-to-massive tears with those of nonpseudoparalytic tears after rotator cuff repair and whether the presence of pseudoparalysis negatively affected the outcome. The study observed evidence of recovery from pseudoparalysis in a large portion of the study group; similar outcomes were noted in postoperative function and cuff healing, whether pseudoparalysis was present or not. Considering the possible complications from treatment with RTSA, the study authors suggest that rotator cuff repair should be the first-line treatment option for large-to-massive tears.

Data from one study noted that the failure rate after arthroscopic rotator cuff repair was significantly higher in patients with lower bone mineral density, a higher grade of fatty infiltration of the infraspinatus, and greater amount of retraction.

Pathology

Rotator cuff pathology can be caused by extrinsic (outside) or intrinsic (from within) causes. Extrinsic examples include a traumatic tear in tendons from a fall or accident. Overuse injuries from repetitive lifting, pushing, pulling, or throwing are also extrinsic in nature. Intrinsic factors include poor blood supply, normal attrition or degeneration with aging, and calcific invasion of tendons.

Rotator cuff tendinitis is the term used to describe irritation of tendons either from excessive pressure on the acromion or, less commonly, from intrinsic tendon pathology. Irritation of the adjacent bursa is known as subdeltoid or subacromial bursitis. Repetitive overhead activities resulting in irritation of tendons and bursae from repeated contact with the undersurface of the acromion is termed impingement syndrome.

Rotator cuff dysfunction is typically a continuum of pathology ranging from tendinitis and bursitis, to partial tearing, to a complete tearing in one or more of the tendons. Although the earlier stages may resolve with conservative care, actual tearing of the tendon can be more problematic. These tears most commonly occur at the tenoperiosteal (tendon-to-bone) junction. Because this area has a relatively poor blood supply, injury to the tendon at this location is very unlikely to actually heal. Additionally, the constant resting tension in the muscle-tendon unit, or muscle tone, pulls any detached fibers away from the bone, preventing their reattachment. Finally, joint fluid from within the shoulder may seep into the tear gap and prevent the normal healing processes from occurring.

Possible causes of rotator cuff pathology are as follows:

                     Outlet impingement

                     Subacromial spurs

                     Type 2 and type 3 acromions

                     Osteoarthritic spurs of the acromioclavicular joint (includes subacromial spurs)

                     Thickened or calcified coracoacromial ligament

                     Nonoutlet impingement

                     Loss of rotator cuff causing superior migration of the humerus (ie, tear, loss of strength)

                     Secondary impingement from an unstable shoulder

                     Acromial defects (os acromiale)

                     Anterior or posterior capsular contractures (ie, adhesive capsulitis)

                     Thick subacromial bursa

Diagnosis

Overview

Patients with rotator cuff pathology commonly present with an activity related dull ache in their upper lateral (outer) arm and shoulder. Activity is usually most difficult above shoulder level. Many people have little or no discomfort with below-shoulder-level activities such as golf, bowling, gardening, writing, or typing. Conversely, tennis, baseball/softball, basketball, swimming, and painting are more problematic.

History

A complete medical history should be obtained to direct the physical examination and make the correct diagnosis. Most of the time, the diagnosis can be made following a systematic history. Relevant history findings, treatments, and test results should complement the history of the present injury. Sometimes, relevant social and family histories are necessary.

Patients with degenerative rotator cuff disease are almost always older than 40 years. Fifty percent of patients have a progressive onset of shoulder pain, whereas the other 50% can identify a specific event responsible for the onset of pain. The evolution of rotator cuff disease is characterized by variable episodes of recurrence following more intensive shoulder activities, followed by remission with rest or treatment.

As the disease progresses, shoulder pain becomes more constant. Overhead and arm-length activities typically increase the pain. Discomfort and night pain can also be present. With time, the individual can notice some weakness during shoulder elevation. Crepitus can also be noted. With evolution of the disease, shoulder pain can be accompanied by cervical and mid-back pain.

The following questions should help the physician assess the patient:

                     What is the patient's age? Shoulder pain in young overhead athletes suggests underlying shoulder instability. 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? A fall on an outstretched arm could indicate a dislocation of the glenohumeral joint or a fracture of the humeral neck. Repetitive overhead motions can cause tendinitis and, in the long run, chronic degenerative changes. A fall or a trauma on the tip of the shoulder can result in an acromioclavicular sprain.

                     What was the onset? Insidious, slow onset may suggest tendinitis or osteoarthritis. Sudden onset is usually due to a trauma causing a fracture, dislocation, or a rotator cuff tear.

                     Where is the pain located? Pain located on the superior or lateral aspect of the shoulder suggests rotator cuff tendinitis. Pain on the anterior aspect of the shoulder may result from bicipital tendinitis, an acromioclavicular sprain, or anterior instability. Neck pain and radicular pain or paresthesias suggest a cervical spine disorder.

                     What is the severity of the pain? An acute burning pain could indicate an acute bursitis. An intermittent dull pain may be due to a degenerative rotator cuff disease.

                     What is the type of pain? Sharp, burning pain suggests a neurologic origin. Bone and tendon pain is deep, boring, and localized. Muscle pain is dull and aching, is not localized, and may be referred to other areas. Vascular pain is aching, cramplike, and poorly localized, and it may be referred to other areas.

                     What is the duration of the symptoms? Frozen shoulder has 3 stages that can last up to 3-4 years. Acute bursitis has a short-term evolution and responds well to nonsteroidal anti-inflammatory drugs (NSAIDs).

                     What is the timing of the pain? Predominantly night pain suggests frozen shoulder. Morning pain and stiffness improved by activity may be caused by a synovitis. Pain that increases with activity is usually the result of a rotator cuff tendinitis.

                     Which activities/positions increase the pain? Pain increased by overhead activities or arm-length activities suggests rotator cuff tendinitis. Pain increased when throwing is likely to be due to anterior instability. 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 paresthesia in the upper extremities? Neurologic symptoms are caused by a cervical radiculopathy or peripheral nerve entrapment/lesion.

                     Are the symptoms constant or intermittent? Intermittent symptoms usually result from soft-tissue or joint disorders. Constant symptoms suggest a neurologic lesion.

                     Is joint-motion restriction present? Passive and active joint restriction in all directions of range of motion (ROM) is caused by a frozen shoulder or glenohumeral synovitis. Restriction in internal rotation suggests an impingement syndrome due to rotator cuff tendinitis. The inability to perform active abduction suggests a rotator cuff tear or a frozen shoulder.

                     Is some crepitus noted? Crepitus is the result of degenerative rotator cuff changes. Crepitus is not a normal finding in the shoulder.

                     Have any changes in the color of the arm occurred? Color changes may be due to ischemia secondary to vascular insufficiency. Reflex sympathetic dystrophy (also termed complex regional pain syndrome, type 1) can cause skin-color changes.

                     Has the patient had any treatments such as 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?

                     Has the pain changed?

                     Has the pain spread or moved?

                     Has the pain subsided or increased? The last 3 questions help in deciding the appropriate treatment and management.

The importance of obtaining a systematic and detailed history cannot be overemphasized. Any attempt to shortcut the process leads to a nonfocused physical examination and an inaccurate diagnosis. Remember that a recent study assessing the interobserver agreement of a diagnostic classification of shoulder disorders based on history and physical examination showed only moderate agreement between experienced observers.

Physical Examination

A systematic examination of the shoulder region includes careful observation; palpation of the bones and soft tissues; assessment of passive and active ROM; and 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 is 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 remove the appropriate amount of clothing to facilitate proper assessment of the bone and soft tissues. The shoulder, cervical region, and entire upper extremity must be assessed. The examiner should assess bones and joints for possible asymmetry or deformities and should assess for soft-tissue changes (eg, swelling, erythema, white shiny skin, loss of hair, atrophy) suggestive of vasomotor abnormalities. 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.

Looking at bony contours, the examiner makes a general assessment. The dominant side may be lower than the nondominant one; the head and neck should be in the midline; the clavicle should be symmetric without any deformity of the acromioclavicular joint and sternoclavicular joint.

Each of these parts is then examined in more detail. Because of its superficial location, a fracture of the clavicle or a subluxation or dislocation of both ends is easy to identify. A step deformity of the acromioclavicular or sternoclavicular joint, with the clavicle side of the joint migrating superiorly, is due to a dislocation of these joints.

Observation of the soft tissues is directed first at the contours of the deltoid. The mass of the deltoid should be round, with the anterior and posterior aspects symmetric. Flattening of the muscle suggests atrophy of the deltoid and is usually due to a neurologic lesion such as an axillary nerve neuropathy, an upper trunk brachial plexopathy (Erb palsy), or a C5-6 radiculopathy. An anterior dislocation of the glenohumeral joint produces flattening of the deltoid with bulging of the anterior aspect of the muscle due to the dislocated head of the humerus, with the patient holding the shoulder in slight adduction and across the trunk. A bulge observed in the middle third of the belly of the biceps when the elbow is flexed suggests rupture of the long head of the biceps tendon.

The side view allows the examiner to assess thoracic spine kyphosis, which is indicated by a protraction of the head or the shoulders. Deltoid atrophy also can be observed.

Looking at bony contours, the examiner seeks evidence of a scoliosis of the thoracolumbar spine and then observes the scapulae. Each scapula extends from the spinous process of T2 (superomedial angle) to the spinous process of T7 (inferomedial angle). The scapulae should be at the same height and at the same distance from the spine. The examiner should check for a winging of the scapula (ie, a displacement of the medial side of the scapula away from the thorax). When the winging is present with medial displacement of the scapula toward the spine, a serratus anterior muscle palsy is suggested. This palsy usually is due to a long thoracic nerve injury. When the winging is noted with lateral displacement of the scapula, a trapezius muscle palsy or, more rarely, a rhomboid muscle palsy must be suspected.

A trapezius muscle palsy can be due to a spinal accessory nerve (cranial nerve XI) injury, and a rhomboid muscle palsy can be due to a dorsal scapular nerve injury. A prominent spine of the scapula may be due to a supraspinatus and infraspinatus muscle atrophy caused by a suprascapular nerve injury in the suprascapular notch or a rotator cuff tear.

Observation of the soft tissues is directed at the posterior aspect of the deltoid muscle. The trapezius muscle is then observed. Atrophy resulting from palsy of the muscle has been discussed previously. Because the rhomboid is overlapped by the trapezius, atrophy of the rhomboids is more difficult to assess.

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

Beginning with the anterior structures, the examiner palpates the sternoclavicular joint. Superior migration of the medial end of the clavicle is palpated if the joint is dislocated. The examiner must remember that the clavicle is superior to the manubrium. Always compare the affected side with the contralateral side. The sternocleidomastoid muscle also must be palpated, looking for tension and spasms. The muscle contracts to turn the head on the contralateral side. The muscle is easier to identify and palpate in this position. The sternal and clavicular heads of the muscle must be palpated. Hands can be moved medially to palpate the suprasternal notch. The first rib, the costochondral joints, and the sternum also should be assessed.

The clavicle should be palpated along its whole length, looking for bumps (suggesting callus formation resulting from fracture), loss of continuity, and crepitus. The acromioclavicular joint is a common site of pain and must be palpated with care. Because the acromioclavicular joint is a superficial joint, swelling, synovial thickening, and/or crepitus can be palpated. Step deformities with superior migration of the lateral end of the clavicle, seen in dislocation or subluxation, are easily palpable.

The coracoid process can be palpated approximately 2.5 cm (1 in) inferior and just medial to the acromioclavicular joint. The coracoid process is the site of origin of the short head of the biceps tendon, the coracobrachialis muscle, and the insertion of the pectoralis minor. The pectoralis major and minor also must be palpated. Muscle tension and spasms are commonly associated with shoulder disorders.

The acromion and subacromial space are palpated. The subacromiodeltoid bursa can be palpated indirectly in the subacromial space. Because it is overlapped by the deltoid muscle, the bursa cannot be felt under the fingers; however, the examiner, through pressure on the deltoid muscle, applies indirect pressure on the inflamed bursa, causing pain.

The examiner follows by palpating the greater tuberosity, the long head of the biceps tendon, and the lesser tuberosity. These structures can be identified easily in a lean patient by an experienced examiner. This identification may be more difficult in an overweight patient or one with abundant muscle mass. By rotating the shoulder medially (eg, by putting the dorsal aspect of the hand on the buttock), the examiner can feel the greater tuberosity on the anterior aspect of the shoulder, just inferior to the acromion. The supraspinatus, infraspinatus, and teres minor tendons all insert into this structure and, when inflamed, can produce pain upon palpation of the greater tuberosity.

Keeping the fingers on the greater tuberosity, the examiner rotates the shoulder laterally. The fingers feel the bicipital groove where the long head of the biceps tendon can be palpated. Pain or thickening of the tendon sheet indicates an inflamed tendon, whereas its absence suggests a rupture or dislocation. By rotating the shoulder more laterally, the examiner can palpate the lesser tuberosity. The tendon of the subscapularis inserts on that structure, and when it is inflamed, the tendon is painful to palpation. With the shoulder back to a neutral position, extension of the shoulder allows palpation of the subacromiodeltoid bursae under the anterior edge of the acromion.

All of these structures must be palpated gently because they may be tender. Any painful palpation must be compared with the contralateral shoulder. A positive finding is when pain is more significant on the affected side than on the contralateral shoulder. Any excessive pain caused by a vigorous palpation makes the examination less sensitive.

The biceps muscle should be palpated, looking for any bulging that indicates a long head of the biceps tendon rupture. The deltoid muscle also must be palpated to look for painful spasm or tension. Tone and atrophy also are assessed.

The examination is continued by palpation of the posterior structures. Bony structures can be rapidly assessed because they are rarely a source of pain. The spine of the scapula is palpated, followed by palpation of the superior medial angle of the scapula. The levator scapulae muscle that inserts on this angle is a common site of pain. The medial border of the scapula is then palpated from the superior to the inferior medial angle. The bony palpation is completed by palpation of the spinous processes of the dorsal and cervical spine.

Because muscle spasm and tension are frequently associated with a rotator cuff disease, the posterior muscles must be palpated with care to identify and treat those muscles. The superior trapezius is commonly tense and painful and must be palpated from its cervical and occipital origin to its insertion on the spine of the scapula and the acromion. Under this muscle, lying in the supraspinatus fossa, the supraspinatus muscle also should be palpated.

The rhomboid muscles, from C7 to T5, run downward to attach on the medial border of the scapula. These muscles, often a source of pain, are difficult to distinguish from the overlying middle trapezius muscle. The rhomboid muscles can be identified by asking the patient to put his or her hand behind the back, with the shoulder internally rotated and the elbow flexed, and to push posteriorly against a resistance. The muscle belly of the rhomboid muscles then becomes palpable. Muscle palpation is completed by assessing the infraspinatus, teres major and minor, and latissimus dorsi muscles.

Range of motion

Both active and passive ROM must be evaluated. Although some authors suggest that an assessment of passive ROM is not necessary if the patient is able to perform 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 ROM.

Movements (with the normal ranges provided) that should be assessed are abduction (70-180), adduction (30-45), flexion (160-180), extension (45-50), external rotation (80-90), and 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 at 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 trapezius or rhomboid muscle weakness. Active flexion is also evaluated. In the presence of a subacromial impingement syndrome, this movement can also be painful. Active flexion may elicit a winging of the scapula caused by a serratus anterior weakness.

Other motions can be evaluated through a combination of active movements. The Apley scratch test is probably the most well known. This test combines internal rotation and adduction of one shoulder with external rotation and abduction of the other.

The evaluation for passive ROM 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).

The same procedure can be used to evaluate full flexion that combines scapulothoracic and glenohumeral motion and flexion performed selectively by the glenohumeral joint. This maneuver is followed by an evaluation of adduction. The external rotation is tested with the elbow held close to the waist and flexed at 90. Then, the arm is rotated externally. The examination is followed by an evaluation of the extension and an assessment of the internal rotation. The full range of internal rotation is achieved with the forearm passing behind the trunk with the shoulder slightly extended.

Impingement tests

Positive impingement tests result from the reproduction of impingement of the rotator cuff tendon by different provocative maneuvers.[25] With anterosuperior impingement syndrome, the impingement occurs underneath the coracoacromial arch. With posterosuperior impingement syndrome, the impingement is on the posterosuperior border of the glenoid cavity. Finally, with anterointernal impingement syndrome, the impingement occurs in the subcoracoid space or in the coracohumeral interval.

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

A of cadaveric shoulders has shown that some provocative impingement testsnamely, the Neer and Hawkins-Kennedy testsappear to elicit contact consistent with impingement.

The Neer impingement test is described as follows:

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

                     When the result is positive, this test produces pain caused by 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.

                     A positive test result suggests an anterosuperior impingement syndrome. The sensitivity of this test, assessed based on operatively observed anatomic lesions, is 89%.

The Hawkins-Kennedy test is described as follows:

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

                     When the result is positive, this test produces pain caused by contact of the bursal side of the rotator cuff on the coracoacromial ligament and by contact between the articular surface of the tendon and the anterosuperior glenoid rim. Contact between the subscapularis tendon and the coracoid process is also observed.

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

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

                     The sensitivity of this test is 87%.

The Yocum test is described as follows:

                     With the examiner standing behind the patient, the hand on the ipsilateral side of the examined shoulder is placed on the contralateral shoulder. The elevation of the elbow is resisted by the examiner.

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

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

The posterior impingement test is described as follows:

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

                     When the result is positive, this test produces pain in the posterior aspect of the shoulder caused by impingement of the articular side of the cuff tendon between the greater tuberosity and the posterosuperior glenoid rim and labrum. Relocation of the humeral head, performed by applying a posteriorly directed force to the humeral head, causes a reduction in pain.

                     The sensitivity of this test is 90%.

Topographic tests

Using resisted isometric contraction of specific muscles of the rotator cuff, the location of the tendon lesion causing the impingement can be identified.

To identify the supraspinatus tendon, use the Jobe test or the full-can test.

In the 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 result is considered positive if pain is noted. When compared with surgical observations, the sensitivity of this test is 86% and the 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 true 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, as if someone is holding a full can right-side-up). Shoulder elevation is resisted. The test result is considered positive if it produces pain. Electromyography (EMG) studies show that this test results in the greatest supraspinatus activation with the least activation from the infraspinatus.

To identify the infraspinatus tendon, use the infraspinatus isolation test or, less optimally, the Patte test.

In the 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 result is considered positive if it produces pain. EMG shows this to be the optimal infraspinatus isolation test.

In the Patte test, the shoulder is placed at 90 of abduction, in 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 result is considered 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 result is positive if the patient is unable to maintain the shoulder in external rotation, suggesting a full tear of the external rotators.

To identify the teres minor tendon, use the same tests used for the infraspinatus tendon. No specific teres minor isolation tests have been developed.

To identify the subscapular tendon, use the Gerber lift-off test or the Gerber push-with-force test.

In 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 result 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 the subscapularis is fully torn.

In the Gerber push-with-force test, the shoulder is placed in the same position as the lift-off test; however, the patient must keep the hand away from the back and must resist 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.

To identify the long head of the biceps tendon, use the Speed palm-up test.

In 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 result is positive if the maneuver 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, is technically difficult and ineffective; therefore, it is not described. Generally, the topographic tests are sensitive but not specific, except for the Gerber lift-off test. The combination of impingement tests and topographic tests helps determine whether a patient's symptoms are caused by rotator cuff disease. As mentioned, 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 all.

Imaging Studies

A wide variety of radiologic 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 and to 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

Plain films are not very specific or sensitive for rotator cuff disease, but they remain the first examination to perform. Radiographs are used for 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 with by other modalities. This is the most useful test in trauma situations or to assess chronic complete tears. In the last stage of complete chronic rotator cuff tear, it could be the only imaging modality needed to confirm the diagnosis (see the image below).

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In this patient's shoulder radiography, the humeral head no longer matches up with the glenoid because the rotator cuff is torn and the strong deltoid muscle is pulling the head superiorly toward the acromion. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.

Plain films are acquired routinely in 3 planes (ie, neutral, internal, external rotation).

Arthrography

The main indication of arthrography is to identify complete rotator cuff tears and intra-articular infiltration of the corticoid. As a diagnostic tool, it is combined generally with CT arthrography scanning.

Arthrography is performed by injecting iodine contrast medium, air, or both into the glenohumeral joint. From 8-12 mL of contrast (or 3-4 mL of contrast and 10-12 mL of air) is 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.

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This image depicts the channel between the articular capsule and the subacromial-subdeltoid bursa in a complete rotator cuff tear. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.

 

In the presence of a complete tear, the contrast floods from the glenohumeral joint into the subacromial-subdeltoid bursa (see the images below).

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Even if the channel cannot be always identified, the presence of contrast medium in the subdeltoid-subacromial bursa signals the presence of a complete rotator cuff tear. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.

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CT-arthrography of the shoulder in the axial plane. Note the presence of air and contrast in the subacromial-subdeltoid bursa. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.

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 in a complete tear. Intratendon tears and tears on the superior aspect of the tendon (bursal side) are not visualized with this technique. Arthrography can also 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

This study, although very accurate (100% sensitivity, 100% specificity) in depicting complete rotator cuff tears, is limited in the evaluation of tendinitis and partial tears, for which its sensitivity drops to 17-43%. On the other hand, this test yields more information than arthrography regarding 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.

CT arthrography is performed exactly like a double-contrast (air and iodine contrast) arthrography but is followed by tomodensitometry imaging (CT scanning). 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 scanning technology, it has become easy to reformat images in multiple planes.

The semiologic signs of rotator cuff tears are essentially the same as seen with conventional arthrography. The presence of contrast in the subacromial-subdeltoid space confirms the diagnosis of complete rotator cuff tears (see images below). The contrast can also 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 are also well depicted.

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CT-arthrography of the shoulder in the axial plane. Note the presence of air and contrast in the subacromial-subdeltoid bursa. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.

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CT-arthrography of the shoulder in the axial plane. Note the presence of air and contrast in the subacromial-subdeltoid bursa. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.

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, can also be diagnosed. Finally, the shape of the acromion can be evaluated on the oblique sagittal reformatted study, which requires a special acquisition.

Magnetic resonance imaging (Arthrography)

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 and of all the soft tissues about the shoulder and in any plane desirable. With this imaging modality, the full continuum of rotator cuff disease, from simple tendinosis to complete tears, can be diagnosed. MRI is much more powerful than the previous modalities when used to identify partial tears, and it also can identify intratendon tears or tears on the bursal aspect of the tendon. As with CT scanning and plain radiography, the bone structures resulting or contributing to the impingement syndrome can be evaluated.

MRI can also yield information about retraction of the muscle, atrophy, bursitis, and bone marrow abnormalities (eg, edema, contusion), which all are associated findings of 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.

This technique takes advantage of the properties of hydrogen protons submitted to a magnetic field and radiofrequency waves. Therefore, the patient is not subjected to radiation exposure. 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 (intravenous or intra-articular) can be added if necessary.

MRI shows great detail of the anatomy in multiple plans. MRI also allows better visualization of the nature of a structure or an anomaly (ie, 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 (see image below).

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Full-thickness tear of the supraspinatus as seen as a hyperintensity line through the full thickness of the tendon in a flash 2-dimensional MRI sequence in coronal oblique plane. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.

Tendinitis is recognized as a gray signal in the tendon. Finally, calcification and cortical bone appear hypointense in all sequences (see image below).


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Calcifications are seen as hypointense foci in flash 2-dimensional images. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.

MRI arthrography is the gold standard as an imaging modality for diagnosis of a rotator cuff tear. It follows the same principle as CT arthrography. This modality can help identify labral tears (see image below) and glenohumeral tears.

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MRI arthrography can help to identify labral tears, as seen in this image. The contrast medium penetrates between the labrum and the articular surface. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.

The size and morphologic features of rotator cuff tears may influence treatment selection and affect final outcomes. Magnetic resonance arthrography allows observation of these features and other intra-articular structures. In one series, Toyoda and colleagues compared MRI with MRI arthrography. To assess the utility of magnetic resonance imaging in assessing size and morphologic features, the authors did a retrospective analysis of 41 shoulders in 37 consecutive surgically treated patients (mean age, 63.2 years) who had MRI followed by magnetic resonance arthrography. The maximum rotator cuff defect size in the anteroposterior direction defined transverse size, and the maximum rotator cuff defect size in the mediolateral direction defined longitudinal size. Sensitivity for detecting full-thickness rotator cuff tears by MRI was 90.2%, compared with 100% for magnetic resonance arthrography.

Magnetic resonance arthrography also allowed morphologic classification of the torn tendon as blunt end, tapering end, indistinct end, horizontal tear, and global tear. There was good agreement in classifying torn edges: the imaging findings agreed with findings at surgery. Magnetic resonance arthrography was more accurate in evaluating both rotator cuff tear size and morphologic features than MRI.

With the aid of fat-suppressed imaging, full thickness and partial cuff tears can be identified with 100% sensitivity and specificity. Fat-suppressed images also showed intratendinous contrast material imbibition in 3 torn cuffs with frayed, friable tendon margins. Fat suppression in MR arthrography is valuable in the differentiation between partial and full-thickness cuff tears and in the detection of small partial tears of the inferior tendon surface.

Ultrasonography

Ultrasound 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. Ultrasound 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 because sound does not penetrate bone very well.

With ultrasound, the normal tendon is an echoic structure, whereas the cartilage and fluids are hypoechoic. All of the tendons, bony landmarks (eg, humerus, greater tuberosity), and intra-articular or intrabursal effusions are easily recognized. 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, because 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 (see image below). 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.

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Ultrasound is another modality to demonstrate a complete rotator cuff tear, as seen here with a gap of more than 2 cm between both extremities of the torn tendon. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.

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 ultrasound 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.

Nuclear medicine imaging

Bone scintigraphy is not used routinely in rotator cuff disease imaging.

Treatment & Management

Conservative Therapies

Physical therapy can be a useful adjunct in the conservative treatment of patients with degenerative rotator cuffs. Although numerous studies have been performed on conservative treatment and surgical approaches of the painful shoulder and, more specifically, the rotator cuff, the conclusion of a review of randomized, controlled trials of interventions for painful shoulder was that little evidence supports or refutes the efficacy of common interventions for shoulder pain.

Drawing firm conclusions about the efficacy of any of these interventions remains difficult because of, among other reasons, the 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. In their approach to conservative patient treatment, clinicians must be critical and try to use an evidence-based medicine approach as much as possible. The clinician must also use a combination of experience and intuition to compensate for the lack of scientific evidence supporting the different therapeutic modalities.

Conservative treatment of the degenerative rotator cuff involves pain relief; avoidance of painful motions and activities; simple analgesics and NSAIDs; manual physical therapy for the glenohumeral, scapulothoracic, acromioclavicular, and sternoclavicular joints and the parascapular and scapula-stabilizer muscles; subacromial corticosteroid injection; bupivacaine suprascapular nerve block; restoration of motion and normal scapulohumeral rhythm; stretching of the glenohumeral capsule and muscles; and manual therapy of the cervicodorsal spine (often necessary because of its close relationship with the shoulder).

Ultrasound

Ebenbichler showed in a randomized, doubled-blind, placebo-controlled study that the use of a pulsed ultrasound performed 5 times a week for 15 minutes (0.89 MHz frequency, 2.5 W/cm2, pulsed mode 1:4) significantly resolves calcification of the shoulder, decreases pain, and improves the short-term quality of life.[37, 38]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 ultrasound is only significantly effective in the short term. The short-term efficacy of ultrasound therapy has been demonstrated only in calcifying tendinitis. Its efficacy in other shoulder disorders has not been shown.

Extracorporeal shockwave therapy

Another modality that looks promising is extracorporeal shockwave therapy. Passing a strong electric current through a flat coil induces a magnetic field and generates shock waves. Shock waves were used first for the treatment of delayed union and nonunion of fractures by stimulating osteogenesis.

In an uncontrolled study, shockwave 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 prospective, randomized, controlled study using a valid functional shoulder scale showed the efficacy of extracorporeal shockwave therapy. At 3-6 months, significant improvement occurred in pain and function. At 6 months, calcium deposits disappeared or disintegrated in up to 77% of patients' radiographs. Comparing different regimens of shockwaves, the authors concluded that the improvement in pain and function and the radiologic disintegration of calcification were dose-dependent.

Extracorporeal shockwave therapy appears to be a promising treatment for calcifying tendinitis. Similar to ultrasound, its efficacy in other shoulder conditions has not been established.

Iontophoresis

Randomized, controlled studies have shown the efficacy of topical steroids, NSAIDs, and acetic acid iontophoresis, as compared with placebo, in different MSDs; however, the studies were not specifically on rotator cuff disease. Moreover, a recent trial did not show any difference in outcomes between no treatment and treatment with acetic acid iontophoresis followed immediately by 9 sessions of ultrasound therapy in a constant mode (0.8 W/cm2 at a frequency of 1 MHz for 5 min) 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, no conclusions can be made regarding the efficacy of iontophoresis in the treatment of rotator cuff disease.

Subacromial corticosteroid injection

As with NSAID therapy, many of the studies on the efficacy of corticosteroid injection for various shoulder conditions are of poor methodological quality. Green, van Der Heijden, and Sibilia performed a systematic review of all the randomized clinical trials on corticosteroid injection. Although the trials selected were essentially the same in the 3 studies, their conclusions differ because of the different assessment methods. Two of these articles suggested that corticosteroid injection may be superior to placebo in the short-term treatment of rotator cuff tendinitis, whereas one suggested that no conclusive evidence was found regarding the efficacy of corticosteroid injection.

Subacromial corticosteroid and local anesthetic agent injection also appear to be more effective than an injection of a local anesthetic alone, although some authors disagree. Corticosteroid injection also appears to be significantly more effective than NSAIDs. Therefore, subacromial corticosteroid injection appears indicated when pain persists after simple analgesics and NSAIDs have been used.

Because some authors have reported poorer surgical outcome in patients who have had 3 or more corticosteroid injections, the recommendation is that no more than 2 injections be given. No trials have compared the different routes of corticosteroid injection; thus, the physician should select his or her preferred route. Additionally, no trial has compared the efficacy of different corticosteroids. Triamcinolone acetonide is the agent most frequently studied.

The action mechanism is inhibition of prostaglandin formation by selective cyclooxygenase (COX)2 activity. The optimal dose has not been evaluated. Recommended doses vary from 20-80 mg in the different trials. This author recommends 20-40 mg of triamcinolone acetonide. Adverse effects can be local or systemic. Although systemic adverse effects can occur following a subacromial injection, only local adverse effects are discussed here. Possible adverse effects include dermal atrophy, necrosis and loss of pigmentation, synovitis, septic arthritis, hemarthroses, cartilage damage and degeneration, tendon rupture, and Charcot arthropathy.

Bupivacaine suprascapular nerve block

The bupivacaine suprascapular nerve block is a relatively unknown, although effective, method to treat different painful shoulder disorders. A few randomized controlled trials have demonstrated its efficacy for painful shoulder associated with rheumatoid arthritis, for chronic rotator cuff disease, and for frozen shoulder. Preliminary data of a study on chronic impingement syndrome conducted at the Montreal Rehabilitation Institute show its efficacy compared with placebo. At 3 months, a significant improvement in pain and function, measured by a valid functional shoulder scale, was observed. The efficacy of this procedure is supported by randomized controlled studies, and it appears to be a very promising new approach in the treatment of rotator cuff disease.

The technique for nerve block is very inexpensive, simple, and safe. It consists of injecting 10 mL of bupivacaine 0.5% in the supraspinatus fossa of the scapula to produce an indirect suprascapular nerve block. In rotator cuff disease, 2 injections are administered 4 weeks apart

Surgical Treatment

Patients with more advanced rotator cuff disease or a more significant injury may not respond to conservative therapies. If the patient believes that his or her quality of life is being significantly impacted by the shoulder dysfunction, then surgical intervention is a reasonable consideration. In some cases, simple debridement of a frayed or partially torn cuff tendon, along with smoothing of the undersurface of the acromion (acromioplasty) above the tendon, may be all that is needed. More significant partial tearing (>50% of tendon thickness) and complete tears require reattachment of the tendon ends back to the humeral head.

Open surgery

Rotator cuff repair is most commonly performed using an open surgical procedure, which typically requires a 2- to 4-in incision at the top of the shoulder. The deltoid muscle is split, and the undersurface of the acromion is smoothed. Strong stitches are placed in the torn ends of the rotator cuff tendons, and they are attached back to the bone of the humerus through specially created tunnels or commercially available suture anchors.

Because the entire shoulder cannot be visualized through the open approach, many surgeons perform an initial diagnostic arthroscopy of the shoulder at the time of the repair to be sure no other coexisting problems are present within the shoulder that could also be addressed at the open procedure. This technique may be performed in an inpatient setting or in an outpatient surgery facility, providing that the patient is comfortable enough to return home the same day.

Standard tendon repair techniques combined with anterior acromioplasty, postoperative limb protection, and monitored physiotherapy can produce consistent and lasting pain relief and improvement in range of motion. Open rotator cuff repair has been known to have excellent outcomes and patient satisfaction since the early 80s. Romeo and colleagues have reported 94% patient satisfaction 4 years after open rotator cuff repair, with lasting relief of pain and improved function.[52] In another series, Baysal has reported that 96% of patients were satisfied or very satisfied with the results of their repair; 78% of patients who were working before surgery returned to work without modification by 1 year postoperatively. For the most part, patient age and size of tear did not influence postoperative range of motion or health-related quality of life.

Arthroscopy

Arthroscopic surgery involves the use of a special camera attached to a long, narrow surgical telescope to visualize the inside of a joint. Working through small incisions about the size of dress-shirt buttonholes, the surgeon can use specially created instruments to repair damaged cartilage, capsule, tendon, and other tissues. The camera transmits the signal to a video monitor for improved visualization and to allow photographic and videographic documentation of the surgical findings and the procedure. In orthopedic surgery, arthroscopy was first used to treat conditions of the knee. With new technology and refined techniques, arthroscopic surgery has become quite common for treating many knee, shoulder, elbow, wrist, hip, ankle, and foot problems.

Arthroscopic treatment of rotator cuff disease initially consisted of rotator cuff inspection and debridement and arthroscopic acromioplasty. If a repairable rotator cuff tear was discovered, an open or miniopen repair of the tendon was then performed. As surgeons' skills improved and more specialized instrumentation was developed, it became possible to fix relatively small tears using arthroscopic techniques to insert anchors, pass sutures, and tie knots. In current practice, surgeons can now perform shoulder arthroscopy to repair even large rotator cuff tears using these techniques.

Arthroscopic rotator cuff repair is a technically challenging procedure (see images below) that requires advanced arthroscopic surgical skills, careful preoperative planning, and a step-wise, systematic approach. The procedure may be performed with the patient in a "beach chair" (sitting) or a lateral decubitus (side-lying) position. Usually, the patient is under general anesthesia.

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View of large tear from posterior (behind). Socket is to the right. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.

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Visualizing torn rotator cuff from within the joint. The biceps tendon is running vertically on the left. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.

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Motorized burr removing under-surface of acromion. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.

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View of large tear from the "50 yard line." Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.

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The side-to-side stitches begin to close the large tear defect. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.

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An arthroscopic knot-tying instrument is used to pass tie knots in the suture to secure the repair. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.

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Small metallic anchors (5 mm) with sutures attached are then inserted into the humerus at the site desired for tendon reattachment. The anchors are recessed below the surface, so only the suture is visible. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.

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Sutures are anchored with the metallic anchors. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.

Small (5-mm) incisions are created in the back, side, and front of the shoulder, and the arthroscope and instruments may be switched between each of these positions as necessary. A complete diagnostic arthroscopy and bursoscopy (inspection of bursa) is initially performed. Care is taken to inspect the biceps tendon within the shoulder, the fibrous ring or labrum that surrounds the glenoid, the capsule and ligaments, the cartilage surfaces of the head and glenoid, and the rotator cuff tendons. Any pathology is addressed only after a complete inspection, so as not to miss any significant findings.

Careful preoperative radiographic evaluation of the shape and size of the acromion, along with a notation of any spurs, serves as a guide for the extent of any acromioplasty (undersurface smoothing) necessary. Because the arthroscope magnifies the structures seen, irregularities in the surface of less than 1 mm can be seen and are removed. The goal is to smooth and flatten the undersurface of the acromion to provide more room for the repair and to relieve pressure from the healing tendon. An overly aggressive acromioplasty must be avoided because excessive removal of the anterior acromion can result in the humeral head sliding forward, up, and out of the socket (anterosuperior subluxation).

The rotator cuff tear is then visualized through the lateral (side) portal from the "50-yard-line view." The size and pattern of the tear are assessed. Any thin or fragmented portions are removed, and the area where the tendon will be reattached to the bone is lightly debrided to encourage new blood vessel ingrowth for healing.

The sutures are once again passed through the tendon and systematically tied. The sutures pull the tendon down to the prepared bone surface, closing the defect. This completes the repair.

At the completion of the procedure, the shoulder is injected with a long-acting local anesthetic to assist with postoperative pain management. Each portal incision is closed with a single nylon stitch and covered with a sterile bandage tape, followed by a dry, sterile dressing. A cryotherapeutic shoulder pad (Cryocuff) is applied to provide postoperative cold therapy. This assists in management of pain and swelling. Finally, a sling (Don Joy UltraSling II) is applied for immobilization and protection. The patient is then taken to the recovery room.

Arthroscopic rotator cuff repair has achieved good-to-excellent results in a large percentage of patients (95% reported in one series), with the results being independent of tear size. U-shaped tears repaired by margin convergence have been shown to have results comparable to those of crescent-shaped tears repaired directly by a tendon-to-bone technique. There is a rapid return to full overhead function after arthroscopic rotator cuff repair (average, 4 months for all tear sizes). A delay between the time of injury and the time of diagnosis, even of several years, is not a contraindication for arthroscopic rotator cuff repair.

The results from one study suggest that patients who underwent arthroscopic rotator cuff repair with or without acromioplasty experienced no difference in function or quality of life.[59]

In a prospective study of 88 patients, Castricini et al showed that augmentation of a double row surgical repair of a small to medium size tear of the rotator cuff with autologous platelet-rich fibrin matrix (PRFM) did not improve the healing.[60]

Prosthetic implants (tissue engineering)

Tissue-engineering techniques are being used to develop therapies for tendon reconstruction. Biologic and synthetic scaffolds can both repair tendon defects and improve healing by allowing for the regeneration of the tendon's natural biologic composition to restore its mechanical capacity. This process can be further enhanced through augmentation methods such as cell seeding, growth factor implantation, and gene therapy.

There are many engineered prosthetic materials being used, but there is no widely accepted treatment for massive irreparable rotator cuff tears. Allografts have been used for repair of large defects but with very little success.

Medications

Simple Analgesics

Acetaminophen is recommended as initial treatment because of the toxicity associated with 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.

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 methodologic quality showed no short-term superiority of NSAIDs over acetaminophen in the treatment of painful shoulder syndrome. Long- and short-term studies comparing the efficacy of NSAIDs with that of acetaminophen for osteoarthritis of the knee have shown similar efficacy for the 2 agents. Moreover, even the presence of inflammatory signs did not predict a better response to treatment with NSAIDs, suggesting that improvements are not necessarily dependent on an anti-inflammatory effect.

Ibuprofen (Ibuprin, Advil, Motrin)

If the patient has no contraindications to the use of ibuprofen, it is usually the drug of choice for the treatment of mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

                     Adult dose - 400 mg PO q4-6h, 600 mg PO q6h, or 800 mg PO q8h while symptoms persist; not to exceed 3.2 g/d

                     Pediatric dose - For age 6 months to 12 years, 10-70 mg/kg/d PO divided tid/qid; begin at lower end of the dosing range and titrate upward; not to exceed 2.4 g/d; for older than 12 years, administer as in adults

                     Contraindications - Documented hypersensitivity; peptic ulcer disease, recent gastrointestinal bleeding or perforation, renal insufficiency, or high risk of bleeding

                     Interactions - Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta blockers; may decrease diuretic effects of furosemide and thiazides; may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently; monitor prothrombin time closely (instruct patients to watch for signs of bleeding)

                     Pregnancy category B - Usually safe but benefits must outweigh the risks.

                     Precautions - Category D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy

Acetaminophen (Tylenol, Feverall, Aspirin-Free Anacin)

The analgesic effect of acetaminophen is mediated by prostaglandin inhibition.

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

                     Pediatric dose - For those younger than 12 years, 10-15 mg/kg/dose PO q4-6h prn, not to exceed 2.6 g/d; for those older than 12 years, 325-650 mg PO q4h, not to exceed 5 doses in 24 h

                     Contraindications - Documented hypersensitivity; known glucose-6-phosphate dehydrogenase deficiency

                     Interactions - Rifampin can reduce analgesic effects of acetaminophen; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity

                     Pregnancy category B - Usually safe, but benefits must outweigh the risks.

                     Precautions - Hepatotoxicity possible in chronic alcoholism following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; acetaminophen is contained in many over-the-counter products, and combined use with these products may result in cumulative doses exceeding recommended daily dose

Nonsteroidal Anti-inflammatory Drugs

Numerous studies on the efficacy of NSAIDs for different shoulder conditions have been published, but because most of them have poor methodologic quality, no conclusions can be drawn about the efficacy of NSAIDs.

Recent review articles, using strict inclusion criteria based on the quality of the methodology, concluded that the trials with the best methodology show a superior short-term efficacy (2 wk) of NSAIDs compared with placebo; however, at 4 weeks, results did not show any statistical differences. Therefore, a short course (10-14 d) of NSAIDs is indicated as a second-line treatment. No evidence supports longer use.

In case of persistent pain, other therapeutic modalities should be sought. A comparison between different types of NSAIDs did not show evidence of the superiority of 1 NSAID with respect to efficacy. Therefore, an NSAID with the fewest adverse effects, such as the newer COX-2 selective molecules or an NSAID with a combination of prostaglandin E1 analogue (diclofenac/misoprostol), should be the drug of choice.

In an aging population taking additional medication that may interact with NSAIDs, drug interactions must be avoided. From 40-60% of drugs consumed are over-the-counter medications, most often analgesics and NSAIDs, increasing the risk of potential adverse gastrointestinal side effects. The patient should be asked whether he or she is taking any medications concomitantly, such as anticoagulants (hemorrhage), corticosteroids (peptic ulcer), diuretics and antihypertensives (decreased blood pressure control), ACE inhibitors (acute renal failure), high-dose methotrexate (increased methotrexate toxicity), lithium, digoxin, aminoglycosides (decreased renal clearance), phenytoin (decreased albumin binding), and antacids (decreased NSAID levels). NSAIDs should be avoided, if possible, in elderly patients with congestive heart failure or renal or hepatic dysfunction and who are taking other medications.

Celecoxib (Celebrex)

Celecoxib primarily inhibits COX-2, which is considered an inducible isoenzymethat is, it is induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID gastrointestinal toxicity, but at therapeutic concentrations, celecoxib does not inhibit the COX-isoenzyme; therefore, gastrointestinal toxicity may be decreased. The lowest dose of celecoxib should be sought for each patient.

                     Adult dose - 200 mg/d PO qd; alternatively, 100 mg PO bid

                     Pediatric dose - Not established

                     Contraindications - Documented hypersensitivity

                     Interactions - Coadministration with fluconazole may cause an increase in celecoxib plasma concentrations because of inhibition of celecoxib metabolism; coadministration of celecoxib with rifampin may decrease plasma concentrations

                     Pregnancy category C - Safety for use during pregnancy has not been established.

                     Precautions - Use with caution in patients with compromised cardiac function, hypertension, and conditions predisposing to fluid retention, because NSAIDs may cause fluid retention and peripheral edema; use with caution in patients with severe heart failure and hyponatremia, because NSAIDs may deteriorate circulatory hemodynamics; use with caution in the presence of existing controlled infections, because NSAIDs may mask the usual signs of infection; evaluate symptoms and signs suggesting liver dysfunction, cardiac dysfunction or renal dysfunction

Ketoprofen (Orudis, Actron, Oruvail)

Ketoprofen is used for relief of mild to moderate pain and inflammation. Small initial dosages are indicated in small and elderly patients and in persons with renal or liver disease. Doses of more than 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patients for response.

                     Adult dose - 25-50 mg PO q6-8h prn; not to exceed 300 mg/d

                     Pediatric dose - For those aged 3 months to 14 years, 0.11 PO mg/kg q6-8h; for those older than 14 years, administer as in adults

                     Contraindications - Documented hypersensitivity; gastrointestinal disease

                     Interactions - Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta blockers; may decrease diuretic effects of furosemide and thiazides; may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently; monitor prothrombin time closely (instruct patients to watch for signs of bleeding)

                     Pregnancy category B - Usually safe, but benefits must outweigh the risks.

                     Precautions - Category D in third trimester of pregnancy; use with caution in patients with congestive heart failure, hypertension, and decreased renal and hepatic function; use with caution in patients with anticoagulation abnormalities or during anticoagulant therapy

Differential Diagnosis

Differential diagnoses include the following:

                     Adhesive capsulitis

                     Biceps rupture

                     Bicipital tendinitis

                     Cervical disk disease

                     Cervical myofascial pain

                     Cervical spondylosis

                     Cervical sprain and strain

                     Complex regional pain syndromes

                     Fibromyalgia

                     Myofascial pain

                     Osteoarthritis

                     Rheumatoid arthritis

                     Rotator cuff disease

                     Shoulder and hemiplegia

                     Thoracic outlet syndrome

Follow-up

Inpatient care

Admit the patient to an orthopedic service in preparation for the operating room (only required if surgery is the treatment of choice).

Outpatient care

Arrange outpatient follow-up care to an orthopedic surgeon and rehabilitation services to continue conservative therapy. A follow-up reassessment examination 6 weeks after beginning conservative therapy is essential to determine if treatment is successful or if further surgical treatment is needed.

Inpatient or outpatient medications

All NSAIDs are equally effective.

Deterrence and prevention

Instruct patients to limit activities to ensure rest of the affected shoulder.

Complications

Failure of conservative treatment requires surgical intervention. Decreased ROM may occur.

Prognosis

An estimated 4% of cuff ruptures develop a cuff arthropathy. Various authors report the success rate of conservative treatment to be 33-90%, with longer recovery time required in older patients. Surgery results in better function regardless of the patient's age.

Patient education

Refer patients to a physical therapist for conservative treatment and postoperative therapy.