The skeletal structure of the shoulder girdle consists of the clavicle, scapula, and the proximal humerus. They are interconnected at the acromioclavicular, coracoclavicular, and glenohumeral articulations. The coracoclavicular, coracoacromial and glenohumeral ligaments are clinically important. This skeletal structure is suspended from the thorax by ligaments at the sternoclavicular joint and by muscles from the cervical spine and the rib cage.

The muscular anatomy of the shoulder girdle can be divided into four functional groups: the pectoral muscles take origin from the anterior rib cage and are the pectoralis major and minor, and the subclavius muscles. The extrinsic back muscles consist of muscles that connect the upper limb to the thoracic wall and the vertebral column. The serratus anterior and rhomboidei originate at the thoracic wall and the trapezius, latissimus dorsi, and levator scapulae originate at the vertebral column. The deltoid, teres major, and rotator cuff muscles (supraspinatus, infraspinatus, subscapularis, and teres minor) have scapular origin and humeral insertion. The glenohumeral joint is also bridged by the brachial muscles that originate on the scapula and insert more distally. These include the long head of the triceps muscles, and the long and short heads of the biceps and the coracobrachialis muscles.

The brachial plexus and the individual peripheral nerves are intimately involved in the shoulder. The specific individual nerves are the supraclavicular branches and the lateral, medial, and posterior cords of the brachial plexus. The subclavian artery enters the shoulder region and becomes the axillary artery at the outer border of the first rib. The first part of the axillary artery ends at the superior border of the pectoralis minor, and the third part ends at the lower border of the teres major muscle. The axillary artery has numerous branches and there are extensive arterial anastomoses around the scapula.

The function of the shoulder is dependent upon the complex interaction of 26 muscles and the motion about the sternoclavicular, acromioclavicular, coracoclavicular, scapulothoracic, and glenohumeral joints. It is the most mobile joint having a normal range of motion of 180° of elevation, 150° of external and internal rotation, and 170° of anterior and posterior rotation in the horizontal plane. Most of the motion occurs in the glenohumeral and scapulothoracic joints. Elevation of the shoulder involves coordinated motion in these two joints. The overall ratio of glenohumeral to scapulothoracic motion is about 2:1. Maximum elevation requires external rotation to clear the greater tuberosity from under the coracoacromial arch, loosen the ligamentous constraints, and appose the glenohumeral articulation. The sequence of axes of rotation determines the final position of the arm.

The shoulder is the most commonly dislocated major joint and chronic instability is not uncommon. About 30 per cent of the humeral head is covered by the glenoid surface which offers little stability to the glenohumeral joint. The labrum deepens the glenoid surface, serves as the attachment of the inferior glenohumeral ligament, and enhances stability. The inferior glenohumeral ligament is the primary ligamentous constraint to anterior and inferior instability. The coracohumeral, superior glenohumeral, and middle glenohumeral ligaments also contribute to stability. The global concept of instability refers to the finding that translation in one direction causes tension in the ligament on the opposite side of the joint.

Radiographs are most useful for evaluating fractures and other bone lesions as well as joint disruptions. An anteroposterior view of the glenohumeral joint (Fig. 1) 2439 in internal and external rotation and an axillary lateral view (Fig. 2) 2440 are routinely obtained. Further studies should be directed specifically to evaluating the suspected problem.

In the evaluation of trauma a tangential scapular Y view (Fig. 3) 2441 is also obtained. Computerized tomography provides additional information about displacement and the degree of comminution of proximal humeral and glenoid fractures.

Plain radiography can be used to provide additional information about glenohumeral instability. Special views include the West Point axillary lateral view to demonstrate an anterior - inferior Bankart fracture or soft tissue calcification. The glenoid and capsular - labral complex can be evaluated with CT arthrography. A Hill - Sachs lesion is demonstrated by the Stryker Notch view. Magnetic resonance imaging demonstrates capsular and tendinous pathology.

The degree of acromioclavicular joint separation can be demonstrated with the anteroposterior stress view. The medial clavicle and sternoclavicular joint are evaluated with a 40° cephalic tilt view; the serendipity view. Tomograms and CT scan are also useful to evaluate the medial end of the clavicle.

Apart from the shoulder problems that will be discussed in the other sections, there are several extrinsic causes of shoulder pain that must be considered in the differential diagnosis. Neurological causes predominate. These include cervical spine disease; intra- and extradural tumours, disc herniation, and spinal and foraminal stenosis, as well as brachial plexus and individual nerve lesions, herpetic neuralgia, and peripheral nerve tumours. Neurovascular syndromes such as thoracic outlet syndrome and reflex sympathetic dystrophy can cause shoulder pain and are difficult to treat. Referred pain from phrenic nerve irritation due to pulmonary, cardiac or subdiaphragmatic disease is common. Occupational cervicobrachial syndrome, repetitive strain syndrome, and droopy shoulder syndrome are postural and muscular lesions that can be the cause of shoulder pain.

Fractures of the proximal humerus occur most commonly in the elderly and are generally the result of minor trauma that fractures the osteoporotic bone. In younger patients proximal humerus fractures are usually due to violent trauma. Electrical shock, convulsive seizure, and pathological lesions are less common causes.

Neer established the four segment classification system. The four segments, the articular segment, the greater and lesser tuberosities and the shaft or surgical neck represent the same segments that were once separated by physeal plates. Displacement is defined as greater than 1-cm displacement or 45° of angulation. The classification assesses disruption of blood supply to the head and helps to predict its viability and correlates well with prognosis.

Patients are examined for neurological and vascular injury. It is difficult to determine the extent of bony injury without radiographs. The shoulder trauma series, including an anterior - posterior film in the plane of the scapula, a tangential scapular lateral, and an axillary lateral, is routinely obtained. Secondary evaluation with plain tomograms or CT scans is useful to assess the degree of displacement, humeral bone stock, and the glenoid fossa.

Return of shoulder function is achieved through anatomical reduction and early rehabilitation. Disability results from scarring of tendons, joint capsule and bursae, and malunion.

Fortunately, about 80 per cent of proximal humerus fractures are non- or minimally displaced one-part fractures. These fractures are best treated with sling and swathe protection and early rehabilitation. Rehabilitation begins with gentle pendulum exercises. If the fracture is not impacted motion is delayed until healing causes the fragments to move as a unit, usually within 2 weeks. Abduction casts and splints are cumbersome and unnecessary. Hanging casts may distract the fragments.

Displaced fractures and fracture dislocations involve greater soft tissue injury and vascular compromise of the head. Dislocations have extensive extra-articular soft tissue damage and displacement of fracture fragments outside the joint.

Two-part fractures have displacement of one of the four segments of the proximal humerus. Surgical neck fractures can often be treated with closed reduction. Unimpacted reduction may be unstable and can be stabilized with percutaneous pinning. When soft tissue interposition prevents closed reduction open reduction is required. Often, the biceps tendon is interposed. After open reduction, the fracture can be stabilized with suture, tension band wire, intramedullary device, T-plate, or traction. Once the fracture is stabilized, range of motion is begun. Displacement of the greater tuberosity can be associated with a longitudinal rotator cuff tear. Though the cuff injury may not be clinically important after healing, malunion of the greater tuberosity frequently causes impingement.

Isolated anatomic neck fractures are rare, but potentially devastating injuries. The blood supply to the articular segment is disrupted, and there is a high incidence of avascular necrosis. Open reduction with internal fixation is indicated in young patients with good bone stock. Otherwise, proximal humeral replacement is indicated.

Displaced lesser tuberosity fractures are also rare and only require open reduction with internal fixation if the fragment is large and blocks medial rotation. This fracture should alert the physician to the possibility of posterior dislocation.

The most common type of anterior fracture dislocation involves fracture of the greater tuberosity. The greater tuberosity often reduces after closed reduction. In this case surgery is unnecessary if there is no further displacement. Open reduction with internal fixation and rotator cuff repair is the best treatment for displaced greater tuberosity fracture.

Three-part fractures generally involve fracture of the surgical neck and one tuberosity. They are actually fracture subluxations because of rotation of the humeral articular surface. In younger patients with good bone stock open reduction with internal fixation (Fig. 5) 2443,2444 is preferable to prosthetic replacement. Limited internal fixation with sutures or wires may give a more reliable result with fewer complications. Prosthetic replacement is recommended for older patients.

In anterior three-part fracture dislocations open reduction provides for a gentler reduction and more accurate reduction. Open reduction with internal fixation with rotator cuff repair is the preferred treatment in younger patients. Prosthetic replacement is indicated when open reduction with internal fixation is not likely to be successful.

Three-part posterior fracture dislocations are often missed. In the setting of the acute injury, closed reduction is sometimes possible. Prosthetic replacement is usually not indicated because the intact greater tuberosity provides additional blood supply to the articular segment. Open reduction with internal fixation is the same as for three-part fractures without dislocation.

This injury causes complete disruption of the blood supply to the articular segment. This has an important influence on treatment selection and outcome. The incidence of avascular necrosis after closed reduction of this injury has been reported to be as high as 33 per cent. Open reduction with internal fixation, arthrodesis and head excision have generally yielded poor results. Consequently, prosthetic replacement is the treatment of choice.

Articular surface fractures present a different problem. Impression fractures, e.g. Hill - Sachs, occur with dislocation. Treatment depends upon the degree of articular involvement. When less than 20 per cent of the articular surface is involved, the joint is stable. With 20 to 40 per cent involvement the joint may be unstable. Reconstruction is performed by transplanting the greater or lesser tuberosity with attached tendon into the defect of the head of the humerus. Prosthetic replacement is reserved for involvement of greater than 50 per cent of the head. Head splitting fractures are uncommon. They involve devascularization of fragments of the articular surface. Comminuted fractures with small fragments are irreparable and should have proximal humeral replacement. Open reduction with internal fixation of large fragments in patients with good bone stock may be successful.

Rehabilitation is an essential aspect of treatment of proximal humerus fractures and fracture dislocations. Passive range of motion is initiated almost immediately. Active assisted range of motion is begun as soon as healing or fracture repair permits the segments to move as a unit. The deltoid and external rotators are strengthened with isometric exercises. Active motion is initiated once the fragments are united and good passive motion is achieved.

Joint stiffness, malunion, avascular necrosis, non-union, and myositis ossificans are the major complications of proximal humerus fractures and fracture dislocations. Malunion usually results after closed treatment. Greater tuberosity malunion can cause impingement. Anterior angulation at the surgical neck restricts forward elevation and is rarely reconstructed. Non-union is most likely to occur after an unimpacted surgical neck fracture. Unstable reduction, soft tissue interposition, a hanging cast, insufficient immobilization, over-aggressive physical therapy and poor bone quality are predisposing factors. Myositis ossificans only occurs after fracture dislocation. It rarely requires excision.

The shoulder is the most commonly dislocated major joint. Most dislocations (about 95 per cent) represent traumatic lesions. A smaller number have an atraumatic origin and may be related to congenital, acquired, or degenerative conditions.

The majority of shoulder dislocations are anterior. They are either subcoracoid (the most common), subglenoid, subclavicular, or intrathoracic. Subglenoid and subclavicular dislocations account for more than 90 per cent. Posterior dislocations are far less common, often missed, and frequently present as unreduced dislocations.

Dislocations are usually caused by indirect force. Combined abduction, extension, and external rotation cause anterior dislocation. Posterior dislocation results when an axial load is applied to an adducted and internally rotated shoulder. Hyperabduction impinges the neck of the humerus against the acromion process and levers the head out of the glenoid fossa inferiorly. In addition, violent muscle contraction about the shoulder such as that caused by electrical shock or convulsive seizure can cause dislocation, usually posteriorly.

In cases of recurrent dislocation, a differentiation must be made between traumatic and atraumatic causes. In atraumatic shoulder dislocation the original injury is not painful, is often self reduced and often both shoulders are involved. Voluntary dislocators often have a psychiatric or emotional disturbance.

Careful physical examination of the dislocated shoulder is essential before any treatment. The direction of the dislocation is often discernible and associated neurological and vascular injuries must be identified. Anterior dislocation is characterized by a subacromial sulcus, prominence of the humeral head anteriorly, and a slightly abducted and externally rotated position of the arm. Posterior dislocations are far more subtle and often lack significant deformity. Posterior shoulder fullness, anterior flattening, a prominent coracoid process, and internal rotation are suggestive findings. Limitation of external rotation is often the most remarkable finding.

Biplane plain film radiography, including an anteroposterior film in the plane of the scapula and a lateral projection, is used to evaluate all acute shoulder injuries. We have found that an axillary lateral view can be obtained in most cases without having to move the painful, injured shoulder appreciably. This view provides additional information about the glenoid fossa and humeral head compression fractures, and confirms the direction of dislocation. Some authors prefer the scapular Y view.

Most anterior shoulder dislocations can be reduced closed. The sooner the reduction is attempted, the easier it is. A gentle closed reduction can usually be performed with intravenous sedation or intra-articular xylocaine. In some cases general anaesthesia may be required.

After reduction the arm is placed in a sling. Abduction and external rotation are prevented. Traditionally, immobilization has been longer for young patients (up to 6 weeks) to prevent recurrence and shorter in older patients to avoid stiffness. However, there are a considerable number of reports refuting these guidelines and recommending shorter periods of immobilization. Rehabilitation should include strengthening of the shoulder girdle muscles, protecting healing anterior soft tissues, and regaining range of motion. The specifics of rehabilitation are probably more important than the exact length of immobilization.

Subclavicular or intrathoracic dislocations should have attempted gentle closed reduction with general anaesthesia. Both may require open reduction.

Irreducible shoulder dislocations either have soft tissue interposition or an associated fracture. In the former case the rotator cuff, glenoid labrum, capsule, or biceps tendon may be interposed in the glenohumeral joint and open surgical reduction is indicated. Other indications for surgery in acute anterior dislocations are a greater tuberosity fracture displaced more than 1 cm after reduction or an anterior glenoid rim fracture, which is almost always associated with recurring subluxation or dislocation.

Recurrence is the most common complication of an anterior shoulder dislocation. The incidence is inversely proportional to the age of the patient; up to 80 to 90 per cent for patients less than 20 years old and 10 to 15 per cent for those over 40. It also appears to be inversely related to the severity of the original trauma. In addition, several studies have failed to show a correlation between the length of the period of immobilization and incidence to recurrence. The posterolateral compression fracture (Hill - Sachs lesion), detachment of the labrum and capsule from the anterior glenoid, or Bankart lesion, and deficiencies of the subscapularis muscle and tendon are associated with recurrence.

Neuropraxia or neurotomesis of the axillary nerve are the most frequently associated neurological injuries. Expectant management is recommended and most deficits recover. The axillary artery or one of the major branches can be injured. This occurs more frequently in older patients with atherosclerotic vessels, and is either the result of the dislocating injury or overly forceful closed reduction. Emergent arteriography is indicated when a vascular injury is suspected. In most cases, disruption of the axillary artery must be treated with repair or vessel grafting.

Occasionally, unreduced anterior dislocations are encountered. These are most common among the elderly or the unconscious multiply-injured patient. Closed reduction should be avoided to prevent neurological and vascular injury. In some elderly patients it is more practical to leave the shoulder dislocated and rehabilitate the patient.

Atraumatic anterior dislocations should generally be treated non-operatively. If rehabilitation of an involuntary dislocator is unsuccessful after 6 to 12 months surgical reconstruction can be considered.

In general, posterior dislocations are more painful and more difficult to reduce without general anaesthesia. Gentle closed reduction can be achieved with the patient supine and traction applied in line with the adduction deformity. Lateral traction on the upper arm or gentle internal rotation may be required to unlock the humeral head. If this is unsuccessful open reduction through an anterior deltopectoral approach is recommended. After reduction the arm is placed into a modified shoulder spica or "cummerbund handshake cast" in neutral rotation and slight extension for about 6 weeks. Isometric deltoid and external rotation exercises are initiated in the cast. After removal, rehabilitation with strengthening and range of motion are initiated.

Early surgery is indicated if there is a displaced lesser tuberosity fracture, a major posterior glenoid fracture, an irreducible dislocation, open dislocation, or an unstable reduction. Unreduced dislocations should have open reduction if greater than 2 weeks old. Surgery is not recommended for elderly patients with a painless unreduced posterior dislocation and acceptable function. If there is significant disability with good glenohumeral bone stock reconstruction is indicated.

Patients who voluntarily dislocate their shoulders should never have surgery. However, involuntary atraumatic dislocators who have failed 6 to 12 months of rehabilitation may benefit from reconstruction.

The acromioclavicular joint and the surrounding ligamentous complex form an important link between the arm and the thorax. Though the sternoclavicular joint and deltoid and trapezius muscles maintain the normal position of the shoulder, the coracoclavicular ligament is the prime suspensory ligament of the upper extremity.

Most acromiclavicular injuries are due to direct force to the point of the shoulder. The soft tissue structure around the acromioclavicular joint undergoes sequential failure. Indirect force in an upward or downward direction is less common.

There are six types of acromioclavicular separation. These are based upon the degree of injury to the acromioclavicular and coracoclavicular ligaments and the deltoid and trapezius muscles. Type I represents acromioclavicular ligament sprain and a stable acromioclavicular joint. In type II injuries the acromioclavicular ligaments are disrupted but the coracoclavicular ligaments are only sprained. Type III injuries (Fig. 12) 2454 are characterized by disruption of the acromioclavicular and coracoclavicular ligaments, increase in the coracoclavicular distance, and avulsion of the deltoid and trapezius muscles. Types IV, V, and VI injuries have severe displacement of the distal clavicle. In type IV the clavicle is displaced into and penetrates posteriorly through the trapezius muscle. In type V injuries the coracoclavicular space is much wider and the distal clavicle is displaced superiorly. The distal clavicle is either under the acromion or coracoid process in type VI injuries.

In all except type II injuries the appearance of the acromioclavicular joint predicts whether the coracoclavicular ligament is disrupted. Cephalad tilt (10°) anteroposterior and axillary lateral radiographs are standard. Weight-bearing stress radiographs are used to differentiate type II and III injuries. Rockwood has found that when coracoclavicular distances are compared a 25 per cent difference correlates with complete coracoclavicular disruption.

Type I injuries are treated with ice and 7 to 10 days of rest. Unrestricted activity is resumed when there is full range of motion and no tenderness.

Closed treatment of type II injuries is usually appropriate. A variety of methods have been devised to reduce the acromioclavicular displacement by applying downward pressure to the distal clavicle and support the arm. The Kenny - Howard sling is an example. Careful attention must be directed to preventing skin slough over the 3- to 6-week treatment period. Alternatively, the shoulder complex can be treated with "skilful neglect" in a sling for about 2 weeks. Excellent results are achieved in most cases.

Type III injuries can be treated in the same non-operative fashion. Surgical repair or reconstruction of acute acromioclavicular dislocation may be appropriate for heavy labourers, young patients, and active older patients. The four major surgical approaches are: (1) acromioclavicular ligament repair, (2) coracoclavicular repair with screw (Fig. 13) 2455, wire, coracoacromial ligament transfer, or biceps tendon transfer, (3) excision of the distal clavicle, or (4) transfer of the coracoid tip with attached muscles to the clavicle. Similar results have been reported for operative and non-operative approaches.

Type IV, V, and VI injuries more commonly require surgery. Though closed reduction can be attempted to convert a type IV to a type III injury it is often not possible and surgery must be performed. The surgical approaches discussed above are appropriate.

Late reconstruction is indicated for chronic symptomatic acromioclavicular dislocation. If the coracoclavicular ligament is intact (type II) then 2 to 2.5 cm of the distal clavicle is excised and the conoid ligament is retained. If the coracoclavicular ligament is disrupted it must be reconstructed.

Associated fractures of the clavicle, acromion, and coracoid processes can occur. Ossification of the coracoclavicular ligament is a fairly common finding that does not appear to affect late function. Osteolysis of the distal clavicle can cause weakness and pain with flexion and adduction but usually resolves with avoidance of the bothersome activities.

Complications are more commonly the result of treatment. Residual deformity, stiffness due to prolonged immobilization, and skin pressure sores are the major complications of non-operative treatment.

Operative treatment can result in more troublesome complications. Failure of fixation and fracture around or due to fixation causes recurrence of deformity as well as potentially impinging retained hardware. In addition, pins have migrated all around the shoulder, neck, and upper thorax.

The rotator cuff is composed of the tendons of the supraspinatus, infraspinatus, subscapularis, and the teres minor muscles. Functionally, it stabilizes the humeral head in its articulation with the glenoid fossa during the motion of the glenohumeral joint and resists the shearing forces of the deltoid muscle during abduction and forward flexion. In addition, the supraspinatus, infraspinatus, and teres minor muscles function as external rotators of the glenohumeral joint, and the subscapularis muscle functions as a strong internal rotator.

Rotator cuff tears generally occur in older patients and are usually superimposed upon degenerative lesions of the rotator cuff tendons. In younger patients they usually follow severe trauma (including injuries of the shoulder without fracture or dislocation, anterior glenohumeral dislocation, and fracture dislocation) or chronic overuse syndromes. Some 95 per cent of rotator cuff tears are initiated by impingement as opposed to circulatory impairment or trauma. There are three pathological stages of impingement: the first is a stage of oedema and haemorrhage of the rotator cuff tendons, the second represents fibrosis or tendinitis, and the third stage represents rotator cuff tears, biceps tendon ruptures, and the bony changes present at the humeral tuberosities and the acromion.

Rotator cuff tears can be either partial or full thickness tears. Partial tears are either intratendinous or on the under surface of the rotator cuff tendons. With partial or incomplete rotator cuff tear, muscle function usually continues and the patient may have pain or locking episodes.

Full-thickness rotator cuff tears expose the humeral head. The supraspinatus tendon is most commonly torn while the subscapularis is rarely torn. Patients with complete rotator cuff tears usually have pain, and may have limited active but unrestricted passive motion. Eventually they can develop spinati atrophy, weakness of external rotation and abduction, and limited passive motion. Soft crepitance can usually be appreciated in the subacromial area. The impingement test described by Neer (10 ml subacromial injection of 1 per cent plain lidocaine) is fairly specific and can help to differentiate impingement and small cuff tears from large tears. In addition injection of the acromioclavicular joint can be used to evaluate or differentiate pain in this joint. If there is marked weakness of abduction due to cuff tear, the drop arm sign, the inability to hold the shoulder in abduction after injection of lidocaine into the subacromial space, will be positive. Weakness of abduction and/or external rotation is a reliable sign of rotator cuff pathology

There are several non-specific radiographic findings associated with rotator cuff disease. These include a decreased space between the humeral head and the inferior acromion. The normal space is about 7 to 14 mm. A space less than 5 mm is compatible with a major tear of the rotator cuff. Prominence on the greater tuberosity at the point of insertion of the supraspinatus tendon, cystic changes in the anatomic neck of the humerus, and traction spurring on the underside of the acromion are also consistent with rotator cuff pathology.

Arthrography is the gold standard for radiographic diagnosis of rotator cuff tears. With a full thickness tear there will be communication of contrast from the glenohumeral joint to the subacromial bursa (Fig. 14) 2456. Arthrography can also demonstrate partial tears. Double contrast studies yield more information about the synovial lining and the thickness of the glenohumeral cartilage. CT-arthrography has also been very helpful in evaluating these patients. More recently, ultrasonography and MRI of the shoulder have been useful in assessing disease of the rotator cuff.

Rotator cuff tears present themselves as either acute or chronic problems. Cadaver studies have shown that there is a 30 to 40 per cent incidence of cuff tear. Clearly, many do not have clinical significance. Acute tears usually occur through unhealthy tendons with long-standing lesions.

Pain is the predominant complaint with chronic rotator cuff tears. It may be worst at night, and in overhead use. Often patients with chronic tears are treated with prolonged physical therapy and anti-inflammatory medications. In some cases, depending on the patient's functional expectations, this is appropriate treatment.

Critical analysis of shoulder function in relation to patient age and activity suggests that early surgical intervention and repair is often indicated. The observed natural history of cuff tears supports appropriate surgical treatment. Prolonged conservative therapy in chronic tears leads to tendon scarring and thickening of avascular scar tissue which is very difficult to repair. There is considerable risk that a superimposed second injury can cause a massive acute extension of a chronic tear. The usual forces of the rotator cuff muscles can pull on small tears and prevent healing. Lastly, the chronic inflammatory reaction of the healing process can actually weaken the tendon.

In most cases, surgical treatment is straightforward. First, the overlying bursa is excised. The defect is defined, and the avascular scarred edges are debrided. The rotator cuff tendons are mobilized. Repair is dependent upon the morphology of the disruption. In avulsion tears, the mobilized tendon is inserted into a trough in the bone. Anterior acromioplasty is always performed to decompress the coracoacromial arch.

Surgical repair of chronic rotator cuff tears can be more difficult. The decision to perform repair should depend on the patient's functional requirements, not on the extent of the tear. Elderly patients with minimal or no pain, extreme weakness, and less than 60° of active elevation tend not to do well. The tendons are scarred, thickened, and extensively avascular at the edges of the tear. It is often difficult to close the gap primarily. Several options are available. These include incorporation of the intra-articular portion of the long head of the biceps tendon, use of cadaver rotator cuff tendon, autograft of fascia lata tissue, or transfer of the subscapularis or teres minor tendons. Other authors have advocated subacromial decompression and debridement of massive tears.

The proximal tendon of the long head of the biceps originates from the supraglenoid tubercle and is an intra-articular, but extrasynovial structure. The tendon leaves the shoulder between the tuberosities in the bicipital groove. More than 90 per cent of patients with a diagnosis of bicipital tendinitis suffer from the impingement syndrome and have secondary involvement of the biceps tendon.

Slatis and Aalto classified three types of biceps tendon disease. Type A is impingement tendinitis, which occurs in conjunction with the impingement syndrome and rotator cuff tears. Type B is subluxation of the biceps tendon and is usually associated with more severe rotator cuff tears. Type C is attrition tendinitis or primary bicipital tendinitis. Primary tendinitis is the most painful and common type to cause complete rupture of the biceps tendon.

Patients have chronic pain in the proximal anterior part of the shoulder. Repetitive motion, especially overhead, exacerbates impingement and bicipital tendinitis. Instability of the tendon may be present. Frank tendon rupture manifests pain, ecchymosis, and obvious change in the contour of the arm.

Primary bicipital tendinitis is a diagnosis of exclusion. It must be differentiated from impingement and rotator cuff tear. Selective injection into the subacromial space may be helpful.

Painful attrition tendinitis can be treated with a limited number of corticosteroid injections. Chronic tendinitis or instability can be surgically treated with proximal tenodesis. Proximal biceps tendon rupture can usually be treated non-operatively. Physiotherapy usually produces good results. Nonetheless, rupture is often not an isolated problem and a rotator cuff tear must be excluded. Early surgical intervention is only advocated for acute traumatic rupture in young patients or in association with a rotator cuff tear in an active patient. At the time of any surgery the coracoacromial arch should be assessed for evidence of impingement.

Glenohumeral arthritis is less common than degenerative conditions of the hip or knee because the glenohumeral articulation is not a weight-bearing joint and is less constrained in its range of motion. The three most common causes are rheumatoid arthritis, osteoarthritis, and post-traumatic arthritis. Cuff tear arthropathy, prior surgery, and osteonecrosis (Fig. 15) 2457 occur less commonly. In addition, there are several rare conditions that cause glenohumeral arthritis. These include old sepsis, radiation necrosis, ankylosing spondylitis, systemic lupus erythematosus, and haemophilia. Differential diagnoses include septic arthritis, neuropathic arthritis, neoplasia, and cervical radiculopathy.

In rheumatoid arthritis all tissues around the shoulder girdle are effected. Glenohumeral arthritis and arthralgia, rotator cuff tendinitis, bicipital tenosynovitis, scapulothoracic pain, frozen shoulder, subacromial bursitis, and calcific tendinitis can all occur in a patient with rheumatoid disease. Glenohumeral arthritis worsens with time in a halting pattern of progression. Symptoms are often less serious than the radiographs suggest, and patients can be quite functional despite tremendous disease.

The three types of glenohumeral arthritis in patients with rheumatoid arthritis are dry, wet, and resorptive. (1) The dry form is stiff, with loss of joint space, and sclerotic and cystic changes. (2) Exuberant synovial disease is the hallmark of the wet form. In this type the head often erodes deeply into the glenoid. (3) In the resorptive type the humeral head and scapula resorb. Within each type there is a spectrum of severity.

In the rheumatoid patient glenohumeral arthritis can be associated with subacromial or subdeltoid bursitis, rotator cuff tears, and acromioclavicular joint arthritis. These conditions must be treated in conjunction with the arthritis. Rotator cuff tears have been reported in 25 to 40 per cent of patients with rheumatoid arthritis with glenohumeral arthritis. Several less common entities can cause pain or dysfunction in the rheumatoid shoulder. These include suprascapular nerve damage, pseudothrombosis, serratus anterior disruption, septic arthritis, chylous or synovial cysts, and neuropathic arthritis secondary to cervical spine abnormalities.

Osteoarthritis of the shoulder is uncommon. Radiographically it is characterized by joint space narrowing, marginal osteophytes, and loose bodies. More advanced disease often includes erosion of the posterior glenoid and posterior subluxation. It is often a bilateral condition. The incidence of associated rotator cuff tear is about 5 per cent.

Post-traumatic arthritis results from incongruity of the glenohumeral articulation. Malunion, with joint incongruity, proximal humeral non-union, and avascular necrosis after fracture or fracture dislocation are the more common causes. Less commonly, recurrent or chronic dislocation leads to post-traumatic arthritis.

Cuff tear arthropathy occurs after long-standing massive rotator cuff tear, particularly in women. Without a functioning rotator cuff the proximal humerus migrates superiorly and articulates with the acromial arch. The humeral head loses the contour of the greater tuberosity and sits in a socket formed by the glenoid and coracoacromial arch.

The first line of treatment is non-operative. Physical therapy to improve shoulder girdle strength and mobility, and oral non-steroidal anti-inflammatory medications are the mainstays of conservative treatment. Although steroid injections may be useful, they should be used sparingly because of the potentially deleterious effect on soft tissue integrity and the risk of iatrogenic infection.

The best surgical results are achieved with prosthetic replacement (either hemi- or total shoulder arthroplasty).

Synovectomy is recommended for rheumatoid patients who have persistent pain despite adequate medical therapy and have intact humeral and glenoid articular cartilage.

Joint debridement has been attempted for non-rheumatoid degenerative joint disease. This effort has rarely been successful because the articular surfaces are usually already involved in the degenerative process.

Resection arthroplasty is seldom indicated. It results in an unstable joint with maximum active abduction of 60 to 80°. Occasionally it is necessary for chronic sepsis, humeral head osteomyelitis, infected implants when prosthetic revision is impossible, or painful neuropathic shoulder.

Arthrodesis can provide a stable, pain-free, and functional shoulder. The functional outcome is dependent upon the mobility of the scapulothoracic articulation. The primary indications are paralysis of the deltoid and rotator cuff muscles, massive unrepairable rotator cuff tears, infection with destruction of glenohumeral cartilage, failed reconstructive procedures, and severe shoulder trauma. A combined intra- and extra-articular approach is most commonly used. The humeral head is approximated to the acromion. Fixation is usually achieved with plates and screws. This procedure generally has a high rate of fusion. Maximum function is achieved when the shoulder is fused in 25 to 40° abduction, 20 to 30° forward flexion, and 25 to 30° of internal rotation. Arthrodesis should be avoided in patients with osteoarthritis, rheumatoid arthritis, and post-traumatic arthritis because they have a better functional outcome after total shoulder arthroplasty.

Prosthetic arthroplasty is the mainstay of the surgical treatment of glenohumeral arthritis. The goal of prosthetic replacement is to relieve pain and restore functional range of motion.

In addition to acute fractures and fracture dislocations, proximal humeral replacement or hemiarthroplasty can be performed for some proximal humeral non-unions, malunion with joint incongruity, chronic dislocation, osteonecrosis with collapse, osteoarthritis in a young active person with a normal glenoid fossa, rheumatoid patients with inadequate bone to support the glenoid component, or long-standing sepsis in young or active patients. Though total shoulder arthroplasty is most commonly performed for rheumatoid and osteoarthritis it can be used for failed reconstructions of cuff tear arthropathy, and previously resolved sepsis. The important contraindications include infection, paralysis that effects the deltoid and rotator cuff muscles, extreme glenoid bone deficiency, psychiatric disorders, alcoholism, and neuropathic joints.

Success is dependent upon meticulous technique and good rehabilitation. The shoulder joint is approached through a deltopectoral incision. Correct component placement is predicated on accurate proximal humeral osteotomy and careful glenoid preparation. The humeral component is retroverted 30 to 40° and is seated above the level of the greater tuberosity. Bony deficiencies of the glenoid must be corrected. Unless deficient, the rotator cuff is repaired. If there is a major internal rotation contracture, a Z-plasty of the subscapularis tendon is performed. Porous, coated humeral stem and glenoid components theoretically permit bony ingrowth to allow stable fixation. Most implant systems rely on cement fixation of the glenoid.

Very good results have been reported. In most series total shoulder arthroplasty has achieved greater than 90 per cent satisfactory pain relief. Range of motion has been variable and is dependent upon the diagnosis and condition of the rotator cuff and capsule. Cofield has reported 140° of active abduction in osteoarthritis and about 105° in rheumatoid arthritis. Neer has reported the largest series. In reviewing outcome he found it necessary to define two patient populations and use either full or limited goals rehabilitation criteria. Follow-up evaluations of the prosthetic components have shown lucency at the glenoid bone cement interface in 30 to 90 per cent of cases.

Septic arthritis of the shoulder is uncommon. It represents approximately 10 to 15 per cent of all septic arthritides, and more commonly affects the glenohumeral joint than the acromioclavicular or sternoclavicular joints.

Most frequently, septic arthritis of the glenohumeral joint affects adults who have debilitating disease such as alcoholism, malignancy, or diabetes mellitus. It is often the result of direct inoculation due to trauma or invasive procedures. These include surgery, arthroscopy, total joint replacement, aspirations, and steroid injections. The presence of a foreign body increases the risk of infection because of the formation of a surrounding glycocalyx membrane that protects bacteria from the body's defences. Young adults are rarely affected unless there is penetrating trauma, intravenous drug use, or immunosuppression. Septic arthritis can occur secondary to contiguous spread from metaphyseal osteomyelitis. Septic shoulders are uncommon in children and are usually secondary to haematological inoculation or to direct extension from metaphyseal osteomyelitis.

The most common bacterial organisms are Staphylococcus aureus and epidermidis, and streptococcus group B. Pseudomonas aeruginosa is found among intravenous drug abusers. Neisseria gonorrhoea is prevalent among sexually active adults. Haemophilus influenzae type B is common in children less than 2 years old. In the neonatal period, group B streptococci, Gram-negative bacilli, and Staphylococcus aureus are most common. In addition, mycobacteria, fungi, and viruses can cause sepsis of the shoulder.

Patients have pain, loss of motion, and effusion. Effusion is difficult to detect and is not a reliable finding. Pain on joint motion is specific for joint inflammation. Fever and leucocytosis, though not always present, are suggestive findings. The erythrocyte sedimentation rate is usually elevated. In the immunosuppressed and rheumatoid patient symptoms may be masked. Infection after prosthetic shoulder arthroplasty is rare and occurs in less than 0.5 per cent of cases. The patient usually has pain, decreased motion, subluxation, and lucency around the implant or cement. Gout, pseudogout, rheumatic fever, juvenile rheumatoid arthritis, trauma, and tumour must also be considered in the differential diagnosis.

Diagnosis is made by aspiration, fluid analysis and culture. Aspiration may require radiographic control. In the case of a negative culture with uncertain diagnosis, synovial biopsy by arthroscopy or arthrotomy can be very helpful. Joint fluid cultures are positive in approximately 90 per cent of cases of established bacterial septic arthritis and in about 75 per cent of tubercular arthritis.

Treatment includes surgical drainage and systemic antibiotics. Numerous reports have demonstrated success with serial aspiration of septic joints. However, it has been our experience that surgical arthrotomy or multiportal arthroscopic irrigation are more efficacious. Unfortunately, many cases go undetected and are treated in a subacute or chronic stage. If recognized early and successfully treated, outcome is usually good.

Anatomy

Romanes GJ, ed. Cunningham's Textbook of Anatomy, 12th edn. Oxford: Oxford University Press, 1981.

Shoulder biomechanics

Morrey BF, An K-N. Biomechanics of the shoulder. In: Rockwood CA, Matsen FA, eds. The Shoulder. Philadelphia: WB Saunders, 1990: 208.

Poppen NK, Walker PS. Normal and abnormal motion of the shoulder. J Bone Joint Surg 1976; 58A: 195.

Radiography

Rockwood CA, et al. X-ray evaluation of shoulder problems. In: Rockwood CA, Matsen FA, eds. The Shoulder. Philadelphia: WB Saunders Co., 1990.

Proximal humerus fractures and fracture - dislocations

Cofield RH. Comminuted fractures of the proximal humerus. Clin Orthop, 1988; 230: 49 - 57.

Hawkins RJ, Bell RH, Gurr K. The three-part fracture of the proximal humerus; operative treatment. J Bone Joint Surg 1986; 68A: 1410 - 14.

Kristiansen B, Christiansen SW. Plate fixation of proximal humeral fractures. Acta Orthop Scand 1986; 57: 320 - 3.

Neer CS. Displaced proximal humeral fractures; part I. Classification and evaluation. J Bone Joint Surg 1970; 52A: 1077 - 89.

Neer CS. Displaced proximal humeral fractures; part II. Treatment of three-part and four-part displacement. J Bone Joint Surg 1970; 52A: 1090 - 1102.

Leyshon RL. Closed treatment of fractures of the proximal humerus. Acta Orthop Scand 1984; 55: 48 - 51.

Stableforth PG. Four-part fractures of the neck of the humerus. J Bone Joint Surg 1984; 66B: 104 - 8.

Rose SJ, Melton J, Morrey BF, Ilstrup DM, Riggs BL. Epidemiologic features of humeral fractures. Clin Orthop 1982; 168: 24 - 30.

Acute shoulder dislocation

Hawkins RJ, Neer CS, Pianta R, Mendoza FX. Locked posterior dislocation of the shoulder. J Bone Joint Surg 1987; 69A: 9.

Hovelius L. Recurrences after initial dislocation of the shoulder. J Bone Joint Surg 1983; 65A: 343.

Hovelius L. Anterior dislocation of the shoulder in teenagers and young adults. Five-year prognosis. J Bone Joint Surg 1987; 69A: 393.

Matsen FA, Thomas SC, Rockwood CA. Anterior glenohumeral instability. In Rockwood CA, Matsen FA, eds. The Shoulder. Philadelphia: WB Saunders, 1990.

Rose CR. Prognosis in dislocations of the shoulder. J Bone Joint Surg 19856; 38A: 957.

Acromioclavicular joint injury

Bjerneld H, Hovelius L, Thorling J. Acromioclavicular separations treated conservatively. Acta Orthop Scand 1983; 54: 743 - 5.

Fujuda K, Craig EV, An K-N, Cofield RH. Anatomic and biomechanical studies of the ligamentous system of the acromioclavicular joint. J Bone Joint Surg 1986; 68A: 434 - 9.

Galpin RD, Hawkins RJ, Grainger RW. A comparative analysis of operative versus nonoperative treatment of grade III acromioclavicular separations. Clin Orthop 193: 150 - 5.

Lancaster S, Horowitz M, Alonso J. Complete acromioclavicular separations: a comparison of operative methods. Clin Orthop 1987; 216: 80 - 8.

Larsen E, Bjerg-Nielsen A, Christensen P. Conservative or surgical treatment of acromioclavicular dislocations: a prospective controlled randomized study. J Bone Joint Surg 1986; 68A: 552 - 5.

Post M. Current concepts in the diagnosis and management of acromioclavicular dislocations. Clin Orthop 1985; 200: 234 - 47.Rockwood CA, Young DC. Disorders of the acromioclavicular joint. In: Rockwood CA, Matsen FA, eds. The Shoulder. Philadelphia, WB Saunders Co., 1990.

Taft TN, Wilson FC, Oglesby JW. Dislocation of the acromioclavicular joint: an end result study. J Bone Joint Surg 1987; 69A: 1045 - 51.

Rotator cuff tears

Bassett RW, Cofield R. Acute tears of the rotator cuff; the timing of surgical repair. Clin Orthop 1983; 175: 18 - 24.

Cofield RH. Tears of the rotator cuff. In Murray DG, ed. Instructional Course Lectures. St Louis; CV Mosby, 1981; 30: 258 - 73.

Ellman H, Hanker G, Bayer M. Repair of the rotator cuff; end-result study of factors influencing reconstruction. J Bone Joint Surg 1986; 68A: 266 - 72.

Gartsman GM. Arthroscopic acromioplasty for lesions of the rotator cuff. J Bone Joint Surg 1990; 72A: 169.

Kunkel SS, Hawkins RJ. Rotator-cuff repair utilizing a trough in bone. Techniques Orthop 1989; 3: 51 - 7.

Neer CS. Anterior acromioplasty for the chronic impingement syndrome in the shoulder. A preliminary report. J Bone Joint Surg 1972; 54A: 41.

Neer CS. Impingement lesions. Clin Orthop 1983; 173: 70 - 7.

Neer CS, Craig EV, Fukuda H. Cuff-tear arthropathy. J Bone Joint Surg 1983; 65A: 1232 - 44.

Nevaiser RJ, Nevaiser TJ. Lesions of musculotendinous cuff of shoulder: diagnosis and management. In: Murray DG, ed. Instruction Course Lectures. St Louis: CV Mosby, 1981; 30: 239 - 57.

Norwood LA, Barrack R, Jacobson KE. Clinical presentation of complete tears of the rotator cuff. J Bone Joint Surg 1989; 71A: 499 - 505.

Post M, Silver R, Singh M. Rotator cuff tear: diagnosis and treatment. Clin Orthop 1983; 173: 78 - 91.

Proximal bicipital tendinitis and rupture

Burkhead WZ. The biceps tendon. In Rockwood CA, Matsen FA, eds. The Shoulder, Philadelphia: WB Saunders, 1990; 791 - 836.

Dines D, Warren RF, Inglis AE. Surgical treatment of lesions of the long head of the biceps. Clin Orthop 1982; 164: 165 - 71.

Nevaiser TJ, Nevaiser RJ. Lesions of the long head of the biceps tendon. In Murray DG, ed. Instructional Course Lecture St Louis: CV Mosby 1981; 30: 250 - 7.

Arthritis

Cofield RH. Total shoulder arthroplasty with the Neer prosthesis, J Bone Joint Surg 1984; 66A: 899 - 906.

Cofield RH. Shoulder arthrodesis and resection arthroplasty. In Stauffer ES, ed. Instructional Course Lecture. St Louis: CV Mosby 1985; 34: 268 - 77. 1985.

Cofield RH. Degenerative and arthritic problems of glenohumeral joint. In: Rockwood CA, Matsen FA, eds. The Shoulder. Philadelphia: WB Saunders, 1990; 678 - 749.

Curran JF, Ellman MH, Brown NL. Rheumatologic aspects of painful conditions affecting the shoulder. Clin Orthop 1983; 173: 27 - 37.

Friedman RJ, Thornhill TS, Thomas WH, Sledge CB. Non-constrained total shoulder replacement in patients who have rheumatoid arthritis and class-IV function. J Bone Joint Surg 1989; 71A: 494 - 8.

Neer CS. Replacement arthroplasty for glenohumeral osteoarthritis. J Bone Joint Surg 1974; 56A: 1 - 13.

Neer CS, Watson KC, Stanton FJ. Recent experience in total shoulder replacement. J Bone Joint Surg 1982; 64A: 319 - 37.

Septic arthritis

Gelberman RH, Menon J, Austerlitz S, Weisman MH. Pyogenic arthritis of the shoulder in adults. J Bone Joint Surg 1980; 62A: 550 - 3.

Gifford DB, Patzakis M, Ivler D, Swezey RL. Septic arthritis due to Pseudomonas in heroin addicts. J Bone Joint Surg 1975; 57A: 631 - 5.

Goldenberg DL, Reed JI. Bacterial arthritis. N Engl J Med 1985; 312: 764 - 71.

Gristina AG, Costerton JW. Bacterial adherence to biomaterials and tissue. The significance of its role in clinical sepsis. J Bone Joint Surg 1985; 67A: 264 - 73.