Fractures

Upper extremity fractures account for more than half of all pediatric fractures¹ and only 7% of geriatric fractures.² The annual incidence of upper extremity fractures in the United States is 67.6 fractures per 10,000 persons.³ The most common shoulder girdle fractures occur in the proximal humerus, with fractures of the clavicle being second most prevalent. The annual incidence of proximal humeral fractures is 83.0 events per 100,000 persons,⁴ while clavicle fractures account for 24.4 injuries per 100,000 person years.⁵ Scapular fractures account for 13 fractures per 100,000 women and 37 fractures per 100,000 men. Glenoid fractures are rarer and account for 10% of scapular fractures with an overall prevalence of 0.1%.⁶

Clavicle

Eighty percent of clavicle fractures occur within the middle third, while 15% involve the distal third, and 5% involve the proximal third.⁷ Distal clavicle fractures can be subclassified into three groups. Type I refers to a clavicle fracture distal to the coracoclavicular (CC) ligament with the ligament remaining intact. Group II refers to a clavicle fracture distal to the CC ligament with (IIB) or without (IIa) disruption of the CC ligament. Type III distal clavicle fractures refer to a fracture with intra-articular extension (Fig. 30–1).

Trauma accounts for the most common etiology of clavicular fractures. Translational force from the lateral shoulder, falling on an outstretched hand, and direct contact with the clavicle may all lead to fracture. Less common causes include childbirth in the neonate, malignancy, and radiation therapy.⁸ In rare cases, stress fractures of the clavicle can be seen. Case reports typically center on gymnasts or weight lifters.

A clavicle radiograph series is used for diagnosis. This series includes an anteroposterior (AP) view of the clavicle, acromioclavicular (AC) joint, and sternoclavicular (SC) joint, as well as an AP view with 15 degrees of cephalad angulation⁹ (Fig. 30–2). Computerized tomography (CT) scans can be performed in instances of equivocal radiographs or in cases of fracture near the AC or SC joint.

The treatment for clavicle fractures with less than 100% displacement or less than 20 mm of shortening is typically conservative. Immobilization with a figure-of-8 brace is preferred for 4 to 6 weeks. Surgical intervention is indicated for neurovascular compromise, >100% displacement, >20 mm of shortening, type II distal clavicle fractures, ipsilateral fracture of the glenoid (floating shoulder), or open fracture. Similar success rates have been seen with intramedullary nails versus plate fixation.¹⁰ In the case of distal clavicular fractures, the coracoclavicular screw must be later removed.

Proximal Humerus

The humerus is composed of the head, surgical and anatomic necks, greater and lesser tubercles, shaft, medial and lateral epicondyles, and olecranon fossa (Fig. 30–3). The Neer classification of fractures of the humerus is defined by the location of the fracture and number of fragments (Fig. 30–4). Proximal humerus fractures involve the head, neck, or tubercles and are roughly six times more prevalent than humeral shaft fractures. Proximal humeral fractures are 10 times more common than distal fractures.⁵ Direct trauma and falls account for the majority of humeral fractures. Patients with proximal humerus fractures typically present with an immobilized shoulder and complain of pain, swelling, and decreased range of motion. Compromise of neurovascular structure can lead to numbness, weakness, or pallor.

On physical examination, a patient with humeral fracture will typically demonstrate decreased active and passive range of motion. Sensation of the lateral shoulder should be tested to evaluate the integrity of the axillary nerve. Radial pulse and capillary refill should be obtained to evaluate vascular structures, including the axillary artery.¹¹

Radiographs are typically used for diagnostic purposes. Three views of the shoulder are used to evaluate the shoulder: AP, axillary, and Y view (Fig. 30–5). Evaluation of the humeral head position is imperative to assess for possible glenohumeral dislocation due to the frequency of concomitant injury.

For nondisplaced and minimally displaced proximal humerus fractures, the treatment is conservative with sling immobilization for 4 to 6 weeks. At 2 to 3 weeks, pendulum exercises and gentle range of motion may be initiated. At 6 weeks, isometric scapular stabilization and shoulder abduction exercises may be initiated.¹² Surgery is indicated with substantial displacement, anatomic neck involvement, or significantly decreased range of motion.¹³ Three-part and four-part fractures typically require surgical fixation. Surgical techniques include percutaneous fixation, intramedullary nail fixation, plate fixation, shoulder hemiarthroplasty, total shoulder arthroplasty, or reverse shoulder arthroplasty.

Midshaft Humerus

Midshaft humeral fractures typically occur from a direct blow to the middle third of the humerus.¹⁴ Patients present with arm pain and guarding. Deformity or arm shortening may be seen with midshaft fractures. Compromise of neurovascular structures may occur—most commonly with radial nerve or brachial artery. Patients with concurrent radial neuropathy may present with wrist and finger extensor weakness as well as dorsal numbness of the lateral hand and first through fourth digits. Brachial artery injury may present with hematoma, ecchymosis, and/or weak distal pulses.

The humerus is evaluated with AP and lateral radiographs. The glenohumeral, humeroulnar, and humeroradial joints should all be included to assess for proximal or distal extension.

Most humeral shaft fractures are managed nonoperatively. Shortening of less than 3 mm or varus deformity of less than 30 degrees has been found to have successful functional outcomes with conservative treatment.¹⁵ Conservative treatment consists of initial immobilization with a coaptation splint until edema resolves, then progression to functional bracing. Slings should be avoided to allow gravity-induced traction. Indications for surgery include open fracture, neurovascular injury, pathologic fractures, concurrent forearm fractures (floating elbow), and nonunion.

Scapula

The scapula is a flat triangular bone located on the posterior aspect of the shoulder girdle and thorax. The scapula serves as the origin and insertion of several muscles, which also serve to cushion and stabilize the structure. Fracture of the scapula usually involves high-force, direct trauma due to its abundant muscular coverage and unique shape. This high-energy mechanism of action leads to concomitant injuries in 90% of cases.¹⁶ Scapular fractures are described by their anatomic location (Fig. 30–6).

A patient with a scapular fracture typically presents with posterior shoulder pain with the affected arm in adduction; the pain is typically worse with any movement. Tenderness with light palpation of the scapula is common, and ecchymosis or hematoma may be present due to the high-energy nature of injury. Radiographs typically demonstrate fracture (see Fig. 30–7. Preferred views include AP, lateral, and axillary scapular views.¹¹ For equivocal radiographs, dedicated CT may be preferred.

Conservative treatment of scapular fracture is preferred and frequently results in proper bone healing.¹⁷ Initially, sling immobilization is utilized with early passive range of motion. Shoulder mobilization and strengthening may be initiated once full range of motion is achieved.¹⁸ Generally, patients have demonstrated good functional outcomes with these conservative measures, although poor functional outcomes have been seen in cases of substantial displacement. Due to these outcomes, surgery is indicated for displacement greater than 10 mm.¹⁹ Surgical intervention is also indicated for bone fragments within the joint capsule²⁰ and displaced scapular spine and neck fractures.²¹

Glenoid

The glenoid articulates with the head of the humerus and is located on the lateral aspect of the scapula. The glenohumeral joint is characteristically unstable due to the small area of articulation between the humerus and glenoid. The location of a glenoid fracture is determined by the mechanism of injury (Figs. 30–7 and 30–8). For rim or avulsion fractures, anterior subluxation or dislocation is the most likely pathophysiology. In the instance of fossa fractures, high-energy trauma with concurrent scapular fractures are common.²²

Patients typically present similarly to those with scapular fractures. A patient may present with an adducted arm and decreased range of motion of the shoulder. Tenderness to palpation is usually present. Recommended radiographs include anteroposterior, lateral, and trans-scapular views. CT scan is useful in determining the extent of fracture and presurgical planning.²²

Most glenoid neck fractures are treated conservatively, while fractures to the glenoid fossa and glenoid rim are treated with open reduction and internal fixation.^23,24 Glenoid fossa fractures with >20% involvement of the anterior aspect are typically treated with surgical correction.²⁴

Dislocation/Subluxation

Acromioclavicular

The AC joint is stabilized horizontally by the acromioclavicular ligament and vertically by the CC ligament (Fig. 30–9). Acromioclavicular joint dislocations account for 9% to 10% of shoulder girdle injuries in the general population, but account for up to 40% of shoulder girdle injuries in athletes.²⁵ The incidence is 2.8 per 10,000 individuals,²⁶ with 2.8% of AC joint dislocations being associated with clavicle fracture.²⁶ The most common mechanism of injury is direct trauma to the shoulder, while indirect trauma from a fall onto the affected arm may also result in AC joint injury.

Patients typically present with anterior shoulder pain and swelling. Shoulder movement is restricted due to pain, and patients may complain of nighttime pain when attempting to sleep on the affected shoulder. Deformity of the AC joint may be present with superior migration of the clavicle with relation to the acromion. On physical examination, the patient demonstrates tenderness with palpation of the joint and pain with cross-arm adduction.

Rockwood classified acromioclavicular separations into six categories²⁷:

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  Type I: Acromioclavicular ligament sprained, coracoclavicular ligament intact

  
  
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  Type II: Acromioclavicular ligament torn, coracoclavicular ligament sprained

  
  
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  Type III: Acromioclavicular and coracoclavicular ligament torn, up to 100% increase in coracoclavicular space

  
  
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  Type IV: Acromioclavicular and coracoclavicular ligament torn with posterior displacement of the clavicle

  
  
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  Type V: Acromioclavicular and coracoclavicular ligament torn, deltotrapezial fascia torn, with 100% to 300% increase in coracoclavicular space

  
  
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  Type VI: Acromioclavicular and coracoclavicular ligament torn with subchoracoid dislocation

Diagnostic evaluation is typically performed with radiographs. At least two perpendicular views are recommended, and additional evaluation of the clavicle and scapula may be beneficial to assess for concurrent injury. Stress radiographs with 10- to 150 pound weights being held in the affected limb may be obtained to evaluate for instability of the joint. Magnetic resonance imaging (MRI) may be utilized to differentiate type II from type III injuries or to evaluate for additional shoulder pathology²⁸ (Fig. 30–10).

Type I and type II AC joint sprains have universally demonstrated positive functional outcomes with conservative treatment. For these separations, treatment has been cataloged into three phases. Rehabilitation during the acute phase consists of sling immobilization, pendulum exercises, and isometric exercises. During the recovery phase, active and passive range of motion with axial loading is typically increased, in addition to kinetic exercises and dynamic stretches. Return to sport is the final stage and includes sport-specific drills and exercises. Reid recommends return to play in 2 to 4 weeks after a grade I injury, 4 to 8 weeks after grade II injury, and 6 to 8 weeks after grade III injury.²⁹ While treatment for grade III injuries remains controversial, a Cochrane Review in 2012 was unable to demonstrate superiority of surgical intervention when compared with nonsurgical intervention.³⁰ Surgical intervention is typically preferred for grade IV to VI joint separations.³¹

Glenohumeral Dislocation

The glenohumeral joint is a ball-and-socket joint that is inherently unstable due to the small surface area that the humerus articulates with the glenoid fossa. The joint capsule predisposes the shoulder to some degree of laxity. Shoulder dislocation frequently occurs with high-energy forces, which displace the humerus from the glenoid fossa. Acute shoulder dislocations due to isolated trauma are relatively rare and have an annual incidence of 1.1 per 100,000 individuals.³² The overall annual incidence of shoulder dislocation is between 23.1 and 23.9 per 100,000, with a much larger incidence occurring among males under the age of 30.³³ The vast majority of glenohumeral dislocations involve anterior displacement of the humerus. Anterior glenohumeral dislocation is approximately 20 times more common than posterior displacement.³²

Shoulder instability is likely multifactorial and can be secondary to osseous elements or soft tissue factors. Defects of the glenoid and humeral head are osseous elements that contribute to instability, while muscular weakness, capsular laxity, and labral pathology are soft tissue factors.³⁴ The anterior portion of the shoulder capsule is stabilized by the superior, middle, and inferior glenohumeral ligaments. In contrast, the posterior capsule is fortified by infraspinatus, teres minor, and subacromial bursa (Fig. 30–11). The glenohumeral joint’s anterior laxity may progress to instability due to trauma or recurrent stresses.¹² Anterior shoulder instability accounts for 80% to 90% of shoulder instability.^32,35 Posterior shoulder instability accounts for approximately 10% of shoulder instability,³² while multidirectional instability (MDI) accounts for less than 5%.³⁶

Patients with a dislocated shoulder present with pain of their shoulder, guarding of the affected limb, and self-limited range of motion. On physical examination an acutely dislocated shoulder will demonstrate decreased range of motion. Physical deformity and possibly a small sulcus may be seen inferior to the lateral aspect of the acromion. Special physical examination maneuvers include anterior apprehension test (for anterior instability), posterior apprehension test (for posterior instability), and sulcus sign (for multidirectional instability)³⁷ (Fig. 30–12). Rotator cuff and neurovascular evaluation must be completed due to frequent association of injuries.

Radiographs are an accessible and cost-effective method to confirm shoulder dislocation. Three views should be obtained (AP, axillary, and trans-scapular). The trans-scapular view demonstrates directionality of displacement (Fig. 30–13).

Anterior dislocations are associated with Bankart and Hill-Sachs lesions. A Bankart lesion (Fig. 30–14) is a fracture of the inferior glenoid that occurs with an anteroinferior labral injury.³⁸ A Hill-Sachs lesion (Fig. 30–15A and B) is a compression defect of the superoposterolateral humeral head that occurs when the humeral head compresses the anterior glenoid.³⁹ Posterior dislocations are consistent with reverse Bankart lesion and reverse Hill-Sachs lesions. A reverse Bankart lesion is an injury to the posterolateral labrum and glenoid. A reverse Hill-Sachs lesion is a compression defect of the anteromedial aspect of the humeral head.

Traumatic anterior dislocations are typically treated with reduction (Fig. 30–16) and immobilization. Immobilization has been shown to prevent recurrence of shoulder dislocation in 50% of traumatic shoulder dislocation patients.⁴⁰ Risk factors for recurrent dislocation include male sex, younger age at initial dislocation, joint hypermobility, and greater tuberosity fractures.³³ Physical therapy is recommended to commence 2 to 3 weeks after dislocation. A strengthening program consisting of progressive band resistance for 6 weeks in duration has demonstrated improvements in strength and range of motion.⁴¹ Although surgical intervention has been demonstrated to be effective for young individuals with traumatic shoulder dislocation,⁴² arthroscopic repair of Bankart lesions reveals a high incidence of recurrent instability.⁴³

For atraumatic or multidirectional instability, physical therapy should consist of a 6-month program including periscapular and rotator cuff strengthening.⁴⁴ Therapy is most effective when each contributing element (glenoid and humeral defects, muscular weakness, capsular laxity, labral pathology) of instability is targeted.⁴⁵ Conservative treatment of chronic shoulder instability has been found to be superior to surgical intervention.⁴¹ For those who undertake surgical intervention, arthroscopic repair demonstrates similar outcomes to open capsular shift.⁴⁶

Muscle/Tendon Injuries

Biceps Tendon, Proximal

The biceps brachii is a muscle that traverses the shoulder and elbow joints. The muscle consists of a short head and a long head (Fig. 30–17). The long head of the biceps tendon originates within the shoulder capsule at the supraglenoid tubercle and attaches to the superior aspect of the glenoid labrum. The long head exits the glenohumeral joint between the supraspinatus and subscapularis tendons and extends through the bicipital groove of the humerus before forming a single muscle belly. Recent evidence indicates the tendon helps stabilize the glenohumeral joint.⁴⁷ The short head originates at the coracoid process and forms a muscle belly that joins with the belly of the long head to form the biceps brachii.

The long head of the biceps tendon (LHBT) has been described as a source of shoulder pain since as early as the seventeenth century.⁴⁸ LHBT rupture is seen most commonly with weightlifters and overhead throwing athletes, while other tendinopathy is associated with degenerative and overuse lesions of the rotator cuff and labrum.⁴⁹ Shoulder impingement is commonly seen in patients with biceps tendinitis with some estimates as high as 95% concurrence.⁵⁰

Patients with injury to the long head of the biceps present similarly to those with rotator cuff pathology. Patients typically complain of anterior shoulder pain that is exacerbated with activity. The “Popeye sign” may be seen with complete rupture of the tendon (Fig. 30–18). Provocative maneuvers for biceps pathology include Speed’s test and Yergason’s test (Fig. 30–19). For Speed’s test, the patient extends the elbow and fully supinates the forearm. A positive test elicits pain when the shoulder is flexed to 90 degrees against resistance. Sensitivity and specificity for the Speed’s test is 32% and 61%, respectively.⁵¹ The Yergason’s test is positive when anterior shoulder pain is elicited with resisted forearm supination and elbow flexion. Given the preponderance of concurrent labral or rotator cuff injuries in the setting of LHBT pathology, additional provocative maneuvers may be completed. These may include O’Brien’s test (glenoid labrum), Hawkins’ maneuver (impingement), empty can test (supraspinatus), resisted external rotation (infraspinatus), and/or lift-off test (subscapularis).

While bicipital injuries are rarely seen on radiographs, they are utilized to rule out bone irregularities. Concurrent abnormalities such as acromioclavicular injury or glenohumeral pathology may also be seen. Diagnostic ultrasound and MRI have demonstrated accuracy in assessment of bicipital injuries. Ultrasound has been shown to be accurate in diagnosing biceps tendon subluxation or complete tear. MRI has been demonstrated to be more sensitive in diagnosing incomplete tears and acute tendinitis.⁵²

Eccentric-based exercise programs are recommended for biceps tendinopathy. Therapy programs should begin at low intensity and low speed with gradual progressions. A minimum of 20 to 30 sessions is recommended.⁵³ Ultrasound-guided steroid injections around the LHBT may provide temporary pain relief for some patients.⁵⁴ Conservative treatment is preferred with proximal ruptures.⁴⁷ Surgical treatment may be indicated for pathology refractory to conservative treatment. Biceps tenodesis is preferred in younger and more active patients, while biceps tenotomy is an option for patients over the age of 60.⁵⁵ No significant differences have been found in outcomes for open versus arthroscopic LHB tenodesis.⁵⁶

Rotator Cuff

The rotator cuff provides dynamic stability to the glenohumeral joint and consists of four muscles and tendons that insert on the humeral tuberosities: supraspinatus, infraspinatus, teres minor, and subscapularis (Figs. 30–20 and 30–21). Rotator cuff pathology is the most common cause of shoulder pain and disability,⁵⁷ but not all rotator cuff pathology is symptomatic. As much as 34% of asymptomatic subjects undergoing MRI were found to have rotator cuff tears; 15% had full-thickness tears, while 20% had partial-thickness tears.⁵⁸ In individuals over the age of 60, the prevalence of rotator cuff tears in asymptomatic individuals increased to 52%. Risk factors for rotator cuff tears include increased age, history of trauma, hand dominance, smoking, hypercholesterolemia, and genetics.⁵⁹

The supraspinatus tendon is the most commonly injured tendon of the rotator cuff. This is thought to be due to compressive forces against the acromion. Repeated shoulder abduction and internal rotation may lead to recurring shoulder impingement and stress on the supraspinatus tendon and subacromial bursa. With injury, the supraspinatus tendon becomes edematous and hemorrhagic. Repeated injury leads to fibrotic thickening and degeneration, which leads to tendinosis or degenerative tears⁶⁰ (Fig. 30–22).

Infraspinatus tendinopathy has increased prevalence among overhead throwing athletes, although this is still less common than supraspinatus tendinopathy.⁶¹ Overhead throwers have been found to have increased range of motion with external rotation. Repeated external rotation forces lead to glenohumeral internal rotation deficits, scapular dyskinesias, and internal shoulder impingement.⁶² Articular-sided tears become prevalent as the distal infraspinatus tendon impinges within the glenohumeral joint.

Patients with rotator cuff pathology present with insidious anterolateral shoulder pain that is worse with overhead activities and sleep. Nocturnal pain is common, although small incomplete tears affect sleep quality more than large, complete tears.⁶³ Physical examination may demonstrate weakness with shoulder abduction and external rotation. The empty can test and full can test both have utility in evaluating for supraspinatus pathology. The empty can test (Fig. 30–23) is performed by placing the affected arm parallel to the ground and internally rotating the arm to 90 degrees. The examiner then applies a downward force upon the arm while the patient provides resistance. A positive test may have pain or weakness. The full can test is performed in a similar manner, but the arm is rotated to 45 degrees of external rotation. Recent evidence has demonstrated less recruitment of middle deltoid and improved isolation of the supraspinatus when the full can test is used.⁶⁴ There is still insufficient evidence to demonstrate improved positive predictive value for one physical examination maneuver over the other.⁶⁵ Pain and weakness with resisted external rotation are indicative of infraspinatus pathology.⁶⁶

Radiographs of the shoulder should be obtained to evaluate for translation of the humeral head or calcific deposits at the insertion of the rotator cuff. Superior migration of the humeral head may be seen with a complete tear of the supraspinatus. Calcific deposits may be seen in enthesopathy or calcific tendinosis. Diagnostic ultrasound and MRI have similar sensitivities, while MR arthrogram has demonstrated the slightly improved positive predictive value.⁶⁷

Conservative treatment with nonsteroidal anti-inflammatory medications and physical therapy is preferred with rotator cuff tendinitis and partial-thickness tears.⁶⁸ Closed chain exercises with a focus on proximal to distal progression have been the preferred therapy algorithm for rotator cuff pathology.⁶⁹ Initial exercises should focus on scapular stabilization with progression to shoulder external rotation and the shoulder abductors and shoulder flexors once improvement has been demonstrated. Physical therapy has been shown to decrease pain, increase range of motion, and improve functional scores.⁷⁰ Subacromial bursa injections may provide temporary relief, although the efficacy of the injection is less when performed in the setting of normative bursa.⁷¹ Recent evidence has demonstrated decreased pain and improved shoulder function with ultrasound-guided platelet-rich plasma injection for partial rotator cuff tears.⁷²

Surgical repair is recommended in acute full-thickness tears in patients of all ages, as well symptomatic, chronic tears in patients under the age of 65.⁵⁸ Aggressive physical therapy immediately after rotator cuff repair has been associated with surgical failure, but tempered physical therapy with range-of-motion restrictions has been shown to be beneficial without increased risk of reinjury.^73–75

Labral Tears

The glenoid labrum is composed of fibrocartilaginous tissue and serves to deepen the glenoid fossa and improve articulation with the humerus. The labrum deepens the socket by approximately 50% and helps reduce subluxation or dislocation.⁷⁶ The labrum also serves as an attachment site for the glenohumeral ligaments and the long head of the biceps brachii. The long head of the biceps brachii attaches at the superior aspect of the labrum, and injuries to the biceps tendon and superior labrum are commonly injured in overhead throwing athletes. Superior labral anterior-to-posterior (SLAP) tears are commonly associated with concurrent biceps tendon injury due to their anatomic relationship. Injury to the inferior labrum and inferior glenohumeral ligament is associated with Bankart lesions (see Fig. 30–9). Although the incidence of labral injuries is unknown in the general population, labral tears have an incidence of 9.8% in those over the age of 65.⁷⁷

Labral tears may occur from acute injury or overuse. Acute tears occur with high-energy forces of the humerus as it translates across the glenoid labrum. Typically, this is seen with a fall onto an outstretched arm. In overhead throwers, the humerus is “cocked” into the end range of external rotation, which causes posterosuperior translation of the humerus. With the subsequent sudden acceleration of the humerus, anterior translation occurs. These events result in a “peel-back phenomenon” and can cause superior labral injury. SLAP tears are classified into five groups (Fig. 30–24):

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  I: Superior labrum fraying

  
  
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  II: Detachment of superior labrum

  
  
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  III: Bucket handle tear with anchored biceps tendon

  
  
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  IV: Labral tear extending into biceps

  
  
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  V: Combination of prior tears

Labral injuries typically present with diffuse, vague shoulder pain. Clicking or popping may be present and indicative of an acute tear. Patients may present with decreased range of motion with shoulder abduction, internal rotation, or external rotation. O’Brien’s test has a positive predictive value of 90%.⁷⁸ Bankart lesions may be seen on radiographs, and MR arthrograms have improved sensitivity, specificity, and accuracy in diagnosing labral injures when compared to MRI (Fig. 30–25).⁷⁹

Conservative treatment, including physical therapy and nonsteroidal anti-inflammatory medications, has demonstrated improved pain, function, and quality of life. Therapy is typically guided toward scapular stabilization, correction of glenohumeral internal rotation deficits, and rotator cuff strengthening. Glenohumeral joint steroid injections may provide 2 to 4 months of relief and are recommended to be used in conjunction with physical therapy. Ultrasound-guided glenohumeral joint injections have demonstrated superior accuracy when compared to landmark-based injections: 92.5% versus 72.5% accuracy, respectively.⁸⁰ Half of all patients with labral tears are able to avoid surgery with conservative treatment.⁸¹

Adhesive Capsulitis

Adhesive capsulitis, or “frozen shoulder,” is a painful shoulder condition associated with profound loss of range of motion. The incidence of adhesive capsulitis has been estimated to be between 2% and 3% of the general population, and as many as 20% of diabetics are diagnosed with this condition.⁸² The incidence of frozen shoulder peaks between the ages of 40 and 70.⁸³ Adhesive capsulitis may be present as an isolated diagnosis or seen in the setting of concurrent shoulder injury. Rotator cuff injury, biceps tendon injury, labral injury, shoulder impingent, cancer, and recent surgery may all contribute to the incidence of secondary adhesive capsulitis.⁸⁴

While synovial hyperplasia and capsular fibrosis contribute to adhesive capsulitis, the exact pathophysiology is still debated. Cytokines, such as platelet-derived growth factor (PDGF) and transforming growth factor–beta (TGF-β), have been implicated in initiating adhesive capsulitis via an autoimmune response.⁸⁵ There are three stages of adhesive capsulitis: freezing, frozen, and thawing. The freezing stage consists of increasing pain and decreasing range of motion. This stage typically lasts 2 to 9 months. The frozen stage is characterized by minimal to no pain but decreased range of motion. The stage can last 4 to 9 months. The thawing stage involves improving range of motion and can take 6 to 24 months.

Patients with adhesive capsulitis present with pain in the shoulder and decreased range of motion. Diffuse tenderness is usually present over multiple shoulder structures. External rotation deficit in the absence of glenohumeral arthritis is the most predictive physical examination maneuver.⁸⁶ While range of motion may be affected with shoulder flexion, abduction, and internal rotation, deficits in external rotation are typically the first clinical manifestation. Range of motion is affected both actively and passively. Full shoulder examination with provocative tests is encouraged to rule out additional contributing pathology. The patient’s strength should be full in the absence of additional pathology.

If adhesive capsulitis is suspected, imaging should be obtained to rule out any other factors that may cause pain and decreased range of motion. Radiographs will help evaluate for fracture, dislocation, and glenohumeral arthritis. The diagnosis of adhesive capsulitis may be made clinically in the absence of clinically significant radiograph findings. Capsular thickening and other contributing conditions may be seen on MRI (Fig. 30–26).

Frozen shoulder is typically a self-limiting condition that lasts 6 to 24 months on average. While physical therapy geared toward range of motion is typically recommended, a 2014 Cochrane Review determined that manual therapy and exercise was not as effective as glucocorticoid injection.⁸⁷ Glenohumeral joint steroid injections have demonstrated improvement in pain scores, range of motion, and shoulder function.^88,89 Patients who do not demonstrate benefit with at least 12 weeks of conservative treatment may be a candidate for shoulder manipulation under anesthesia. Risks of manipulation include humeral fracture, glenohumeral dislocation, and rotator cuff injury.⁹⁰ For those with persistent symptoms, surgical release has been shown to provide benefit.⁹¹

Neurovascular

Axillary Nerve Injury

The axillary nerve (Fig. 30–27) is a branch off the posterior cord of the brachial plexus and receives contribution from C5 and C6. The nerve provides sensation to the lateral shoulder and motor innervation to the deltoid and teres minor. The axillary nerve is located inferior to the glenohumeral joint capsule and may be injured with subluxation or dislocation of the humerus. Approximately 25% of anterior glenohumeral dislocations are associated with injury to the axillar nerve. Axillary neuropathy may also be seen after humeral fractures or after arthroscopic capsular release.⁷⁶

Patients with axillary neuropathy present with shoulder abduction weakness and lateral shoulder numbness. Electromyography (EMG) may be performed 3 to 6 weeks after injury. This may be repeated at 12 weeks to evaluate for reinnervation patterns. Most cases of axillary nerve injury will spontaneously recover. Treatment is geared toward physical therapy, rest, and time. If nerve function does not recover in 3 to 6 months, then surgical intervention may be performed. Axillary nerve grafting has demonstrated improvement in deltoid function in 73% to 88% of cases.⁹² Sensory function typically returns prior to motor recovery.

Long Thoracic Nerve Injury

The long thoracic nerve branches from the roots of C5, C6, and C7 and provides innervation to the serratus anterior. The serratus anterior protracts and stabilizes the scapula against the chest wall. The nerve is superficial and may be injured by compressive forces on the shoulder, such as carrying heavy objects or weightlifting.⁹³ Patients may present with shoulder pain, weakness, and medial winging of the scapula. In medial winging, the medial aspect of the scapular spine moves superior and medial (Fig. 30–28).

Injury to the long thoracic nerve may occur from trauma or may occur without specific injury. Conservative treatment is preferred and includes physical therapy, time, and rest. Most patients demonstrate improvement in 12 to 24 months. For refractory cases surgical intervention may be performed. Scapulothoracic fusion has demonstrated improved pain and function scores but has complication rates of around 50%.⁹⁴ The scapula may also be stabilized by transfer of the sternal head of the pectoralis major to the inferior angle of the scapula. This has also demonstrated improvement in pain, function, and scapular winging.⁹⁵

Radial Nerve Injury

The radial nerve (Fig. 30–29) is a branch from the posterior cord of the brachial plexus and receives contribution of the C5, C6, and C7 nerve roots. The nerve first provides innervation to the triceps and anconeus as it enters the spiral groove of the humerus. After the spiral groove, the radial nerve innervates the brachioradialis, extensor carpi radialis longus, extensor carpi radialis brevis, and supinator. The nerve branches into a superficial sensory branch and the posterior interosseous nerve (PIN). Please see the elbow neurovascular section for information regarding PIN.

The radial nerve is the most common peripheral nerve injury associated with humeral fractures due to the nerve’s course through the spiral groove.⁹⁶ Up to 22% of humeral fractures are associated with radial nerve injury.⁹⁷ Patients with injury to the radial nerve present with wrist drop, finger extensor weakness, and sensory deficit to the dorsal aspect of the radial hand. EMG may be performed at 3 to 6 weeks post-injury and may be repeated at a later date to evaluate for reinnervation patterns.

Sixty percent to 92% of radial nerve injuries associated with humeral fractures will improve without interventions.⁹⁸ Average conservative recovery time has been found to be as low as 7.3 weeks.⁹⁹ Conservative treatment includes physical therapy, time, and rest. Routine surgical intervention with radial nerve exploration is not recommended but has been shown to provide benefit when recovery of the nerve is delayed.¹⁰⁰ Surgical intervention performed more than 5 months post-injury has been associated with poor outcomes. As a result, surgery is recommended at 4 to 5 months post-injury.¹⁰¹ Tendon transfers have demonstrated improved functional abilities for those patients with persistent symptoms over a year after injury.¹⁰²

Suprascapular Nerve Injury

The suprascapular nerve arises from C5 and C6 and provides motor innervation to the supraspinatus and infraspinatus. The nerve also supplies sensation to the posterior glenohumeral capsule.¹⁰³ The nerve may become entrapped in the suprascapular notch by the transverse scapular ligament or in the spinoglenoid notch.¹⁰⁴ The nerve is commonly compressed in athletes who excessively abduct the arm in full rotation.¹⁰⁵

Patients may present with vague posterior shoulder pain and weakness with shoulder abduction and external rotation. Abduction is typically most affected in the first 30 degrees. Electromyography and nerve conduction study have been shown to have a 91% positive predictive value.¹⁰⁶ MRI may show atrophy of the infraspinatus and supraspinatus muscles. Suprascapular nerve blocks with local anesthetic can also help confirm the diagnosis of suprascapular neuropathy (Fig. 30–30).

Conservative treatment consists of activity modification, nonsteroidal anti-inflammatory medications, and physical therapy. A 6- to 12-month physical therapy program consisting of shoulder strengthening and range of motion has demonstrated benefit.¹⁰⁶ Conservative treatment of suprascapular nerve entrapment has demonstrated better outcomes when the etiology is overuse when compared to compressive lesion, such as a mass or cyst.¹⁰⁷ Surgical correction typically involves release of the transverse scapular ligament and removing compressive masses.¹⁰⁸

Parsonage-Turner Syndrome

Brachial plexus neuritis (Parsonage-Turner syndrome [PTS]) presents with sudden onset of shoulder pain and upper extremity weakness. PTS is an idiopathic neuropathy of the brachial plexus (Fig. 30–31). The incidence of PTS has been estimated at 1.64 cases per 100,000 person-years.¹⁰⁹ The upper trunk is most commonly affected, but single or multiple mononeuropathies may be present.¹¹⁰ Like other neuropathies, diagnosis may be made by EMG 3 to 6 weeks after onset of symptoms. Imaging of the cervical spine should be performed to rule out cervical spine pathology.

Motor and sensory recovery usually occurs in 6 to 12 weeks and is self-limited.⁹³ Ninety percent of patients achieve full recovery within 3 years of onset.¹¹¹ Initial treatment is symptom management with nonsteroidal anti-inflammatory medications, opioids, and neuroleptics. Oral steroids may be used during the acute phase, although evidence has not demonstrated their efficacy.¹¹² Physical therapy is recommended to focus on strengthening, range of motion, and modalities such as transcutaneous electrical nerve stimulation (TENS).¹¹³

Shoulder Impingement

Rotator cuff impingement is a generic term that refers to compression of the rotator cuff. The shoulder may be compressed externally or internally. External shoulder impingement refers to the superficial aspect of the rotator cuff compressing between two bones. External impingement may have primary or secondary etiologies. Secondary impingement syndrome is due to abnormal glenohumeral or scapulothoracic motion. Instability of the shoulder joint may secondarily cause the rotator cuff to compress against osseous structures. Internal impingement refers to the deep aspect of the rotator cuff compressing within the glenohumeral joint.

Subacromial Impingement

Subacromial impingement syndrome (SAIS) is the most common disorder of the shoulder and affects one in three adults.¹¹⁴ Over half of all patients with shoulder pain have subacromial impingement.¹¹⁵ SAIS refers to the compression of the bursal side of the supraspinatus between the acromion and humeral head (Fig. 30–32). Compression may occur due to the morphology of the acromion (primary impingement) or to superior migration of the humeral head (secondary). There are four types of acromial morphology: I, flat; II, curved; III, hooked; and IV, convex.¹¹⁶ A hooked acromion is most commonly associated with shoulder impingement.¹¹⁷

Patients typically present with insidious lateral shoulder pain, which is worse with shoulder abduction and internal rotation. The patient may also complain of nocturnal pain. Neer’s test may be performed by internally rotating the affected arm and passively flexing the shoulder to 160 degrees while stabilizing the scapula (Fig. 30–33). The Hawkins-Kennedy test may also be performed. The examiner flexes the subject’s elbow to 90 degrees and abducts the shoulder to 90 degrees. The shoulder is then maximally rotated internally (Fig. 30–34). Sensitivity for the Neer’s test and Hawkins-Kennedy test are similar (79%), although specificity for Hawkins-Kennedy is higher (59% vs. 53%).⁵¹

For the Hawkins-Kennedy test, the arm is passively flexed forward to 90 degrees and the elbow is flexed to 90 degrees. When the examiner internally rotates the shoulder, pain indicates impingement of the supraspinatus tendon.

SAIS is typically a clinical diagnosis, although radiographs may be performed to evaluate for the morphology of the acromion. Diagnostic dynamic ultrasound may be performed to evaluate for compression of the supraspinatus under the acromion with internal rotation of the shoulder. Acromiohumeral distance may also be measured to diagnose and prognosticate subacromial impingement.¹¹⁸ MRI may be used to evaluate for subacromial osteophytic spurs, subacromial bursitis, or supraspinatus tendinopathy.¹¹⁹

Physical therapy has demonstrated strength and functional improvements, although there is a lack of established protocol.¹²⁰ In the instance of secondary impingement syndrome, therapy should be guided toward correction of abnormal shoulder movement. Anti-inflammatory medications and avoidance of overhead activities may provide some relief. Subacromial bursa steroid injections may provide up to 6 months of relief.¹²¹ Platelet-rich plasma injections have demonstrated benefit but were not as effective as a physical therapy program.¹²² Recent evidence has shown physical therapy may provide similar benefits when compared with acromioplasty.

Subcoracoid Impingement

Subcoracoid impingement refers to the compression of the subscapularis between the coracoid process and lesser tuberosity. Although the exact prevalence of subcoracoid bursal impingement is unknown, the condition is much less common than subacromial bursitis.¹²³ Due to its low prevalence, coracoid impingement is an underrecognized cause of anterior shoulder pain. The tendon is typically impinged with shoulder flexion, shoulder adduction, and internal rotation. Patients typically present with anterior shoulder pain, which worsens with any of the aforementioned movements.¹²⁴ Physical examination may reveal tenderness on the anterior coracoid.

Radiographs may be performed to evaluate the coracohumeral distance. MRI may be performed to assess the integrity of the subscapularis. MRI has long been the gold standard for diagnosing subcoracoid impingement, although ultrasound has recently demonstrated diagnostic utility.¹²⁵

Physical therapy focusing on flexibility of the scapular protractors and strengthening of scapular stabilizers has demonstrated benefit. Subcoracoid bursa injection and botulinum toxin injections to the subscapularis have both demonstrated improvement in pain.¹²⁶ For refractory cases, coracoplasty may be performed, although there is limited evidence to support surgical intervention.¹²⁷

Internal Impingement

Internal (posterosuperior) impingement is a common cause of posterior shoulder pain in overhead throwing athletes. Excessive external rotation and inadequate internal rotation lead to posterior shoulder tightness and anterior laxity. This results in friction of the articular side of the rotator cuff against the labrum. Articular infraspinatus tears develop as the deep portion of the infraspinatus is compressed between the humeral head and the posterior labrum. Maximal impingement is present during late cocking and early acceleration phases and can cause “peel-back” of the posterior labrum (see the labral tear section for further details).

Patients present with insidious onset of vague posterior shoulder pain, which may be associated with loss of velocity or control.¹²⁸ They typically demonstrate posterior glenohumeral joint tenderness and more than 20 degrees decreased internal rotation when compared to the contralateral side. Internal rotation resisted strength test and positive posterior impingement test are usually positive. For the posterior impingement test, the patient is placed in the supine position, the shoulder is abducted to 90 degrees, the elbow is flexed to 90 degrees, and the shoulder is maximally externally rotated. A positive test re-creates posterior shoulder pain. For the resisted internal rotation strength test, the patient’s shoulder is abducted to 90 degrees and the elbow is flexed to 90 degrees. The patient is then asked to provide resistance with both internal and external rotation. Weakness of internal rotators when compared to external rotators is indicative of pathology.

Radiographs may show calcification of the posterior capsule (Bennett’s lesion). Diagnostic ultrasound has been used to evaluate for internal impingement syndrome.¹²⁹ MRI will typically demonstrate posterior labral tears, biceps tendinopathy, and articular-sided infraspinatus tears at the supraspinatus-infraspinatus junction.¹³⁰

Physical therapy should be guided toward posterior capsule stretches, glenohumeral internal rotation, scapular stabilization, and eccentric rotator cuff exercises.^131,132 Glenohumeral joint injections have provided more diagnostic than therapeutic benefit.¹³³ No single surgery has demonstrated superiority. Surgical intervention may include infraspinatus repair, labral repair, posterior capsule release, or anterior stabilization.

Fractures

Radial Head

Radial head fractures account for one-third of all elbow fractures and are the most common fracture of the elbow and forearm.¹³⁴ The incidence is estimated at 25 to 28 fractures per 100,000 person-years.¹³⁴ The peak incidence in males is between the ages of 30 and 40, while the peak incidence for women rises after the age of 50 due to the increasing prevalence of osteoporosis.¹³⁵

Fractures occur when falling onto a partially flexed or pronated elbow or when sustaining high-energy valgus force onto the elbow.¹³⁶ In 1954, Mason classified radial head fractures into three classes (Fig. 30–35). Type I involves a nondisplaced radial head fracture. Type II involves a single displaced fracture. Type III is a comminuted fracture. In 1962, Johnson added a fourth type to Mason’s classification. He classified radial head fractures associated with elbow dislocation as type IV.¹³⁷ The radiocapitellar joint is an important valgus stabilizer, and injury to the radial head commonly leads to concurrent injury. Ligamentous injury, ulnar fracture, capitellar injury, and elbow dislocation are seen in 39% of radial head fractures.¹³⁸

Patients present with lateral elbow pain and guarding of the affected arm. Pain is exacerbated with pronation or supination of the elbow. Elbow swelling and tenderness at the radial head may also be indicative of fracture. Anteroposterior and lateral radiographs should be obtained and may demonstrate radiolucency anterior to the distal humerus. This “fat pad sign” (Fig. 30–36) is indicative of edema or hematoma secondary to fracture. An oblique view may be obtained to better visualize the radial head.

Type I (nondisplaced) fractures are treated conservatively with sling and early mobilization.¹³⁹ Patients with the earliest mobilization have been found to have the best outcomes.¹⁴⁰ Joint aspiration may be performed to decrease pressure and short-term pain.¹⁴¹ Treatment of type II (displaced) fractures has been controversial. Both conservative treatment and surgical fixation have demonstrated good outcomes.¹⁴¹ A review of nine retrospective series was unable to demonstrate superiority of either treatment option.¹⁴² Open reduction and internal fixation (ORIF) or elbow arthroplasty is indicated for type III (comminuted) fractures. Comminuted fractures with two to three fragments have demonstrated good outcomes with ORIF but unsatisfactory outcomes when more than three fragments are present.¹⁴³ A recent study demonstrated superiority of elbow arthroplasty when compared to open reduction and internal fixation.¹⁴⁴

Supracondylar

Supracondylar fractures (Fig. 30–37) are the most common fractures seen in children and have a peak incidence from 5 to 10 years old.¹⁴⁵ Supracondylar fractures are the most common type of humeral fracture in the pediatric patient and are estimated at 60% of all pediatric elbow fractures.^146,147 Fractures classically occur onto an outstretched arm with the elbow hyperextended.

Patients typically present with elbow pain, swelling, and tenderness. Guarding is present with decreased elbow range of motion. AP and lateral radiographs should be obtained. Anterior or posterior fat pad sign may indicate nondisplaced supracondylar fracture (Fig. 30–38). MRI may be completed to evaluate for concurrent injury.

Supracondylar fractures are classified by Gartland’s classification.¹⁴⁷ Type I is a nondisplaced fracture. Type II refers to posterior angulation of the distal fragment with intact periosteal hinge. Type III fractures are completely displaced.

Type I supracondylar fractures may be treated with 3 to 4 weeks of cast immobilization. Closed reduction and percutaneous pin fixation are recommended for type II fractures. The elbow should be immobilized with a fixated pin for 4 to 6 weeks. Neurovascular examination should be performed with any type III fracture to rule out injury to the brachial vessels. Emergent angiogram should be performed if pulses are absent. Injury to the brachial artery is a surgical emergency, and treatment should not be delayed. Pin fixation and immobilization should be performed in the absence of neurovascular injury.³¹

Olecranon

Olecranon fractures account for 10% of elbow fractures¹⁴⁸ and 20% of all proximal forearm fractures.¹⁴⁹ Olecranon fractures are usually caused by high-energy direct trauma but may also occur with forceful triceps contraction. Patients present with posterior elbow pain, guarding of the affected arm, elbow swelling, joint crepitus, elbow defect, and/or localized tenderness.

Anteroposterior and lateral radiographs are recommended for diagnosis. The Mayo classification is used to distinguish type of olecranon fractures and guide treatment. Type I is a nondisplaced fracture. Type II is a displaced, ulnohumeral-stable fracture. Type III is a displaced, ulnohumeral-unstable fracture. Letter “A” indicates noncomminuted, while letter “B” indicates comminuted.

Conservative treatment is preferred for nondisplaced olecranon fracture.¹⁴⁸ Cast immobilization is recommended for 4 to 6 weeks, and rehabilitation should include elbow extensor strength and range of motion.¹⁵⁰ Open reduction and internal fixation of displaced, olecranon fractures has demonstrated improved pain, functional scores, and range of motion.¹⁵¹ Recent studies have demonstrated improved functional elbow scores with conservative treatment of displaced, noncomminuted olecranon fractures in older, lower-demand patients.^152,153

Dislocation

The elbow is the most commonly dislocated joint in the pediatric population, and the second most commonly dislocated joint after the shoulder in the adult population.¹⁵⁰ The annual incidence is 5.21 per 100,000 person-years with the highest incidence from ages 10 to 19 years old.¹⁵⁴ Elbow dislocations are commonly associated with sports such as football, wrestling, gymnastics, and ice skating. Elbow dislocations are classified into three groups: posterior, anterior, and divergent (Fig. 30–39). Posterior dislocations are the most common dislocations and account for over 90% of elbow dislocations.¹⁵⁵ While anterior dislocations are uncommon, divergent locations are the rarest. Divergent dislocations occur when the radius and ulna dissociate in opposite directions.

The elbow is commonly dislocated after falling onto an outstretched hand with rotation of the forearm and axial compression. O’Driscoll and colleagues proposed that rupture of the lateral ulnar collateral ligament results in posterolateral instability causing the forearm to externally rotate and displace, with circumferential tearing of the capsuloligamentous structures.¹⁵⁶ In the instance of radial head dislocation, the radial head becomes trapped underneath the annular ligament.

Patients present with pain and guarding of the elbow with the joint flexed at 45 degrees. Bony landmarks are seen in the acute phase, but edema obscures anatomic landmarks as time passes. In posterior dislocations, the olecranon is displaced posteriorly and resembles a displaced supracondylar fracture.¹⁵⁷ Neurovascular examination should be completed, as vascular injury occurs in 5% to 13% of cases.¹⁵⁸ Neurologic examination may demonstrate injury to the ulnar, radial, and/or median nerve.