Once an accurate diagnosis has been made with a thorough history, physical examination, and appropriate diagnostic testing, an effective treatment program can be developed. Kibler ⁸³ has proposed three broad stages of rehabilitation, including the acute stage, recovery stage, and the functional stage. The acute stage of rehabilitation focuses on reducing the patient’s symptoms and facilitating tissue healing. In specific circumstances, immobilization through splinting or casting might be used during the acute stage of rehabilitation.

RICE (rest, ice, compression, and elevation) is frequently used in this phase of rehabilitation. Rest should not be absolute. It is important for the patient to maintain cardiovascular fitness, strength, and flexibility during this phase. In fact, core strengthening and aerobic conditioning should be emphasized during this phase of rehabilitation. The patient should be instructed on appropriate activities that can be performed during the acute stage of rehabilitation that will not aggravate symptoms nor be detrimental to tissue healing. For example, if a volleyball player has rotator cuff tendonitis, activities that could be done include passive glenohumeral joint range-of-motion (ROM) exercises to maintain flexibility and glenohumeral joint health, riding a stationary bicycle for cardiovascular fitness, and performing scapular stabilizing exercises in preparation for more advanced rehabilitative exercises of the shoulder. Kinetic chain deficits should be identified and treated during the acute rehabilitation stage.

During the acute phase of rehabilitation, cryotherapy can be used for acute injuries to decrease pain, inflammation, muscle guarding, edema, and local blood flow.^70,⁸² Heat increases blood flow, reduces muscle “spasm,” reduces pain, and can be used in the acute phase of rehabilitation for chronic injuries.⁸² High-frequency electrical stimulation is often used during the acute phase of rehabilitation to reduce muscle guarding and increase local circulation.¹⁸⁹

Opioid and nonopioid analgesics might be required for pain control during the acute phase of rehabilitation. Nonsteroidal antiinflammatory drugs (NSAIDs) are often used for their analgesic and antiinflammatory properties. Randomized, placebo-controlled trials have demonstrated reduced pain, edema, and tenderness, and a faster return to activity in NSAID-treated athletes than in those treated with placebo.^4,¹⁸⁶ It is important to remember, however, that NSAIDs are not entirely benign and can cause significant gastrointestinal, renal, cardiovascular, hematologic, dermatologic, and neurologic side effects.^32,^60,¹⁷⁵ Because of these concerns, NSAIDs should be used only if local physical modalities and less toxic medications such as acetaminophen are not effective.

Oral and injected corticosteroids have also been used for pain control and reduction of inflammation during the acute phase of rehabilitation. Because of the possibility of significant systemic and localized consequences of corticosteroid use, however, their use should be limited to very select cases.^53,¹⁵⁶ These side effects include suppression of the hypothalamic–pituitary–adrenal axis, osteoporosis, avascular necrosis, infection, and tendon or ligament rupture.

The patient can advance to the recovery phase of rehabilitation when the pain has been adequately controlled and tissue healing has occurred.⁸³ This is indicated by full pain-free ROM and the ability to participate in strengthening exercises for the injured limb. The emphasis of the recovery phase of rehabilitation involves the restoration of flexibility, strength, and proprioception in the injured limb. Strength and flexibility imbalances and maladaptive movement patterns and muscle substitutions should be corrected in this phase of rehabilitation. Open kinetic chain exercises can be beneficial when correcting strength imbalances, whereas closed chain exercises are frequently used to provide joint stabilization through muscle co-contraction. Cardiovascular and general fitness should be maintained. Progression to functional activities is begun toward the end of this phase.

The patient can begin the functional stage of rehabilitation when the injured limb has regained 75% to 80% of normal strength compared with the uninjured limb, and when there are no strength and flexibility imbalances.⁸³ The patient’s rehabilitation needs to continue to address maladaptive movement patterns and muscle substitutions, and full strength should be obtained. Functional activities should be incorporated into the rehabilitation program with a vocational/avocational-specific progression that eventually leads to a return to normal activities.

Musculoskeletal Problems of the Upper Limb

Conditions of the Shoulder

Sternoclavicular Joint Sprains

Sternoclavicular joint dislocations account for less than 1% of all joint dislocations. Two thirds of sternoclavicular joint dislocations occur anteriorly, whereas one third of dislocations occur posteriorly. The etiology is usually traumatic.³⁸

The diagnosis of sternoclavicular joint injuries is made with an accurate history, physical examination, and radiologic evaluation. Anterior sternoclavicular joint injuries can cause the medial end of the clavicle to become more prominent, whereas posterior joint injuries typically have more pain with a less prominent medial clavicular end. Posterior dislocations can also be associated with vascular compromise to the ipsilateral upper limb, neck and upper limb venous congestion, difficulty breathing, or difficulty swallowing.

Ligament injuries are commonly graded on a scale of 1 to 3 (Table 38-1).³⁸ The presence of tenderness at the sternoclavicular joint without subluxation or dislocation indicates a grade 1 injury; tenderness with subluxation indicates a grade 2 injury; and tenderness with associated dislocation indicates a grade 3 injury.¹⁹⁰

Table 38-1 Ligamentous Injury Grading Scale

Grade	Signs
1	Tenderness to palpation without joint laxity
2	Tenderness to palpation with joint laxity but a good endpoint
3	Tenderness to palpation with significant joint laxity and no endpoint

The radiologic evaluation of sternoclavicular joint injuries includes an anteroposterior radiograph of the chest or sternoclavicular joint and a serendipity view, which involves a 40-degree cephalic tilt view of the sternoclavicular joints (Figure 38-1).¹⁵⁷ Often standard radiographs leave the diagnosis in question, and computed tomography (CT) scan is frequently used for definitive evaluation of sternoclavicular joint injuries.

FIGURE 38-1 The serendipity view of the sternoclavicular joints.

The treatment of grade 1 and 2 injuries is nonoperative and involves the application of the previously described rehabilitation principles. Sling immobilization can be used for comfort and protection during the acute rehabilitation phase. Activity can progress as tolerated with an anticipated return to activity after 1 to 2 weeks for a grade 1 injury and 4 to 6 weeks for a grade 2 injury.

Grade 3 sternoclavicular joint sprains frequently can be treated nonoperatively as described for grade 1 and 2 injuries.⁴¹ Those that remain unstable postreduction, however, might require surgical intervention.¹⁹⁰ Because complications frequently arise with grade 3 posterior dislocations, a thorough evaluation to rule out pulmonary or vascular damage should be undertaken. If mediastinal compression is present, posterior grade 3 dislocations require immediate surgical intervention.¹⁹⁰ Because of the significant risk of vascular complications, posterior sternoclavicular joint dislocations should be reduced in the hospital setting with a vascular surgeon present.

Clavicle Fractures

A majority of clavicular fractures occur in childhood and adults less than 25 years of age. Eighty percent of clavicular fractures occur in the middle third of the clavicle, whereas approximately 15% occur in the lateral one third and 5% in the medial one third. Most clavicular fractures occur as a result of a direct blow to the point of the shoulder, but a small percentage occur from a fall onto an outstretched arm.¹⁷

Most patients know when they have fractured their clavicle. It is important to rule out associated neurovascular and pulmonary injuries during the physical examination and radiologic evaluation. Routine anteroposterior radiographs of the clavicle are usually adequate for visualization of clavicular middle third fractures. For proximal third fractures, the addition of a serendipity view is often used. When a lateral third fracture is suspected, a 15-degree cephalic tilt anteroposterior view centered on the AC joint using a soft tissue technique (Zanca view) and an axillary lateral view are usually diagnostic when combined with anteroposterior radiographs. Occasionally, CT scanning is required for more definitive evaluation.¹⁷

If the fracture has good alignment, partial immobilization is the treatment of choice using an immobilization device such as a sling or figure-of-eight bandage. If 15 to 20 mm of shortening occurs as a result of displacement, surgical intervention should be considered.¹⁴³ Other common indications for surgical intervention include displaced fractures with tissue interposition between the fracture ends, open fractures, neurovascular compromise, tenting of the skin over the fracture site that might lead to tissue necrosis, and displaced fractures located in the lateral third of the clavicle.¹⁷

Acromioclavicular Joint Sprains

AC joint sprains account for only 9% of all shoulder injuries, are most frequent in males in their third decade of life, and are usually partial rather than complete sprains.¹⁰⁵ Most injuries occur as a result of direct trauma from a fall or blow to the acromion. Physical examination demonstrates point tenderness, a positive horizontal adduction test, and a positive O’Brien test.

Rockwood ¹⁵⁸ classified AC joint sprains into six types (Figure 38-2). Type 1 sprains involve a mild injury to the AC ligaments, and radiologic evaluation is normal. Type 2 injuries involve the complete disruption of the AC ligaments but with intact coracoclavicular ligaments. Radiographs might demonstrate clavicular elevation relative to the acromion but less than 25% displacement. Type 3 sprains result in the complete disruption of the AC and coracoclavicular ligaments, but the deltotrapezial fascia remains intact. Radiographs reveal a 25% to 100% increase in the coracoclavicular interspace relative to the normal shoulder. Type 4 sprains involve complete disruption of the coracoclavicular and AC ligaments, with posterior displacement of the distal clavicle into the trapezius muscle. In type 5 sprains, the coracoclavicular and AC ligaments are fully disrupted along with a rupture of the deltotrapezial fascia. This results in an increase in the coracoclavicular interspace to greater than 100% of the normal shoulder. Type 6 sprains involve complete disruption of the coracoclavicular and AC ligaments, as well as the deltotrapezial muscular attachments, with displacement of the distal clavicle below the acromion or the coracoid process.

FIGURE 38-2 The Rockwood classification of acromioclavicular joint sprains.

Radiographic evaluation of the AC joint should include anteroposterior and lateral views of the AC joint, and a Zanca view. Stress views do not provide additional clinically useful information.¹⁰⁵

Type 1, 2, and 3 AC joint sprains are usually treated nonoperatively, using the previously described principles of rehabilitation. A brief period of sling immobilization might be required for pain control. Indications for surgical intervention for type 3 sprains include persistent pain or unsatisfactory cosmetic results. Some authors advocate operative treatment of type 3 sprains in heavy laborers and athletes who participate in sports that place a high demand on the upper limbs,^30,^89,¹⁴¹ but the current literature favors nonoperative treatment for type 3 sprains because of the similar outcomes between operative and nonoperative management and higher complication rates after operative intervention.¹⁷¹ Type 4, 5, or 6 sprains require surgical treatment.¹⁰⁵

Intraarticular AC joint fractures are treated similarly to type 1 through 3 AC joint sprains, unless the injury is open or involves neurovascular compromise. Posttraumatic arthrosis in the AC joint can occur. Persistent pain, despite an appropriate nonoperative treatment program, necessitates surgical resection of the distal clavicle.¹⁰⁵

Osteolysis of the Distal Clavicle

Repetitive overload of the distal clavicle can result in osteolysis. Young weight lifters who perform a significant amount of bench press and military press lifts are the most susceptible to this condition.²⁶ The athlete usually presents with gradual onset of AC joint pain that is increased with overhead presses or bench press, particularly when the bar is lowered all the way to the chest because this results in a significant sheer stress to the AC joint. It frequently occurs bilaterally.¹⁶⁷

Radiographic evaluation is the same as for AC joint injuries. The pathologic changes found on radiographs include distal clavicular subchondral bone loss and cystic changes. Widening of the AC joint can occur in late stages. Bone scans are positive during active disease and can be used to confirm the diagnosis.¹⁰⁵

Nonoperative treatment of distal clavicular osteolysis involves avoidance of the aggravating activities, and application of the previously discussed rehabilitation principles. Occasionally, AC joint intraarticular corticosteroid injections can assist in pain control. For many athletes, however, activity modification is not practical or does not result in significant pain relief. In those athletes who fail to improve with nonoperative measures or are unable to adequately modify their activities, distal clavicular resection is the surgical procedure of choice.¹⁶⁷

Scapulothoracic Crepitus

Multiple authors have reported the occurrence of pathologic sounds at the scapulothoracic joint, often referred to as a snapping scapula or scapular crepitus.^116,^140,¹⁴⁴ The three primary types of sound that can occur at this joint include a gentle friction sound, a louder grating sound, and a loud snapping. Although the gentle friction sound is probably physiologic, a loud grating sound suggests soft tissue disease such as bursitis, fibrotic muscle, muscular atrophy, or anomalous muscular insertions.¹¹⁶ Occasionally an excessive thoracic kyphosis or thoracic scoliosis can cause pathologic crepitus at the scapulothoracic articulation. Scapulothoracic dyskinesis or scapular winging can also cause painful friction between the scapula and the thorax.⁸⁴ A loud snapping sound is frequently caused by bony pathology such as an osteophyte, a rib or scapular osteochondroma, hooked superomedial angle of the scapula, or malunion of rib fractures.^117,^140,¹⁵⁴

The physical examination of individuals with symptomatic scapulothoracic crepitus or snapping should include localization of pain and crepitus or snapping through palpation, evaluation of scapulothoracic mechanics for quality and quantity of scapulothoracic motion, and a neurologic examination of the upper limb. Electrodiagnostic studies should be used when nerve injury is suspected. Tangential and anteroposterior radiographic evaluation of the scapula might identify osseous causes of the scapular crepitus or snapping. The radiologic workup might require further evaluation by CT or magnetic resonance imaging (MRI) for selected cases.

Treatment is warranted when the scapular snapping or crepitus is symptomatic. Nonoperative treatment involves correction of biomechanical deficits such as scapulothoracic dyskinesis, strength and flexibility imbalances, and poor posture. Soft tissue mobilization, NSAIDs, and local modalities might assist in pain control. An injection of corticosteroids into the painful area has been advocated by some authors,^33,¹⁰⁶ but caution must be exercised because complications such as pneumothorax can occur. For those who fail to improve with nonoperative measures, several surgical procedures have been described for treatment of this condition.¹⁰⁶

Rotator Cuff Tendonitis and Impingement

Injuries to the rotator cuff are common. Although macrotrauma can cause rotator cuff injuries, repetitive microtrauma and outlet impingement between the acromion and greater tuberosity of the humerus are more common.¹¹⁵ Neer categorized this type of rotator cuff injury into three stages.¹²² Stage 1 injuries involved inflammation and edema in the rotator cuff. Stage 2 rotator cuff injuries had progressed to fibrosis and tendonitis. When a partial or complete rotator cuff tear occurred, this was considered a stage 3 injury. In the overhead athlete, underlying instability patterns of the glenohumeral joint with associated excessive translation of the humeral head frequently led to outlet impingement and rotator cuff disease.⁶

On cadaveric examination, Bigliani ²¹ found a relationship between the acromial shape and the presence of rotator cuff tears. He classified the acromions into three types (Figure 38-3). Type 1 acromions were relatively flat, whereas type 2 acromions demonstrated a curve, and type 3 acromions were hooked. The incidence of rotator cuff tears increased as the acromion progressed from a type 1 to a type 3 shape. This was presumably related to the greater outlet impingement of the rotator cuff caused by an increasing acromial curve.

FIGURE 38-3 A, Type 1 acromion. B, Type 3 acromion.

A phenomenon referred to as internal impingement has recently been reported in young overhead athletes.^40,¹⁸⁴ When the arm is abducted 90 degrees and maximally externally rotated, there is contact between the undersurface of the rotator cuff and the posterosuperior glenoid rim. This is augmented by anterior glenohumeral joint instability and posterior glenohumeral joint capsular tightness. Internal impingement causes pathologic changes to the undersurface of the rotator cuff.

Impingement can be primary or secondary. Examples of causative factors leading to primary impingement include a hooked acromion or a thick coracoacromial ligament. Secondary impingement has many causes, including glenohumeral joint instability, weak scapular stabilizers, or scapulothoracic dyskinesis and instability.^66,⁶⁷ Lack of adequate scapular control or weakness in the scapular stabilizers can lead to poor scapular positioning during arm elevation. This can result in an acromion that does not retract during overhead activities, creating secondary impingement. Regardless of whether the impingement is primary or secondary, the underlying cause must be determined to formulate an appropriate treatment program.

Rotator cuff microtrauma can also be caused by “eccentric overload” of the shoulder external rotators during the deceleration phase of throwing.

Microvascular studies of the rotator cuff have found a hypovascular zone in the leading edge of the supraspinatus tendon during shoulder adduction compared with shoulder abduction and on the articular compared with bursal surface of the supraspinatus.^97,¹⁴⁹ These hypovascular areas have been implicated as a cause of rotator cuff degeneration and correlate with the higher incidence of articular-sided partial-thickness tears of the rotator cuff.

Patients with rotator cuff injuries frequently note anterior or lateral shoulder pain that occurs with overhead activity and also at night while trying to sleep. Symptoms such as stiffness, weakness, and catching might also be present. It is important to try to elicit any symptoms of underlying glenohumeral joint instability such as numbness, tingling, feelings of subluxation, or previous “dead arm” episodes.

The physical examination of patients with suspected rotator cuff pathology should include an evaluation of the cervical spine because problems originating in the cervical spine frequently refer symptoms to the shoulder. During inspection, the examiner should be sure to assess for proper scapulothoracic mechanics. Strength testing of the rotator cuff muscles can detect weakness as a result of a rotator cuff tear or pain inhibition caused by tendonitis or tendinosis. The Neer-Walsh and Hawkins-Kennedy impingement tests should be performed. Elimination of the pain provoked by impingement testing after injection of 10 mL of 1% lidocaine into the subacromial space confirms the diagnosis of impingement.

The examination of individuals with suspected rotator cuff pathology should also include maneuvers to detect underlying glenohumeral joint instability. The anterior apprehension test can be used to detect both anterior instability of the glenohumeral joint and also internal impingement. If the patient has a sensation of anterior apprehension during the test that is relieved with the relocation test, then there is likely anterior instability. If, however, there is pain in the posterior aspect of the shoulder during the anterior apprehension test that is relieved with the relocation test, then internal impingement is occurring.

Radiographic evaluation of patients with suspected rotator cuff pathology should include anteroposterior, supraspinatus outlet, and axillary radiographs. Anteroposterior radiographs should be performed in the neutral, external, and internal rotation positions to adequately visualize the glenohumeral joint and the greater and lesser tuberosities. Large rotator cuff tears can be indicated by an acromiohumeral distance of less than 7 mm and sclerosis on the undersurface of the acromion. The supraspinatus outlet view allows for categorization of the acromion type and will reveal AC joint osteophytes. Double-contrast arthrograms identify full-thickness rotator cuff tears, partial-thickness articular surface tears, and biceps tendon pathology. Bursal surface and intrasubstance partial-thickness rotator cuff tears are poorly evaluated with this technique. Ultrasound and MRI have high levels of sensitivity and specificity for rotator cuff pathology.^13,⁷³

Nonoperative treatment should include application of the previously described rehabilitation principles. Strengthening exercises for the scapular stabilizing muscles rather than the rotator cuff should be emphasized in the acute rehabilitation stage. Specifically, strengthening muscles that retract and depress the scapula (e.g., serratus anterior and inferior trapezius) and stretching muscles that protract and elevate the scapula (e.g., pectoralis minor and upper trapezius) reduce impingement. Posterior glenohumeral joint capsular tightness should be corrected, particularly in patients with internal impingement. It is imperative to reestablish normal scapulothoracic kinematics through neuromuscular retraining. This can begin once shoulder ROM is pain-free. Rotator cuff muscle strengthening should begin with closed chain exercises to promote stability and proprioception. Open chain exercises can be used to correct strength imbalances, such as weakness of the shoulder external rotators relative to the internal rotators. Some patients benefit from a subacromial corticosteroid injection, although studies of corticosteroid injections have shown mixed results.^68,^112,¹²¹ Patients recalcitrant to these measures might benefit from extracorporeal shock-wave therapy or, if calcific tendonitis is present, ultrasound-guided percutaneous lavage and aspiration of the calcification.^42,¹³⁰ If the patient fails to respond to the above measures, surgical evaluation should be considered.

Patients who have sustained an acute full-thickness rotator cuff tear should receive early surgical intervention to maximize their postoperative recovery potential. If the rotator cuff tear is chronic or degenerative, an initial trial of nonoperative rehabilitation measures can be used with the goal of restoring the patient to a functional level. In the young or active subgroups, however, nonoperative measures frequently fail to restore the patient to an adequate level of function, and surgical intervention is required.

Long Head of the Biceps Tendon Strains

Rupture of the long head of the biceps brachii tendon usually occurs in patients more than 40 years of age with a prolonged history of outlet impingement and rotator cuff disease. The patient frequently experiences a “pop” at the time of the injury, which often occurs during lifting or pulling activities. Some patients, however, just present with a painless retraction of the biceps distally resulting in an exaggeration of the biceps muscle contour. Pain can occur with an acute rupture but is not usually a factor in chronic cases. Because rupture of the long head of the biceps brachii tendon results in a loss of approximately 8% of elbow flexion strength and 21% of supination strength,¹⁰³ function is not significantly affected in most individuals.

This injury is best evaluated radiographically with MRI or ultrasound, which demonstrate the biceps tendon’s absence in the bicipital groove.

Treatment in patients more than 40 years of age who are relatively sedentary includes sling immobilization for comfort and application of the rehabilitation principles previously described. Strengthening exercises of the rotator cuff, shoulder girdle, and arm musculature should be undertaken when the patient is able to tolerate it. This allows for maximal restoration of function.

In younger or physically active patients, early surgical intervention might be warranted. Mariani et al.¹⁰³ reported that 93% of the surgically treated patients and 63% of the nonsurgically treated patients were able to return to full work capacity.

Pectoralis Major Strain

Pectoralis major muscle strains are most commonly seen in athletes who perform forceful shoulder adduction and/or internal rotation against resistance, such as weight lifters and football players.¹¹⁰ Pectoralis muscular strains can be categorized into three grades, with grade 1 being minimal muscle disruption and grade 3 a complete rupture. The strain can be located in the muscle belly, musculotendinous junction, or tendon.

Pectoralis major muscle strains are characterized by sudden pain in the pectoral region during a forceful shoulder adduction or internal rotation. Chest wall and proximal anterior arm region edema and ecchymosis can develop, and the anterior axillary fold often demonstrates a visible defect when the shoulder is abducted 90 degrees. The defect in the muscle can also be palpated on examination. Weakness and pain with shoulder adduction and internal rotation are usually present. Radiographs are normal, but ultrasound or MRI examinations can demonstrate the injury.

Treatment is conservative for grade 1 or grade 2 strains, intramuscular grade 3 strain, or rupture from the sternal or clavicular origins. Conservative treatment should use the previously described rehabilitation principles.

If the patient sustains a complete rupture of the pectoralis major tendon at the humeral insertion, nonathletes can undergo a conservative treatment program if they are willing to accept permanent shoulder adduction and internal rotation weakness. In athletes and those who wish to improve their postinjury strength potential, however, surgical intervention is needed.

Glenohumeral Joint Instability

The glenohumeral joint is a diathroidal joint with a rather large humeral head in relation to the small glenoid fossa. This anatomic relationship allows for the significant mobility seen in the glenohumeral joint but comes at the price of poor bony stability. Glenohumeral joint stability is provided by a combination of static and dynamic stabilizers.

The static stabilizers of the glenohumeral joint include the bony congruence between the humeral head and the glenoid fossa, the glenoid labrum, the negative intraarticular pressure, the glenohumeral joint capsule, and the glenohumeral ligaments.¹

The dynamic stabilizers of the glenohumeral joint include the scapular stabilizing muscles, the rotator cuff muscles, and the long head of the biceps.⁹⁰ The importance of optimal scapular function for glenohumeral joint stability cannot be overemphasized. The scapular stabilizing muscles orient the scapula properly in relation to the humerus for optimal static and dynamic stability of the glenohumeral joint and stabilize the scapula during glenohumeral joint movements.⁵¹ The primary scapular stabilizing muscles include the serratus anterior, trapezius, pectoralis minor, rhomboideus minor and major, latissimus dorsi, and levator scapulae.⁵¹

The rotator cuff muscles include the supraspinatus, infraspinatus, subscapularis, and teres minor. These muscles contribute to dynamic glenohumeral joint stability through a number of mechanisms. Concavity compression, first described by Lippitt et al.,⁹⁵ refers to the compressive forces placed on the glenohumeral joint during rotator cuff muscle co-contractions. These forces press the humeral head into the glenoid fossa, center the humeral head within the glenoid fossa, and help resist glenohumeral translation. Because the glenohumeral ligaments are lax in the midranges of glenohumeral joint motion, coordinated rotator cuff muscle contraction and concavity compression are particularly important mechanisms for glenohumeral joint stability in these ranges.⁹⁰

At the distal insertion of the rotator cuff muscles on the humerus, there is an intertwining of the joint capsule with the rotator cuff tendons. With rotator cuff muscle contraction, it is possible that the glenohumeral joint capsule develops tension and increases in stiffness, consequently acting as a dynamic musculoligamentous stabilizing system.⁹⁰

The rotator cuff muscles also provide glenohumeral joint stability through passive muscle tension and act as barriers to glenohumeral joint translation during active motion.^25,³¹ The subscapularis appears to be an especially important stabilizer for both anterior and posterior glenohumeral joint stability.^22,⁴³

Proprioception and neuromuscular control refer to the mechanism by which the position and movements of the shoulder girdle are sensed (proprioception), processed, and result in an appropriate motor response (neuromuscular control).¹²⁰ Glenohumeral joint instability is often associated with a concomitant decrement in proprioception.⁹³ The abnormal proprioception is restored after surgical correction of the joint instability, suggesting that one of the mechanisms causing proprioceptive deficits in unstable glenohumeral joints is a lack of appropriate capsuloligamentous tension.⁹⁴

The classification of glenohumeral joint instability includes the degree, frequency, etiology, and direction of instability.¹⁴ The degree includes dislocation, subluxation, or microinstability. A dislocation implies that the humeral head is disassociated from the glenoid fossa and often requires manual reduction. A subluxation occurs when the humeral head translates to the edge of the glenoid, beyond normal physiologic limits, followed by self-reduction. Microinstability is due to excessive capsular laxity, is multidirectional, and is frequently associated with internal impingement of the rotator cuff.¹⁴

The frequency of instability can be either acute or chronic.¹⁴ Acute instability involves a new injury resulting in subluxation or dislocation of the glenohumeral joint. Chronic instability refers to repetitive instability episodes.

The etiology of glenohumeral joint instability can be traumatic or atraumatic.¹⁴ Unidirectional instability is frequently caused by a traumatic event resulting in disruption of the glenohumeral joint. Atraumatic instability refers to glenohumeral joint instability resulting from congenital capsular laxity or repetitive microtrauma. Atraumatic instability can be subclassified into voluntary and involuntary categories. Voluntary instability refers to an individual who volitionally subluxes or dislocates his or her glenohumeral joint, whereas those with involuntary instability do not. Some patients with voluntary instability have associated psychologic pathology, which often portends a poor outcome if surgical stabilization is performed.¹⁶¹

Glenohumeral joint instability can be unidirectional or multidirectional. Unidirectional instability refers to instability only in one direction. The most frequent type of unidirectional instability is traumatic anterior instability.¹⁴ Multidirectional instability is instability in two or more directions and is usually due to congenital capsular laxity or chronic repetitive microtrauma.¹⁴

Traumatic anterior glenohumeral dislocation frequently tears the anterior–inferior glenohumeral joint capsule (e.g., the middle glenohumeral ligament and/or anterior band of the inferior glenohumeral ligament [IGHL]) and avulses the anterior–inferior glenoid labrum with or without some underlying bone from the glenoid rim.⁹⁰ The latter of these two entities is frequently referred to as a Bankart lesion.¹⁶ Other anatomic lesions that contribute to anterior glenohumeral joint instability include humeral avulsion of the glenohumeral ligament, superior labral anterior to posterior (SLAP) lesions, injury to the rotator interval, or rotator cuff tears (particularly to the subscapularis muscle).⁹⁰ Acute anterior glenohumeral joint dislocations are also frequently associated with a compression fracture of the posterolateral aspect of the humeral head, referred to as a Hill-Sachs defect.¹⁶³

Inferior glenohumeral joint instability typically does not occur in isolation. Causes of inferior glenohumeral joint instability, however, include capsuloligamentous laxity, absence of the glenoid fossa upward tilt, and lesions to the rotator interval, IGHL, superior glenohumeral ligament (SGHL), coracohumeral ligament (CHL), and the inferior glenoid labrum.

Congenital glenoid hypoplasia or excessive glenoid or humeral retroversion has been reported to contribute to posterior glenohumeral joint instability. The more common lesions that lead to posterior glenohumeral joint instability, however, include excessive capsuloligamentous laxity, or an injury to the rotator interval, SGHL, posterior band of the IGHL, coracohumeral (CHL), or subscapularis muscle.⁹ A tear of the posterior inferior glenoid labrum causing separation from the glenoid fossa rim, often referred to as a “reverse Bankart lesion,” or a fracture of the posterior inferior glenoid fossa rim can also cause posterior glenohumeral joint instability.^9,¹⁴⁶ A “reverse Hill-Sachs defect” can also be present, representing an impaction fracture of the anterior humeral head.^9,¹⁴⁶

Multidirectional instability can be caused by primary or secondary capsuloligamentous laxity. It is frequently seen bilaterally and can be accompanied by generalized ligamentous laxity.¹⁴ Recurrent unilateral joint instability occasionally stretches the glenohumeral capsuloligamentous structures to the point that multidirectional instability develops secondarily.¹⁴ Another possible cause for secondary multidirectional instability is the presence of an underlying connective tissue disorder such as Marfan or Ehlers-Danlos syndromes.¹⁴

Although many patients with glenohumeral joint instability have vague symptoms, common complaints of patients with shoulder instability include pain, popping, catching, locking, an unstable sensation, stiffness, and swelling.¹⁸ A history of acute trauma or chronic, repetitive microtrauma should be obtained. Some patients might have a history of glenohumeral joint dislocation, and the examiner should find out the direction of dislocation, the duration of the dislocation, whether it has recurred, and whether it required manual reduction or spontaneously reduced. Subluxation episodes are commonly associated with a burning or aching dead feeling in the arm. Repetitive overhead activities such as baseball pitching can cause enough microtrauma to lead to symptomatic laxity.¹⁸ Patients should be asked whether they or their family members have a history of generalized ligamentous laxity or connective tissue disorders.

The physical examination should include inspection, palpation, glenohumeral joint ROM, analysis of scapulothoracic kinesis, upper limb strength, sensation (including proprioception), reflex evaluations, and special tests for glenohumeral joint instability.

The most common initial radiographic views for the evaluation of glenohumeral joint instability include the anteroposterior shoulder view, axillary lateral view, and scapular “Y” view.¹⁴ The anteroposterior view allows visualization of the osseous structures of the shoulder, including the scapula, clavicle, upper ribs, humeral head, and glenoid rim.¹⁶³ With internal rotation, the anteroposterior view can also allow visualization of a Hill-Sachs defect.¹⁶³ The scapular Y view can help in the assessment of glenohumeral joint alignment after acute dislocations.¹⁶³ The axillary lateral view can assess anterior or posterior subluxation or dislocation, as well as fractures of the anterior or posterior glenoid rim.¹⁶³ Other specialized views include the Garth view and the West Point view, both of which are useful in the detection of Bankart fractures. The Stryker Notch view can be used for evaluation of Hill-Sachs defects and stress views for the documentation of the degree of glenohumeral joint instability.¹⁶³Magnetic resonance arthrography provides optimal visualization of the labrum, cartilage, and joint capsule. Imaging of nondisplaced injuries to the IGHL and anteroinferior glenoid labrum is improved by placing the arm in an abducted and externally rotated position.

The treatment options for glenohumeral joint instability and dislocation include nonoperative and operative approaches. After glenohumeral joint subluxation episodes and in patients with multidirectional instability or unidirectional posterior or inferior instability, a comprehensive rehabilitation program that addresses kinetic chain deficits, scapulothoracic mechanics, and shoulder girdle strength, flexibility, and neuromuscular control is appropriate. Operative intervention should be considered only in those patients who have failed to improve after a comprehensive nonoperative treatment program.

For patients with glenohumeral joint instability, the strengthening program should begin with closed chain exercises that promote co-contraction of the glenohumeral joint–stabilizing musculature. The patient can eventually progress to functional open chain exercises as stability is achieved. Proprioceptive closed and open chain exercises are also important to recoordinate the stabilizing shoulder girdle musculature and attain engrams that respond appropriately to a dynamically changing environment.

For patients who have suffered a first-time traumatic anterior glenohumeral joint dislocation, the decision between a trial of nonoperative treatment versus immediate surgical stabilization is more controversial. In the older, less active patient, nonoperative management frequently is successful.³ In the younger, more active patient involved in contact sports, studies have shown a very high redislocation rate in those treated nonoperatively compared with those receiving early operative intervention.^11,^12,^85,¹⁷³

Regardless of whether a patient opts for early surgical intervention, closed reduction confirmed by radiologic examination should be performed on all patients who sustain an acute glenohumeral joint dislocation that does not spontaneously reduce. Radiologic studies should be performed in two planes, such as anteroposterior with the humerus in internal rotation and axillary lateral views, to confirm relocation and exclude an associated fracture.¹⁶³ Sensory testing over the deltoid muscle is important to rule out an associated axillary nerve injury.¹⁴

Standard sling immobilization can be used for comfort but does not change future redislocation rates.^71,^72,¹⁶⁶ If initiated within the first 24 hours postinjury, 3 weeks of shoulder immobilization with the humerus externally rotated 30 degrees can reduce the risk of recurrent dislocation by nearly 100%, but the benefits of this type of immobilization are not statistically significant if begun after the first day.⁷⁵^–⁷⁸ The previously described shoulder instability rehabilitation program can be used to treat patients who opt for nonoperative treatment of their shoulder dislocation.

Adhesive Capsulitis

Adhesive capsulitis, or “frozen shoulder,” is characterized by painful, restricted shoulder ROM in patients with normal radiographs.^61,¹²³ Adhesive capsulitis occurs in approximately 2% to 5% of the general population, is 2 to 4 times more common in women than men, and is most frequently seen in individuals between 40 and 60 years of age.^27,³⁵

Adhesive capsulitis is usually an idiopathic condition but can be associated with diabetes mellitus, inflammatory arthritis, trauma, prolonged immobilization, thyroid disease, cerebrovascular accident, myocardial infarction, or autoimmune disease. Pathologic evaluation can reveal perivascular inflammation, but the predominant abnormality is fibroblastic proliferation with increased collagen and nodular band formation.²⁷

Adhesive capsulitis has been divided into four stages (Table 38-2).⁶⁴ Stage 1 occurs for the first 1 to 3 months and involves pain with shoulder movements but no significant glenohumeral joint ROM restriction when examined under anesthesia. In stage 2, the “freezing stage,” symptoms have been present for 3 to 9 months and are characterized by pain with shoulder motion and progressive glenohumeral joint ROM restriction in forward flexion, abduction, and internal and external rotation. During stage 3, or the “frozen stage,” symptoms have been present for 9 to 15 months and include a significant reduction in pain but maintenance of the restricted glenohumeral joint ROM. In stage 4, frequently referred to as the “thawing stage,” symptoms have been present for approximately 15 to 24 months and ROM gradually improves.

Table 38-2 Stages of Adhesive Capsulitis

Stage	Symptom Duration	Signs and Symptoms
1	1-3 mo	Painful shoulder movement, minimal restriction in motion
2	3-9 mo	Painful shoulder movement, progressive loss of glenohumeral joint motion
3	9-15 mo	Reduced pain with shoulder movement, severely restricted glenohumeral joint motion
4	15-24 mo	Minimal pain, progressive normalization of glenohumeral joint motion

Routine radiographic evaluation is usually normal, but glenohumeral joint arthrography typically shows a significant reduction in the capsular volume.

Treatment during stages 1 and 2 of adhesive capsulitis includes physical modalities, analgesics, and activity modification to reduce pain and inflammation. Up to three intraarticular corticosteroid injections can be used during stages 1 and 2 of adhesive capsulitis to reduce inflammation and pain, facilitate rehabilitation, and shorten the duration of this condition.^64,¹⁶⁵ Postural retraining to reduce kyphotic posture and forward humeral positioning should be undertaken. Aggressive ROM exercises should be avoided until the patient’s pain has been adequately controlled.¹⁷⁸ Otherwise, the patient’s symptoms can worsen, leading the patient to immobilize his or her shoulder, thus resulting in a further loss of shoulder ROM. Early in the rehabilitation process, however, passive joint glides and nonpainful passive ROM exercises might be beneficial. Early scapular stability exercises and closed chain rotator cuff exercises can be instituted. As the patient’s symptoms improve, active-assisted and active ROM activities can be added, along with open chain and proprioceptive exercises. Most patients will have restoration of normal function over a 12- to 14-month period.^63,¹¹⁸ In patients who do not improve after 6 months of nonoperative treatment, more aggressive treatments such as capsular hydrodilatation, manipulation under anesthesia, and arthroscopic lysis of adhesions can be considered.^∗

Superior Labral Anterior to Posterior Lesions

Andrews et al.⁷ were the first to report the importance of the superior labrum and biceps tendon complex as a source of pain and shoulder dysfunction. The term SLAP lesion, which stands for superior labral anterior to posterior injury, has been used to name injuries to the superior labrum and biceps tendon complex.¹⁶⁹ The glenoid labrum, which serves to deepen the glenoid socket, increases the contact area of the humeral head by approximately 70%.¹⁴⁵ In addition to increasing the static stability of the glenohumeral joint, the superior aspect of the glenoid labrum serves as an attachment point for the long head of the biceps tendon. Research has demonstrated the importance of the long head of the biceps in providing dynamic stability to both anterior–posterior and superior–inferior humeral head translation.^135,¹⁵⁹

Snyder et al.¹⁶⁹ proposed a classification system for SLAP lesions (Figure 38-4). Type 1 lesions involve a fraying injury to the superior labrum without detachment of the biceps tendon. In type 2 lesions, the biceps tendon is detached from the supraglenoid tubercle. Type 3 lesions are characterized by bucket handle tearing of the superior labrum without detachment of the biceps tendon. Type 4 lesions involve a tear of the superior labrum that extends into the biceps tendon.

FIGURE 38-4 Classification of superior labral anterior to posterior (SLAP) lesions.

Mechanisms of injury for SLAP lesions include falling on an outstretched arm, traction injuries, torsional peeling back of the labrum during the late cocking phase of overhead throwing, and traction forces from the long head of the biceps tendon during the deceleration phase of overhead throwing.^7,^28,^98,^169,¹⁷⁸

The most common complaints of individuals with a SLAP lesion are pain with overhead throwing, and mechanical symptoms such as clicking, catching, or grinding. SLAP lesions can, however, mimic the symptoms of many different diagnoses, such as impingement, AC joint pain, bicipital tendonitis, or glenohumeral joint instability. Consequently a high degree of suspicion is important to make this diagnosis. Physical examination often shows an underlying glenohumeral joint instability. A positive O’Brien test also suggests a SLAP lesion.

Standard radiographic imaging of the shoulder is usually normal. Gadolinium-enhanced MRI scans of the shoulder have improved the ability to detect SLAP lesions. The gold standard for diagnosing SLAP lesions, however, remains arthroscopy.

There currently are no studies of nonoperative SLAP lesion treatment, and surgery is the standard treatment. Patients who have been diagnosed with clinically significant SLAP lesions should be referred for surgical consultation to receive definitive treatment. Correction of strength and flexibility deficits and normalization of scapulothoracic mechanics should help with the postsurgical recovery.

Conditions of the Elbow

Lateral Epicondylitis

Lateral epicondylitis is a common tendinopathy of the lateral elbow and is frequently referred to as tennis elbow. This malady dates back to 1883 when it was described as an injury resulting from lawn tennis.³⁸ It is reported to occur in up to 50% of tennis players.¹²⁶ Any activity that places excessive repetitive stress on the lateral forearm musculature, however, can cause this condition.

Lateral epicondylitis is more common in patients more than 35 years of age and peaks in those between 40 and 50 years old.^81,¹²⁵ It is more common in male than in female tennis players but does not display a gender predilection in the general population.³⁷ When lateral epicondylitis results from a work-related injury, conservative measures are less successful, and surgical intervention occurs more frequently.⁵⁸

Lateral epicondylitis is a misnomer for this condition because the pathologic changes (i.e., angiofibroblastic hyperplasia) are not inflammatory but rather degenerative.^125,¹⁵¹ A more appropriate term for this condition is lateral epicondylosis rather than epicondylitis. The degenerative changes occur most commonly in the origin of the extensor carpi radialis brevis but also involve the extensor digitorum communis origin in 30% of cases.¹²⁵ The origins of the extensor carpi radialis longus or extensor carpi ulnaris are only rarely involved.

Patients with lateral epicondylosis frequently report a gradual onset of symptoms, which usually occur after specific activities. Traumatic or sudden onset of symptoms can also occur. The backhand swing in tennis frequently exacerbates the symptoms, as does gripping and activities that require repetitive wrist extension and forearm pronation and supination. Physical examination can reveal point tenderness over the lateral epicondyle and a positive Cozen’s test. Entrapment of the posterior interosseous branch of the radial nerve can mimic lateral epicondylosis, but the tenderness associated with this condition is 3 to 4 cm distal to the lateral epicondyle rather than directly over it.¹⁸⁷

Although standard anteroposterior and lateral radiographs are usually normal, an oblique view of the lateral epicondyle might reveal punctuate calcifications in the extensor tendon origin.³⁷

Treatment involves discontinuation of provocative activities, oral analgesics, physical modalities, and bracing (e.g., lateral counter-force strap or neutral wrist splint). It is important to correct kinetic chain deficits, training errors, and inappropriate tennis racquet grip size and string tension. Eccentric strengthening of the wrist extensors appears to be the most effective exercise regimen for the treatment of lateral epicondylosis.¹⁷⁷ Peritendinous corticosteroid injections are occasionally used, but their long-term efficacy is questionable.^5,¹²⁴ Promising new treatments include ultrasound-guided percutaneous needle tenotomy, autologous blood injections, and platelet-rich plasma injections.^48,^113,¹¹⁹ Extracorporeal shock-wave therapy for lateral epicondylosis has been reported to be successful in 48% to 73% of cases recalcitrant to other nonoperative measures.¹³⁰ Recalcitrant cases can also be treated with surgical debridement of the degenerative tissue with approximately 85% of surgically treated patients reporting good to excellent results and only 3% reporting no improvement.^47,¹²⁶

Medial Epicondylitis

Medial epicondylitis, frequently referred to as golfer’s elbow, has the same degenerative pathologic changes as those described in lateral epicondylitis and is more correctly termed medial epicondylosis.¹³² This condition occurs 3 to 7 times less frequently than lateral epicondylosis, and the degenerative changes are most frequently found in the pronator teres and flexor carpi radialis (FCR) origins.¹³² Risk factors for medial epicondylosis include training errors, faulty equipment, repetitive activities requiring wrist flexion and forearm pronation, and biomechanical abnormalities (such as poor strength, flexibility imbalances, and joint instability).

Patients often report a gradual onset of pain over the medial epicondyle that is exacerbated by activities that require repetitive gripping, wrist flexion, and forearm pronation and supination. The patient might report a feeling of grip strength weakness. This condition occasionally occurs traumatically as a result of an acute rupture of the UCL of the elbow. Symptoms of a concomitant ulnar neuropathy can also be present. Physical examination demonstrates tenderness to palpation over the medial epicondyle, weakness in grip strength, pain when a tight fist is made, and pain with resisted wrist flexion and forearm pronation.

Oblique radiographs of the medial epicondyle can reveal punctuate calcifications in the region of the flexor tendon origins.³⁷ It is also important to rule out degenerative changes in the posterior medial aspect of the olecranon because this condition can cause symptoms similar to those seen with medial epicondylosis.

Nonoperative treatment should include discontinuation of aggravating activities and use of analgesic medications, physical modalities, bracing (e.g., medial counter-force strap and neutral wrist splint) for pain control, and correcting kinetic chain deficits and training errors. Eccentric exercises can be used for the treatment of tendinopathy. Corticosteroid injections have been used to treat this condition but can lead to further tendon degeneration and predispose to tendon rupture. Autologous blood injections might be beneficial.¹⁷⁶ Medial epicondylosis can also be responsive to extracorporeal shock-wave therapy.¹³⁰ Operative treatment can be warranted for those who fail to improve with conservative measures.

Distal Biceps Tendonitis and Rupture

Distal biceps brachii tendonitis is uncommon and can develop as a result of eccentric overload of the biceps during the deceleration and follow-through phases of throwing. Patients report antecubital fossa pain during repetitive elbow bending activities and the follow-through phase of throwing. Physical examination typically shows tenderness to palpation over the distal biceps tendon and pain with resisted elbow flexion and/or forearm supination. Radiologic evaluation is usually normal.

Initial treatment includes activity modification, ice, and analgesics. Kinetic chain abnormalities should also be addressed early in the rehabilitation process. When the patient is able to participate in an active strengthening program, eccentric exercises should be used. The patient should resume functional activities in a planned, gradually escalating manner and should not return to full unrestricted activity until full strength and ROM has been restored.

Rupture of the distal biceps brachii tendon is also an uncommon injury. This usually occurs in patients between 30 and 50 years of age, with a significant predilection for men and the dominant limb.^10,^15,⁴⁴ The injury usually occurs during a heavy lifting activity while the elbow is at 90 degrees of flexion.⁵⁶ The rupture usually involves the distal biceps brachii tendon at the radial tuberosity insertion site, with variable involvement of the lacertus fibrosus.⁴⁴ Although prodromal symptoms are usually absent, pathologic examination of the avulsed tendon frequently shows degenerative changes in the distal biceps brachii tendon.¹⁴⁷

A distal biceps brachii tendon rupture causes acute pain and a popping or tearing sensation in the antecubital fossa during a heavy lifting activity. The patient might report a reduction in elbow flexion or forearm supination strength. Clinical findings include ecchymosis, edema, and erythema in the antecubital fossa, and a palpable absence of the distal biceps brachii tendon. The biceps brachii muscle belly might have a deformity during contraction as a result of balling up of the muscle, but elbow flexion and forearm supination should still be intact because of the presence of the brachialis and supinator muscles, respectively.

Radiologic evaluation should be performed to rule out an avulsion fracture from the radial tuberosity. MRI or ultrasound can be helpful in cases where the diagnosis is not clear.

Treatment of biceps brachii tendon ruptures is surgical, and early intervention is recommended.

Distal Triceps Tendonitis and Rupture

Activities that require repetitive elbow extension such as throwing, weight lifting, or using a hammer can result in distal triceps brachii tendonitis. This condition can be found in conjunction with loose bodies in the posterior compartment of the elbow or with lateral epicondylitis.¹⁷⁰

Symptoms of triceps brachii tendonitis include aching and burning pain in the distal triceps. The pain frequently occurs after specific aggravating activities in the early manifestations of this condition, but eventually the symptoms are experienced during activity. Physical examination shows tenderness over the distal triceps tendon and pain with resisted elbow extension. Radiologic evaluation is usually normal.

Treatment for triceps tendonitis includes activity modification, physical modalities, and analgesics for pain control. ROM exercises should be used initially, and a more aggressive strengthening program should be started as the pain resolves. Eccentric strengthening exercises of the triceps brachii should be considered in those who have experienced chronic symptoms. Surgical intervention is rarely required.

Triceps tendon rupture can occur in individuals who fall onto an outstretched hand or receive a direct blow to the distal triceps brachii tendon. An audible “pop” might occur at the time of the injury. Elbow extension weakness, erythema, ecchymosis, and edema at the area of the tendon rupture are usually present. Minimal trauma might be all that is required for tendon disruption in those who have received previous corticoteroid injections around the distal triceps tendon, or in people who have been treated with chronic oral corticoteroids for other system conditions.^170,¹⁸³ The most common site of disruption is at the distal insertion site on the olecranon, and a small avulsion fracture from the olecranon might be present.

Physical examination demonstrates these findings, along with a palpable defect. The ability to actively extend the elbow is typically still present because of an intact anconeus muscle, but strength will be significantly reduced.

Standard radiographs of the elbow might reveal a small avulsion fracture on the lateral view.⁵² Ultrasonography or MRI readily demonstrates the pathology.¹⁷⁹

Surgical repair of the disrupted triceps tendon is recommended.

Snapping Triceps Tendon

Occasionally a pathologic band over the medial side of the distal triceps can cause a snapping sensation over the medial epicondyle during elbow flexion and extension.⁴⁶ The astute clinician should try to differentiate this condition from ulnar nerve subluxation, but both conditions can occur at the same time. The patient might report a history of medial elbow popping or snapping during elbow flexion and extension activities. The snapping of the band over the medial epicondyle is frequently palpable on examination. Conservative treatment for this condition includes deep tissue massage, stretching of the triceps muscle, and occasionally local corticosteroid injection. Patients who do not respond to this regimen might require surgical intervention.

Olecranon Bursitis

The olecranon bursa lies subcutaneously over the olecranon process. Olecranon bursitis can be septic or aseptic. Aseptic bursitis is either acute hemorrhagic bursitis resulting from a macrotraumatic insult to the bursa or chronic bursitis caused by repetitive microtrauma. Aseptic bursitis is frequently seen in athletes who participate in football or hockey.⁸⁷

Aseptic bursitis can begin with a direct blow to the area, but some patients report an insidious onset of symptoms after a small abrasion or laceration to the area. If the injury is chronic and recurrent, the patient can experience an initial period of swelling that feels like a small liquid pouch. This pouch eventually organizes into a permanently thickened bursa with intrabursal bands.

Septic bursitis can occur as a result of a localized or systemic infection. It is associated with significant edema, erythema, and hyperthermia in the area of the infected bursa and is frequently accompanied by systemic symptoms of infection. Physical examination reveals an edematous area over the olecranon that is usually tender to palpation. Elbow ROM can be limited because of tissue tightness and pain. If the bursa is infected, the area can feel warm, and the patient can have an increased white blood cell count.

Radiographic evaluation should be performed to determine whether the patient has an osteophyte over the tip of the olecranon or calcification within the bursal sac.

The initial treatment of an acute traumatic aseptic bursitis includes sterile aspiration of the bursa followed by application of a compressive dressing. The patient should begin an NSAID medication and frequently apply ice to the area. The olecranon should be protected from further insult by using an elbow pad.

For those with chronic bursitis, treatment should include ice, intermittent NSAIDs, and protection of the area from further insult. If edema is present, a compressive dressing should be applied. An intrabursal injection of corticosteroid medications can be helpful. For aseptic bursitis that is recalcitrant to standard treatment, sclerotherapy using a tetracycline injection into the bursa has been advocated.⁶⁵ Surgical excision is also an option for patients who do not obtain relief with the above measures.

For patients with septic bursitis, the bursa should be aspirated for symptomatic relief and to obtain a fluid sample for laboratory analysis, including Gram stain, culture and sensitivity, and crystal analysis. The area should then be wrapped in a compressive dressing, and the patient should be instructed to elevate the arm. Intravenous antibiotics are warranted in patients with systemic symptoms, but oral antibiotics might be adequate for those experiencing only localized symptoms. If the patient does not improve with the above measures, referral for incision and drainage should be made.

Ulnar Collateral Ligament Sprain

Injuries to the UCL of the elbow are a result of valgus stress to the elbow. This can be caused by a single traumatic episode but is frequently seen with the repetitive microtrauma associated with throwing. The late cocking phase of overhead throwing is characterized by a valgus torque of approximately 64 N-m across the elbow.⁵⁴ During the acceleration phase of overhead throwing, the valgus forces across the elbow are increased, leading to further stress on the UCL.

The UCL is composed of an anterior, posterior, and transverse bundle. It is primarily stabilized by the anterior bundle.¹⁸⁰ The anterior bundle has a thin superficial and thick deep layer, and the superficial or deep layer can be torn individually or as a unit.¹⁸¹

Patients with UCL injuries complain of medial elbow pain exacerbated by the late cocking and acceleration phases of throwing. If the injury was acute, an audible pop might have been heard. More frequently, however, the symptoms have an insidious onset. Throwing athletes can experience a decrement in throwing velocity and accuracy. Ulnar nerve traction and neuritis can occur because of the increased laxity of the elbow. Physical examination frequently shows a 5-degree elbow flexion contracture, UCL tenderness, and pain with or without laxity during UCL instability testing.

Anteroposterior, lateral, and oblique radiographs of the elbow should be obtained. Calcification of the UCL can occur, and avulsions from the humeral or ulnar attachments should be ruled out.¹⁶⁴ CT or MRI arthrograms can further define the injury, particularly if the injury is a partial tear of the UCL that only involves the deep fibers.¹⁶⁴ MRI has the advantage of excellent soft tissue visualization.

Partial UCL injuries should be initially treated with nonoperative measures. Conservative treatment includes discontinuation of throwing activities for 3 to 6 weeks and initiation of gentle elbow ROM, modalities, and analgesics. Progressive strengthening of the medial forearm musculature should be done because these muscles are dynamic stabilizers of the medial elbow against valgus stress. Occasionally a hinged elbow brace is used for initial support and comfort. Taping the medial elbow to resist valgus stress can be helpful. When the patient has full pain-free ROM and symmetric strength, an interval throwing program can be initiated with the overhead-throwing athlete (Box 38-1). Proper throwing mechanics should be ensured. Patients who fail to improve after conservative management can be candidates for UCL reconstruction.

BOX 38-1 Interval Throwing Program

Athletes are allowed to progress from one phase to the next as soon as they are able to complete the phase pain-free.

45-ft phase

• Step 1: Warm up, 25 45-ft throws × 2 with 15-min rest between sets

• Step 2: Warm up, 25 45-ft throws × 3 with 15-min rest between sets

60-ft phase

• Step 1: Warm up, 25 60-ft throws × 2 with 15-min rest between sets

• Step 2: Warm up, 25 60-ft throws × 3 with 15-min rest between sets

• 90-ft phase

• Step 1: Warm up, 25 90-ft throws × 2 with 15-min rest between sets

• Step 2: Warm up, 25 90-ft throws × 3 with 15-min rest between sets

• 120-ft phase

• Step 1: Warm up, 25 120-ft throws × 2 with 15-min rest between sets

• Step 2: Warm up, 25 120-ft throws × 3 with 15-min rest between sets

• 150-ft phase

• Step 1: Warm up, 25 150-ft throws × 2 with 15-min rest between sets

• Step 2: Warm up, 25 150-ft throws × 3 with 15-min rest between sets

• 180-ft phase

• Step 1: Warm up, 25 180-ft throws × 2 with 15-min rest between sets

• Step 2: Warm up, 25 180-ft throws × 3 with 15-min rest between sets

• Step 3: Begin throwing off of the mound or return to the athlete’s respective positions

Patients with full-thickness UCL injuries are less likely to respond favorably to nonoperative measures, and ligament reconstruction is often required for definitive treatment.

Valgus Extension Overload of the Elbow

Valgus extension overload (VEO) is a common disorder in overhead-throwing athletes, accounting for approximately 65% of surgeries for medial elbow pain in professional baseball players.⁸ This disorder is characterized by impingement of the posteromedial olecranon against the medial wall of the olecranon fossa from the valgus elbow stress during overhead throwing. Over time, repetitive impingement at this site can result in olecranon osteophyte formation, intraarticular loose bodies, and deposition of fibrous tissue in the olecranon fossa (Figure 38-5).¹⁸⁸

FIGURE 38-5 Posteromedial osteophytes of the olecranon caused by valgus extension overload.

The patient often presents with posteromedial elbow pain during the acceleration phase or follow-through phase of throwing. Physical examination shows tenderness to palpation over the posterior medial tip of the olecranon, and pain during passive elbow hyperextension with a valgus loading.

Radiographic evaluation should include anteroposterior, lateral, and axial radiographs. These can demonstrate an olecranon osteophyte or intraarticular loose bodies. Osteophytes are best viewed on lateral radiographs. MRI can provide further delineation of the pathologic lesions, but normal radiographs and MRI do not exclude this condition.

The initial treatment of VEO is conservative. The patient should discontinue aggravating activities, particularly throwing, and localized modalities and ROM exercises should be initiated. Analgesics can reduce the pain and facilitate rehabilitation. It is important to address kinetic chain deficits (particularly of the scapula and core), ensure proper throwing mechanics, and strengthen the medial forearm musculature to reduce the valgus stress across the elbow during throwing. Once all these factors have been addressed and the patient has full pain-free elbow ROM and strength, an interval throwing program can be initiated (see Box 38-1). Symptoms frequently return when the athlete returns to throwing activities, and surgical intervention might be required.

Medial Epicondylar Traction Apophysitis and Stress Fracture

Injuries to the medial elbow in young throwing athletes have been referred to as “little leaguer’s elbow” and include medial epicondylitis, traction apophysitis, stress fractures through the medial epicondylar epiphyses, and avulsion fractures of the medial epicondyle.²⁴ These injuries classically occur in the dominant arm of throwing athletes between the ages of 9 and 12 years.²³ Excessive throwing can cause chronic repetitive valgus stress to medial elbow, resulting in a traction injury to the immature medial epicondyle. The medial epicondylar apophysis does not close until 14 years of age in females and 17 years of age in males, and is the last elbow physis to close (Figure 38-6).²³ Following the currently recommended number of pitches and rest intervals for young overhead-throwing athletes might prevent this type of injury.¹¹¹ The currently recommended number of pitches and rest intervals by Little League can be found at: http://www.littleleague.org/Assets/old_assets/media/RS_Pitching_Regulation_Changes_Baseball_2008.pdf.

FIGURE 38-6 The average age for distal humeral ossification centers to fuse.

The patient frequently presents with medial elbow pain that is exacerbated by throwing. Physical examination reveals tenderness over the medial epicondyle, and there can also be mild edema in the painful region and a slight flexion contracture of the elbow.

Radiologic evaluation should include anteroposterior, lateral, axial, and comparison views of the elbow. Common radiologic abnormalities include medial epicondylar enlargement, fragmentation, beaking, and avulsion of the medial epicondyle (Figure 38-7).²⁴ In the past, three-phase bone scan followed by tomograms or CT scan through the areas of increased activity have been used. MRI, however, currently has the advantage of evaluating for both osseous and soft tissue injuries that might not be identified with other techniques.

FIGURE 38-7 Valgus stress to the immature elbow can result in an avulsion fracture of the medial epicondylar ossification center.

The initial treatment is 4 to 8 weeks of rest from throwing activities. Ice, analgesics, elbow ROM exercises, and correction of kinetic chain deficits should be instituted early. As symptoms reside, progressive strengthening of the medial forearm musculature should be performed. An interval throwing program can begin when full pain-free ROM has been restored, and there are no strength asymmetries (see Box 38-1). When pitching is resumed, the athlete should follow the currently recommended rest intervals and limitations on the number of pitches to prevent injury recurrence (refer to the earlier mentioned Little League website).¹¹¹ If pain resumes with throwing activities, several months of rest from throwing activities should be initiated. This should be followed by the same gradually progressive resumption of throwing activities. If after 6 months of treatment the patient is still symptomatic, surgical consultation is warranted.

If a displaced avulsion fracture occurs, surgical treatment for appropriate anatomic reduction is required.

Osteochondrosis and Osteochondritis Desiccans of the Capitellum

Panner’s disease is an osteochondrosis of the capitellum that occurs in children 7 to 10 years of age. It begins with degeneration or necrosis of the capitellum, followed by regeneration and calcification of this area.¹³⁹ The cause of Panner’s disease is unknown, but it appears to be related to disordered endochondral ossification in association with trauma or vascular impairment.

Patients with Panner’s disease present with dull, aching lateral elbow pain that is aggravated by throwing activities. Effusion of the elbow is frequently present, but ROM is usually not restricted.

Treatment of Panner’s disease is nonoperative and initially involves discontinuation of throwing activities. Occasionally a posterior long arm splint is used for pain control. Repeat radiographs should be performed to ensure adequate healing because late articular collapse of the capitellum, although uncommon, can occur.

Osteochondritis desiccans of the capitellum can also occur and has several unique characteristics that enable clinicians to differentiate it from osteochondrosis of the capitellum. Osteochondritis desiccans occurs in throwing athletes 9 to 15 years of age, whereas osteochondrosis occurs in 7 to 10 year olds.²³ Osteochondritis desiccans involves focal lesions to the capitellum, whereas osteochondrosis involves the entire capitellum.²³ Osteochondritis desiccans frequently leads to loose body formation. Osteochondrosis is usually self-limited and resolves with rest and time.²³

Patients with osteochondritis desiccans present with the insidious onset of lateral elbow pain, accompanied by an elbow flexion contracture of 15 degrees or more. Catching or locking of the elbow can also be present. An elbow effusion might also be present.

Radiographic evaluation should include anteroposterior, lateral, and oblique views of the elbow. Although CT arthrogram and tomograms were previously used to define the lesion, MRI is quickly becoming the study of choice for osteochondritis desiccans.

Treatment should begin with rest, ice, and analgesics. Elbow immobilization with a posterior long arm splint might provide symptomatic relief. Gentle progressive ROM and strengthening exercises should begin once pain has resolved, and protection from forceful activities should continue for a minimum of 6 weeks to allow healing. Once full strength and ROM have been restored, the patient can begin a gradual return to functional activities. Serial radiographic evaluation should be performed to ensure adequate healing of the lesion, although in some cases symptomatic improvement can occur despite persistent radiologic abnormalities. In patients with large loose bodies, persistent mechanical symptoms, or pain recalcitrant to nonoperative measures, surgical intervention might be required.

Elbow Dislocations

Elbow dislocations involving the proximal ulna and distal humerus most frequently occur in a posterolateral direction and are a result of a fall on an outstretched arm with the elbow in hyperextension (Figure 38-8).¹²⁹ Anterior, lateral, and posteromedial dislocations also occur but are much less frequent. When a posterolateral elbow dislocation occurs, associated injuries include disruption of the ulnar and radial collateral ligaments of the elbow, and occasionally disruption of the flexor pronator forearm musculature, or periarticular and intraarticular fractures.^80,^127,¹⁸² Injuries to the brachial artery or to the median, ulnar, or radial nerve should be identified and treated. Acute anterior forearm compartment syndrome can also occur with elbow dislocations.

FIGURE 38-8 Posterior dislocation of the elbow.

Clinical evaluation should include a complete neurovascular examination of the injured limb and standard anterior–posterior, lateral, and oblique radiographs to correctly classify the direction of the dislocation to identify any associated fractures.

Treatment should begin with reduction of the dislocation. Prereduction and postreduction films should be obtained to ensure proper reduction. If the elbow cannot be reduced in a closed manner, then open reduction should be performed. Postreduction neurovascular examination is very important to rule out new or continued neurovascular compromise. If the flexor–pronator musculature has been disrupted along with the UCL, early surgical intervention is warranted.¹²⁷ Gross medial elbow instability without flexor–pronator musculature rupture can be treated nonoperatively if the patient does not participate in overhead-throwing sports. Overhead-throwing athletes with complete disruption of the UCL, however, frequently require surgical intervention to reduce their postinjury morbidity.

Conservative treatment of elbow dislocations includes a sling or posterior long arm splint for 2 to 3 days followed by progressive ROM exercises. Prolonged immobilization should be avoided because flexion contractures are a frequent complication of this injury. A hinged elbow brace that allows flexion and extension of the elbow can be used to facilitate early ROM activities. Ice and analgesics can assist in patient comfort. Progressive strengthening activities should begin when the patient’s pain level allows, and full return to activities should be expected in approximately 8 weeks. A majority of patients have had 90% restoration of function by 3 months postinjury.^79,¹⁵⁵ In addition to the surgical indications previously mentioned, surgical intervention can be warranted in patients who experience chronic recurrent elbow instability.

Conditions of the Forearm and Wrist

The following are general treatment strategies for many forearm and wrist disorders: activity modification, modalities, analgesics, and rehabilitation. Wrist and hand orthoses are commonly used and will be listed under each specific diagnosis. When prescribing such an orthosis, the patient should be reminded to remove the splint at least twice daily to allow for wrist and finger ROM to prevent complications of immobility. Some recalcitrant cases respond to corticosteroid injections, but the potential complications of steroid injections should be kept in mind. Once there is adequate pain control, a rehabilitation program to correct strength, endurance, and flexibility deficits of the forearm musculature should be used. Kinetic chain deficits should be identified and corrected. It is important to ensure that athletes use correct technique in their sport and that they train appropriately. A gradually progressive return to functional activity should occur as the patient’s symptoms resolve.

Flexor Carpi Ulnaris Tendonitis

Flexor carpi ulnaris (FCU) tendonitis occurs as a result of repetitive microtrauma from activities requiring wrist flexion and ulnar deviation such as racquet sports or golf.⁶⁹ Because the pisiform bone is embedded in the FCU tendon, pisotriquetral compression syndrome with eventual pisotriquetral osteoarthritis can be associated with this condition.¹⁵³

Patients with FCU tendonitis typically report the insidious onset of volar ulnar wrist pain. Activities requiring repetitive wrist flexion and ulnar deviation frequently aggravate this condition. The patient might also experience crepitus in the region of the pisotriquetral joint during wrist movements. Physical examination can show localized edema and tenderness to palpation over the distal FCU tendon. Compression of the pisiform against the triquetrum can cause pain if osteoarthritis is present in this joint. Lateral wrist radiographs with slight supination and extension can also demonstrate pisotriquetral joint osteoarthritis.¹⁵³

Wrist hand orthoses with the wrist in 25 degrees of flexion can assist in symptom control.¹⁵³

Patients who do not respond to a comprehensive nonoperative treatment program can consider surgical resection of the pisiform bone with or without Z-plasty lengthening of the FCU tendon.¹³⁸

Flexor Carpi Radialis Tendonitis

The FCR tendon passes through a tunnel formed by the transverse carpal ligament, trapezial ridge, and scaphoid tuberosity before inserting on the second metacarpal base.¹⁵³ Although tendonitis in the FCR is relatively uncommon, activities that require repetitive gripping with wrist flexion and radial deviation predispose to this condition.⁴⁵

Symptoms usually develop slowly and include radial wrist pain with gripping, and forceful wrist flexion with radial deviation. Physical examination reveals tenderness to palpation over the distal FCR tendon and pain with passive wrist extension or with resisted wrist flexion combined with radial deviation.

If splinting is required, a wrist hand orthosis with 25 degrees of wrist flexion is appropriate.¹⁵³

De Quervain’s Syndrome

The first dorsal compartment of the wrist contains the abductor pollicis longus and extensor pollicis brevis tendons. These tendons run beneath a sheath over the dorsal aspect of the radial styloid process, along the inferior portion of the anatomic snuff box. Shear and repetitive microtrauma in this area can result in a stenosing tenosynovitis referred to as de Quervain’s syndrome.¹⁵³ De Quervain’s syndrome is the most common tendonitis of the wrist and is most frequently seen in patients who perform activities requiring forceful gripping with ulnar deviation of the wrist or repetitive use of the thumb.^34,⁹⁶

Patients with this condition present with insidious onset of pain over the dorsal radial aspect of the wrist aggravated by activities such as racquet sports, golf, or fly fishing. Patients can also report a sensation of wrist crepitus. Physical examination frequently demonstrates mild edema localized to the dorsal radial wrist and tenderness to palpation over the first dorsal compartment. Finkelstein’s test is pathognomonic for the diagnosis.¹⁵³ Finkelstein’s test is performed by placing the patient’s elbow in extension, with the forearm in neutral rotation and the wrist in radial deviation. The patient should be asked to place the thumb in the palm and grip the thumb with the fingers. The examiner should then passively bring the wrist into ulnar deviation. A positive test results in pain provocation in the first dorsal wrist compartment tendons.

Treatment for de Quervain’s syndrome includes rest, modalities, analgesics, and a thumb spica splint. First dorsal compartment peritendinous corticosteroid injection reduces symptoms in 62% to 100% of cases.^86,¹⁹¹

Intersection Syndrome

The abductor pollicis longus and extensor pollicis brevis tendons cross the extensor carpi radialis longus and brevis tendons 4 to 6 cm proximal to Lister’s tubercle. An inflammatory condition can develop at this crossing as a result of the friction from the tendons repetitively rubbing against each other. This condition is called intersection syndrome and is most frequently seen in oarsmen, weight lifters, and racquet sport athletes.^36,^134,¹⁵³

Intersection syndrome presents with the insidious onset of dorsoradial distal forearm pain aggravated by activities requiring repetitive wrist extension.¹⁵³ Physical examination reveals mild edema and acute tenderness 4 to 6 cm proximal to Lister’s tubercle, frequently associated with crepitation during wrist flexion and extension.

A neutral wrist–hand orthosis is commonly used in treatment. Corticosteroid injection into the point of maximal tenderness is used if the patient does not respond to initial treatment. Rarely does intersection syndrome require surgical intervention.

Extensor Carpi Ulnaris Tendonitis and Subluxation

The second most frequent tendonitis of the wrist is extensor carpi ulnaris (ECU) tendonitis. Repetitive wrist extension with ulnar deviation, such as occurs in the nondominant hand of the tennis two-handed backhand, predisposes to this condition.¹⁵³ Rupture or attenuation of the overlying tendon sheath can result in subluxation of the ECU tendon.¹⁶²

ECU tendonitis usually presents with insidious onset of dorsoulnar wrist pain that occurs during activities requiring forceful or repetitive wrist extension and ulnar deviation. Patients with tendon subluxation often report a history of a “pop” after a forceful volar wrist flexion and ulnar deviation with subsequent pain.¹⁶² Physical examination reveals tenderness to palpation over the ECU tendon and pain with resisted wrist extension with ulnar deviation. Subluxation can be induced by having the patient perform active ulnar wrist deviation while the forearm is fully supinated. The ECU tendon might palpably and/or visually sublux ulnarly over the ulnar styloid process.¹⁵³

A neutral wrist–hand orthosis is commonly used in treatment. If the patient does not respond to the typical conservative treatment program, a search for other diagnoses that mimic ECU tendonitis, such as triangular fibrocartilage complex injury, should be undertaken.

Acute ECU tendon subluxations can be treated with cast immobilization of the wrist in a pronated and dorsiflexed position for 6 weeks.²⁹ Early surgical repair for acute injuries, however, has also been advocated to improve predictability of outcome.¹⁶² In injuries characterized by chronic recurrent subluxation, surgical reconstruction of the subsheath should be performed.

Scapholunate Instability

Scapholunate instability resulting from ligamentous injury is the most common type of wrist ligament injury.¹⁰⁴ This can occur when a person falls on a pronated outstretched hand with the wrist in extension and ulnar deviation. After scapholunate ligament disruption, the scaphoid moves into a flexed position, whereas the lunate and triquetrum become extended. This pattern is referred to as dorsal intercalated segmental instability, or a “DISI” pattern (Figure 38-9).⁹² If this injury is not diagnosed early and treated properly, joint stress will ultimately lead to progressive wrist arthrosis and scapholunate advanced collapse.¹⁵²

FIGURE 38-9 A, Normal scapholunate angle between 30 and 60 degrees. B, Scapholunate angle greater than 60 degrees indicating a dorsal intercalated segmental instability (DISI) pattern suggestive of scapholunate dissociation.

Patients who sustain a scapholunate injury typically report falling on their outstretched hand with subsequent wrist edema, ecchymosis, and restricted ROM. Physical examination shows tenderness over the scapholunate joint, particularly on the dorsum of the wrist. The patient typically has a positive result on the Watson test.¹⁰⁰ To perform the Watson test, the patient’s wrist should be placed passively into ulnar deviation. The examiner should place his or her thumb over the scaphoid tubercle, located on the volar surface of the wrist. The patient’s wrist should be brought passively from ulnar to radial deviation while the examiner places a dorsally directed force against the scaphoid tubercle with his or her thumb. A positive test result is indicated by a painful click and dorsal shift of the scaphoid bone relative to the lunate bone during this movement.

Radiographic evaluation should include anteroposterior, anteroposterior with a clenched fist, lateral, and oblique radiographs.¹⁵² The presence of associated fractures should be assessed. The lateral radiograph can reveal the presence of a DISI pattern injury (see Figure 38-9). This is characterized by a scapholunate angle of more than 60 degrees.¹⁵² A gap of more than 3 mm between the scaphoid and lunate on anteroposterior radiographs is also diagnostic for scapholunate instability (Figure 38-10).¹⁵² The clenched fist view exaggerates this finding. Radiographic evaluation should include comparison studies with the opposite wrist.

FIGURE 38-10 A gap between the scaphoid and lunate on anteroposterior radiographs indicates scapholunate dissociation.

If standard radiographs are not diagnostic, further studies including arthrography or MRI can be obtained. The sensitivity and specificity of these studies, however, are variable.¹⁵² Wrist arthroscopy has become the gold standard for diagnosing this entity.

Acute scapholunate ligament injuries should be treated surgically. Chronic scapholunate injuries are more difficult to treat but also require surgical intervention. Partial wrist arthrodesis can improve chronic scapholunate instability, and a proximal row carpectomy is frequently used to treat advanced scapholunate collapse.¹⁵²

Scaphoid Fracture

Approximately 6% of all fractures involve the carpal bones, and 70% of carpal fractures involve the scaphoid.⁴⁹ The scaphoid is positioned distal to the radius and is part of the proximal row of carpals. The scaphoid is the primary restraint to excessive wrist extension and is therefore prone to injury. The scaphoid fractures in the middle third 80% of the time, the proximal third 15% of the time, and the distal third 4% of the time. Only 1% of scaphoid fractures occur through the distal tubercle.⁴⁹

The scaphoid receives its blood supply from a branch of the radial artery that enters the scaphoid through its distal pole. Consequently, proximal or middle third fractures of the scaphoid are prone to avascular necrosis and nonunion as a result of a disruption in the blood supply.⁴⁹

Patients who sustain scaphoid fractures usually fall on an extended wrist and experience dorsal radial wrist pain, mild anatomic snuff box edema, and ecchymosis. On physical examination, the anatomic snuff box will be tender to palpation. Neurovascular function should be assessed.

Radiologic evaluation of the wrist should include anteroposterior, lateral, right and left oblique, and anteroposterior clenched fist views.⁴⁹ Scaphoid fractures can be very subtle and not readily apparent on radiographs. Associated carpal instability patterns should be assessed radiographically with particular attention paid to scapholunate dissociation, which is suggested by a 3-mm or larger gap between the scaphoid and lunate during clenched fist anteroposterior views, or with a DISI pattern on lateral radiographs.⁴⁹

Because minimal edema occurs with this fracture, early cast immobilization can be used. For nondisplaced middle or proximal third fractures, the first 6 weeks of immobilization should use a long arm–thumb spica cast with the elbow in 90 degrees of flexion and the wrist in neutral flexion–extension and neutral deviation incorporating the first metacarpophalangeal joint with the thumb in slight extension and abduction.⁴⁹

If the fracture occurs in the distal third of the scaphoid, or if there is a high index of suspicion for a scaphoid fracture that was not seen on radiographs, a short arm–thumb spica cast with the wrist and thumb positioned the same as described previously can be used.⁴⁹

Patients with nondisplaced middle or proximal third fractures can be switched from the long arm–thumb spica cast to a short arm–thumb spica cast after 6 weeks, with the total duration of immobilization being for 12 to 20 weeks depending on when radiographic union occurs.⁴⁹ Patients with nondisplaced distal third fractures typically require between 10 and 12 weeks of immobilization in a short arm–thumb spica cast.⁴⁹ Radiographs should be repeated every 2 to 3 weeks until radiographic union is documented.⁴⁹

If a scaphoid fracture is suspected, and after 2 weeks of short arm–thumb spica cast immobilization the patient continues to have anatomic snuff box tenderness and repeat radiographs are still negative, then a bone scan or MRI can be performed to confirm or exclude this diagnosis. If the bone scan or MRI reveals a nondisplaced fracture, then standard treatment as outlined above should be performed.

During cast immobilization, the patient should be encouraged to perform ROM and strengthening exercises of the nonimmobilized upper limb regions. After immobilization, the patient should begin an exercise program to restore full pain-free ROM of the immobilized joints and strengthening the immobilized musculature.

Patients with displaced fractures, those who sustain scapholunate dissociation, or those who develop avascular necrosis or a nonunion should be referred to an orthopedist for management.

Distal Radial Fractures

The distal radius is one of the most frequently fractured areas of the body. Postmenopausal women and children appear to be particularly susceptible to this fracture.⁵⁰ The distal radius has three articulations, including the distal radioulnar joint, the radioscaphoid joint, and the radiolunate joint. The distal radius normally displays a volar tilt of approximately 11 degrees, a radial inclination along the articular surface as viewed on the anterior–posterior radiograph that is 23 degrees, and a 12-mm distance between the tip of the radial styloid process to a line drawn perpendicular to the distal ulnar articular surface (this can be measured on a standard anteroposterior radiographic image) (Figure 38-11).⁵⁰

FIGURE 38-11 Normal scaphoid volar tilt is approximately 11 degrees.

Frykman proposed a classification system for distal radial fractures in which types 1 and 2 are extraarticular fractures and types 3 and 4 are intraarticular fractures involving the radiocarpal joint.⁵⁰ Type 5 and 6 fractures are intraarticular fractures involving the radioulnar joint, whereas types 7 and 8 are intraarticular fractures that involve both the radioulnar and radiocarpal joints (Figure 38-12). The even-numbered fractures indicate the presence of an associated ulnar styloid fracture. The potential for adverse outcome increases as the Frykman classification number increases.

FIGURE 38-12 Frykman classification of distal radius fractures.

A majority of patients who sustain a distal radius fracture report falling on an extended wrist. Physical examination often reveals localized edema, ecchymosis, and deformity at the fracture site. The fracture site is tender to palpation. It is important to document normal neurovascular function during the examination.

Distal radial fractures can be assessed using anteroposterior, lateral, and oblique radiographs.⁵⁰ The anteroposterior view allows measurements of the radial inclination and length, whereas the lateral view allows evaluation of the volar tilt.

The most common distal radius fracture is a Frykman type 1 fracture called the Colles fracture.⁵⁰ This fracture is characterized by a fracture line 2 cm proximal to the distal radius with dorsal angulation of the distal fragment and radial shortening. Minimally displaced Frykman type 1 or 2 fractures can be managed with closed reduction and immobilization with a double sugar-tong splint with the wrist in slight flexion and ulnar deviation.⁵⁰ The forearm should be in a neutral position, and the elbow should be flexed 90 degrees.⁵⁰ Satisfactory reduction requires that there is less than 5 mm of radial shortening, no dorsal tilt of the distal radius, and less than 2 mm of displacement of fracture fragments. The patient should be evaluated again in 3 days for repeat radiographs.⁵⁰

By approximately 3 days postinjury, patients with a nondisplaced fracture can be placed in a short arm cast with the wrist in a neutral position for approximately 6 weeks, with repeat radiographs every 2 weeks for the first 6 weeks.⁵⁰ Patients with a minimally displaced fracture who are status postreduction should receive repeat radiographs at the 3-day follow-up evaluation to ensure maintenance of the reduction, and should be placed in a long arm cast with the wrist in slight flexion and ulnar deviation, the forearm in a neutral position, and the elbow flexed to 90 degrees for 3 to 4 weeks.⁵⁰ This can then be switched to a short arm cast with the wrist in a neutral position for 3 to 4 more weeks until healing has occurred.⁵⁰ Patients with minimally displaced fractures status postreduction should receive repeat radiographs weekly for the first 3 weeks and then every 2 weeks until healing is complete.⁵⁰

The patient should be instructed on ROM exercises for the joints that are not immobilized, and after discontinuation of the cast, a rehabilitation program should be instituted to ensure restoration of full joint ROM and upper limb strength.

Patients with Frykman type 3 fractures or higher, comminuted fractures, or fractures with significant displacement or that are unstable should be referred to an orthopedist for management.

Kienbock’s Disease

Kienbock first described a condition characterized by progressive collapse of the lunate in 1910.¹⁰⁷ This entity, now commonly referred to as Kienbock’s disease, is hypothesized to result from repetitive compressive forces to the wrist causing microfractures in the lunate leading to vascular compromise, avascular necrosis, and eventual collapse of the lunate.^57,¹⁰⁷ This condition occurs more frequently in patients who have ulnar-minus variant wrists (Figure 38-13).⁵⁷ Kienbock’s disease presents with pain and stiffness in the wrist. Physical examination can reveal limited wrist ROM and tenderness to palpation over the lunate on the dorsum of the wrist.

FIGURE 38-13 Ulnar-minus variant.

Radiographic evaluation typically reveals an ulnar-minus variant in the wrist.⁵⁷ The lunate can appear normal in early cases but frequently becomes sclerotic with cystic changes, followed by fragmentation and collapse.¹⁰⁷ Bone scans might demonstrate increased uptake even when radiographs are still negative.¹⁰⁷ MRI can also be helpful in diagnosing Kienbock’s disease.

In early cases of Kienbock’s disease, the wrist should also be immobilized in an attempt to allow revascularization.¹⁷² If the patient has an ulnar-minus wrist variant, an attempt at relieving lunate trauma through an ulnar lengthening procedure or radial shortening procedure can be performed.¹⁰⁷ For more advanced cases of Kienbock’s disease, partial wrist arthrodesis or lunate excision with soft tissue or silicone replacement might be required.¹⁰⁷

Triangular Fibrocartilage Complex Injuries

The triangular fibrocartilage complex (TFCC) is composed of an avascular central articular disc and vascular dorsal and palmar radioulnar ligaments.¹⁵² The TFCC is the primary stabilizer of the distal radioulnar joint and can be injured in an acute traumatic event such as falling on an outstretched hand or through repetitive microtrauma such as in gymnastics. Axially loading the wrist results in 18% of the load being born through the TFCC and the remaining 82% through the radiocarpal joint.¹³⁷ A positive ulnar variance results in an increase in the load-bearing function of the TFCC, which results in a higher incidence of TFCC injuries (see Figure 38-13).¹³⁷

Patients who sustain a TFCC injury might report either an insidious onset or a single traumatic event. Traumatic tears occur more frequently in young athletes, whereas degenerative tears are more common in older patients. Patients with acute injuries often report an axial load to the wrist associated with rotational stress.¹⁵² The patient can also report wrist catching and locking. The physical examination can show tenderness to palpation in the hollow between the FCU tendon and the extensor carpi ulnaris tendon, just distal to the ulnar styloid process.¹⁵²

Radiographic evaluation of the wrist can reveal an ulnar-plus variant on the anteroposterior view. Tricompartment wrist arthrogram, MRI, and MRI arthrogram can provide more specific information regarding TFCC pathology.¹⁵²

When the central articular disc of the TFCC has been acutely injured, surgical debridement is the treatment of choice. A 90% good-to-excellent result with this treatment was reported by Bednar and Osterman.¹⁹ Peripheral tears of the TFCC also respond well to surgical intervention, but the postoperative recovery process is slower than for central articular disc injuries.¹⁵² Patients with degenerative tears of the TFCC should be evaluated for an ulnar-plus variant, and if this is present, an ulnar shortening procedure should be considered along with surgical debridement of the TFCC.¹⁵²

Conditions of the Hand and Fingers

Extensor Tendon Central Slip Disruption

A rupture of the central slip of the extensor tendon at the base of the middle phalanx results in a boutonnière injury (Figure 38-14). A boutonnière injury is characterized by the inability to actively extend the proximal interphalangeal (PIP) joint, but patients with this injury are able to maintain full PIP joint extension if they are passively placed in this position.⁵⁹ The reason the PIP joint is held in flexion is due to the migration of the lateral bands of the extensor mechanism volarly below the axis of rotation in the PIP joint resulting in a flexion force at this joint.⁵⁹ The lateral bands, however, continue to exert an extension force on the distal interphalangeal (DIP) joint.

FIGURE 38-14 A boutonnière deformity caused by rupture of the central slip and volar migration of the lateral bands.

This injury can result from a rupture of the central slip tendon itself or an avulsion fracture at the central slip’s insertion on the dorsal proximal aspect of the middle phalanx. Mechanisms of injury include a crush injury, forced flexion of the interphalangeal joints, or lateral volar PIP joint dislocation.¹⁵³

The patient usually reports a specific injury to the digit resulting in an inability to extend the flexed PIP joint. Physical examination will reveal a boutonnière deformity of the affected digit and can reveal tenderness to palpation over the dorsum of the PIP joint. In acute cases, when the PIP joint is fully extended, the patient will be able to actively maintain the extension. This deformity can occur without antecedent trauma in patients with uncontrolled rheumatoid arthritis.

Standard radiographic evaluation of the PIP joint should be performed to check for an associated avulsion fracture of the dorsal proximal aspect of the middle phalanx. If the injury is evaluated within approximately 6 weeks, and the patient has full passive extension of the PIP joint, then treatment should involve continuous extension splinting of the PIP joint for 5 to 6 weeks (Figure 38-15).⁵⁹ The DIP joint can be left unsplinted, and flexion exercises of the DIP joint should be initiated early in the treatment program. It is important to educate the patient that even a single episode of PIP joint flexion over this time period can prevent successful treatment of this condition, as compliance is critical.

FIGURE 38-15 Dorsal extension splint of the proximal interphalangeal joint.

In patients who have a chronic boutonnière deformity, or if the PIP joint is not able to be passively extended, an aggressive rehabilitation program involving serial casting or splinting to restore full passive ROM should be implemented.¹⁵³ If adequate passive joint ROM is obtained and symptoms are minimal, no further treatment is required. If the patient is not able to regain significant PIP joint extension ROM, however, then surgical intervention to repair the extensor mechanism can be warranted. Surgical results are variable, however, and a trial of nonoperative treatment should be used in all patients before considering surgical intervention.⁵⁹

If a large displaced avulsion fracture from the dorsal proximal aspect of the middle phalanx accompanies the boutonnière deformity, early surgical intervention is the treatment of choice.¹⁵³

Terminal Extensor Tendon Disruption

Disruption of the distal extensor tendon at its insertion on the dorsal proximal aspect of the distal phalanx results in an injury called a mallet finger (Figure 38-16).⁵⁹ This can be caused by a tendon rupture or an avulsion fracture of the dorsal proximal distal phalanx. This injury usually occurs as a result of a hyperflexion force to an extended DIP joint. A zone of hypovascularity within the distal extensor tendon predisposes to this injury.¹⁸⁵

FIGURE 38-16 A, An extensor tendon rupture (top) or avulsion fracture (bottom) resulting in a mallet finger deformity (B).

The patient frequently reports an injury resulting in DIP joint pain and the inability to extend the DIP joint. Physical examination reveals a DIP joint in a flexed position that the patient is unable to extend actively. The patient might experience tenderness to palpation over the dorsal aspect of the DIP joint, and if the injury was recent, there can be accompanying erythema, ecchymosis, and edema.

Radiologic studies of the DIP joint should be performed to check for an avulsion fracture of the dorsal proximal aspect of the distal phalanx.

The treatment for this injury is usually nonoperative unless a large avulsion fracture is present, in which case surgical intervention can be required.⁵⁹ Nonoperative treatment involves splinting the DIP joint in extension 24 hr/day for 6 to 8 weeks (Figure 38-17).⁵⁹ The patient should be reminded of the importance of never allowing DIP flexion during this period because any flexion can prevent adequate healing and predispose to a permanent extension lag. After an adequate period of splinting, the patient should be placed in a rehabilitation program to restore full joint ROM and to ensure adequate strength, flexibility, and endurance in the forearm and hand musculature.

FIGURE 38-17 The distal interphalangeal joint can be splinted in extension with a dorsal padded aluminum splint (A), a volar aluminum splint without a pad (B), or a stack splint (C).

Flexor Digitorum Profundus Rupture

Distal disruption of the flexor digitorum profundus (FDP) tendon can occur with vigorous gripping activities, such as when a football player is making a tackle by gripping the opponent’s jersey. Because of this mechanism of injury, distal FDP tendon disruptions are frequently referred to as a “jersey finger.”⁸⁸ Biomechanical studies have revealed that the flexor digitorum tendon to the ring finger has a lower breaking strength than the other FDP tendons, which might explain the increased incidence of disruption in the tendon to this digit compared with other digits.¹⁰²

The history of patients with a jersey finger usually includes a vigorous gripping activity resulting in a sudden severe pain, frequently associated with a “pop.” The patient will subsequently be unable to actively flex the affected DIP joint. Physical examination shows an inability to actively flex the DIP joint, which becomes apparent when the patient is asked to make a fist (Figure 38-18). The retracted tendon mass can be palpable in the palm of the hand.

FIGURE 38-18 When asked to make a fist, patients with a ruptured flexor digitorum profundus tendon will be unable to flex the affected digit (in this case, the ring finger).

Radiographic evaluation of the DIP joint should be performed to rule out an associated avulsion fracture of the proximal volar aspect of the distal phalanx.

The primary treatment for this injury is surgical repair. If the tendon has retracted to the palm, then the repair should be performed within 7 to 10 days of the injury to prevent adhesion formation.⁸⁸ If the tendon does not retract below the PIP joint, however, then delayed repair can be performed within 6 to 8 weeks of the injury.⁸⁸ Associated fractures should be addressed at the time of surgery.

Proximal Interphalangeal Joint Dislocations

The PIP joint is the most frequently dislocated joint in the hand.⁵⁹ Dislocations can occur in dorsal, volar, and lateral directions, with dorsal dislocations being the most frequent.¹⁵³ Dorsal dislocations occur as a result of an axial load to the joint combined with hyperextension.¹⁵³ Dorsal dislocations result in various levels of injuries to the volar plate of the PIP joint and radial and UCLs and can also be accompanied by a fracture.

Volar PIP joint dislocations are usually due to a varus or valgus force across the joint combined with a volar force to the middle phalynx.¹⁵³ Associated injuries with volar PIP joint dislocations include radial and UCL sprains, central slip injuries, partial volar plate injuries, and fractures.

Dislocations usually present with deformity, pain, ecchymosis, and edema. The patient can report falling on the affected joint. Physical examination reveals tenderness to palpation over the injured structures. After reduction, the radial and UCL injuries can be assessed by performing varus and valgus stress to the PIP joint. Disruption of the central slip can be assessed by determining whether the patient is able to passively extend a flexed PIP joint. Dorsal and volar instability can be determined by performing a digital block for anesthesia followed by stabilizing the proximal phalanx and exerting a translational volar and dorsal force to the middle phalanx.

Radiologic evaluation should include standard radiographs of the PIP joint to assess for associated fractures. Avulsion fractures from the volar proximal aspect of the middle phalanx are commonly seen with dorsal dislocations. Postreduction films should also be performed to ensure that adequate reduction has been achieved. After a digital block for local anesthesia, the joint’s stability can be assessed by having the patient actively flex and extend the PIP joint under fluoroscopy.⁵⁹

After relocation, treatment for dorsal dislocations of the PIP joint includes a 45-degree extension block splint of the PIP joint to allow for healing of the volar plate injury and associated collateral ligament injuries (Figure 38-19).⁵⁹ The extension block splint angle can be reduced by 10 degrees each week, with a return to full extension in the fifth week. When the splinting is discontinued, buddy taping the injured finger to the adjacent finger for a few weeks can provide some stability for the joint as tissue healing continues and ROM exercises are instituted.

FIGURE 38-19 A dorsal extension splint with a reduction in extension block by 10 degrees each week for 4 weeks.

If stable closed reduction of a volar PIP joint dislocation can be attained, then nonoperative treatment can proceed with splinting of the PIP joint in full extension for 4 to 5 weeks (see Figure 38-15).⁵⁹ This can be followed by buddy taping the injured finger to an adjacent digit for approximately 2 weeks and resumption of normal activities as tolerated.

Surgical indications for PIP joint injuries include radiologic or gross instability after reduction, fractures involving greater than 50% of the articular surface, inability to reduce the dislocation, pilon fractures (i.e., fractures that extend from the volar to dorsal aspects of the phalanx, include intraarticular involvement, and are usually comminuted), or recurrent instability.⁵⁹

First Metacarpophalangeal Joint Ulnar Collateral Ligament Sprain

Radially directed forces across the first metacarpophalangeal (MCP) joint can result in an UCL injury. This injury, often referred to as “gamekeeper’s thumb,” is frequently seen in skiers and athletes who participate in sports such as basketball and football.¹⁵³ UCL injuries to the first MCP joint can be categorized into a three-grade severity scale of ligament sprains (see Table 38-1).

When a grade 3 UCL sprain of the first MCP joint occurs as a result of avulsion of the distal end of the ligament from the base of the first proximal phalanx, there is the possibility of interposition of the adductor pollicis aponeurosis between the base of the first proximal phalanx and the ruptured end of the UCL.¹⁷⁴ This is called a Stener lesion and can prevent adequate healing of this injury, leading to chronic joint pain and instability.

Patients who sustain first MCP joint UCL injuries report a radially directed force across the first MCP joint. They might report an associated “pop” and a feeling of instability in the joint. Physical examination reveals tenderness to palpation over the UCL. If a Stener lesion is present, a palpable mass on the ulnar side of the first MCP joint might be present, representing the avulsed UCL.²

UCL stress examination should be performed after local anesthesia via a wrist block, although an initial examination without local anesthesia can be attempted. The stress examination should be performed with the joint in both full extension and 30 degrees of flexion. A complete tear is indicated by an angular difference between the injured and uninjured first MCP joint during stress examination of greater than 15 to 30 degrees.^74,¹³⁶ A lack of an endpoint during stress examination also suggests complete UCL disruption.

Radiologic evaluation should include anteroposterior, lateral, and oblique radiographs to detect the presence of fractures or joint subluxation. MRI allows better visualization of the soft tissue injuries, but its sensitivity and specificity for this condition is still being examined.

Treatment of partial tears involves modalities, analgesics, and immobilization in a thumb spica cast for 10 to 14 days, followed by a wrist–hand–thumb spica orthosis for 2 weeks and a hand-based thumb spica orthosis for 2 to 4 more weeks.⁵⁹ Patients who participate in contact sports should continue to wear a thumb spica splint during competition for the remainder of the season. Local taping for stability during activity can be used after the period of splinting is completed. Gentle progressive ROM exercises should begin after cast immobilization by removing the splint twice daily, and activity should be progressed as tolerated.

Early surgical repair has been advocated for complete ruptures of the UCL, particularly if a Stener lesion is present.^55,^91,^108,^133,¹⁶⁸ Surgery is also indicated for individuals with an avulsion fracture of the base of the proximal phalanx with angulation and displacement greater than 3 mm, or with chronic recurrent instability.¹¹⁴