Chapter 280: Shoulder Pain

The shoulder is designed for mobility in all directional planes, but stability is less than other joints. To meet the many demands placed on it, the shoulder uses three bones, four joints, and a specialized set of soft tissues consisting of muscles, tendons, ligaments, and bursae. The most common causes of nontraumatic shoulder pain in descending order of frequency are rotator cuff tendinopathy, acromioclavicular joint disease, adhesive capsulitis, and referred pain.¹

BONES AND JOINTS

The humerus, clavicle, and scapula are the bones of the shoulder complex. The scapula consists of the body plus three bony extensions: the glenoid, the coracoid, and the acromion.

The four joints of the shoulder are the glenohumeral, acromioclavicular, sternoclavicular, and scapulothoracic. The glenohumeral joint is a ball-and-socket joint and is the central axis of shoulder motion. The glenohumeral joint is the most mobile and least sTable joint in the body. Stability is derived from three components. The first is the glenoid labrum, which is a fibrous ring of tissue encircling the glenoid cavity. The glenoid labrum increases the surface contact area of the humeral head within the relatively shallow glenoid fossa. The second component consists of three glenohumeral ligaments, which aid stability by reinforcing the joint capsule. Finally, four specialized muscles, known as the rotator cuff, encompass the glenohumeral joint and provide stability during motion.

The sternoclavicular and acromioclavicular joints together contribute to glenohumeral motion, but their primary function is to suspend and stabilize the shoulder girdle. Rotation at the acromioclavicular joint and elevation at the sternoclavicular joint allow complete arm elevation. The scapulothoracic joint represents the articulation of the scapula on the posterior wall of the thorax. Scapular motion is essential for overall shoulder motion: every degree of scapulothoracic motion allows 2 degrees of glenohumeral motion.

SHOULDER MUSCLES

The deltoid, which drapes the shoulder complex and forms its contour, acts as a powerful and independent elevator of the arm. Along with the pectoralis, the deltoid is the primary source of movement of the upper extremity.

The rotator cuff consists of four muscles: supraspinatus, infraspinatus, teres minor, and subscapularis (Figures 280-1 and 280-2). All originate on the scapula, traverse the glenohumeral joint, and insert on the proximal humerus. The rotator cuff muscles also contribute to the power of the upper extremity, providing 30% to 50% of the power in abduction and 90% in external rotation.

The supraspinatus muscle originates on the posterior and superior aspect of the scapula and passes beneath the acromion, inserting onto the great tuberosity of the humeral head. It initiates arm elevation and abducts the shoulder. It also balances the power of the deltoid, keeping the humerus centered in the glenoid during deltoid contraction. The infraspinatus originates on the posterior scapula just inferior to the scapular spine. It inserts on the posterior aspect of the greater tuberosity and acts primarily as an external rotator of the arm (Figure 280-1). The teres minor originates on the lateral border of the scapula just inferior to the infraspinatus and inserts on the posterior aspect of the humerus. It works with the infraspinatus to provide external rotation (Figure 280-1). The subscapularis is the only rotator cuff muscle that arises from the anterior aspect of the scapula. It attaches to the lesser tuberosity of the humeral head and provides internal rotation of the arm (Figure 280-2).

The long head of the biceps tendon, although not part of the rotator cuff, assists in rotator cuff function. The long head of the biceps tendon courses superiorly in the bicipital groove of the humerus between the greater and lesser tuberosities, passes between the subscapularis and supraspinatus tendons, and penetrates the glenohumeral joint to insert on the labrum (Figure 280-2). During arm elevation, the tendon of the long head of the biceps depresses the humeral head, helping it remain centered in the glenoid.

BURSAE

The bursae facilitate frictionless motion between the components of the shoulder. Although there are eight bursae in the shoulder complex, only the extra-articular subacromial bursa is clinically significant. Its roof adheres to the undersurface of the deltoid, and its floor to the underlying rotator cuff. The bursa is lubricated by synovial fluid and surrounded by a layer of peribursal fat.

CORACOACROMIAL ARCH

The coracoacromial arch is formed by the coracoid posteriorly, by the acromion anteriorly, and by the coracoacromial ligament that forms the anterior roof of the arch (Figure 280-3). The humeral head provides the floor of the arch. This arch defines the space within which the tendons of the rotator cuff, the tendon of the long head of the biceps, and the subacromial bursa must function.

PATHOPHYSIOLOGY

Repetitive overhead use of the arm or movement of the shoulder above the horizontal causes encroachment on the subacromial space by the humeral head (Figure 280-4).^2,3,4 Repetitive subacromial encroachment or "impingement" produces pathologic changes of the bursa, rotator cuff, and biceps tendon that result in a loss of the normal gliding mechanism between the rotator cuff and related soft tissues within the coracoacromial arch. Impingement syndrome is the encompassing term used for the conditions of subacromial bursitis, rotator cuff tendinitis, supraspinatus tendinitis, and painful arc syndrome.^2,3,4,5

Repetitive impingement of the subacromial space evolves in a progressive pattern classified in three stages.^3,4 In stage 1, reversible edema and hemorrhage about the rotator cuff occur. Although possible at any age, it is classically seen in young athletes <25 years old who have excessive overhead use of the shoulder. During this stage, patients complain of a dull ache over the anterolateral shoulder that is aggravated by activity and improved by rest. The clinical course at this point is typically reversible.

Repeated mechanical trauma from the impingement can progress to stage 2, where tendinitis of the rotator cuff creates fibrosis and thickening of the tendons of the rotator cuff and bursa. This stage is typically seen in patients between the ages of 25 and 40, and the prolonged duration (weeks to months) or recurrence of symptoms is useful in making this diagnosis. During this stage, patients complain of a recurrent or chronic aching pain with daily activities, pain with vigorous activity, and night pain (caused by irritation triggered by a relaxed supporting muscle tone).

Continued overuse can lead to stage 3 with rotator cuff tears, rupture of the long head of the biceps, and subacromial spurs. Patients at this stage have progressive symptoms and disability, and they often require surgical decompression of the subacromial space.

CLINICAL FEATURES

The primary symptom with impingement syndrome is pain, developing insidiously over a period of weeks to months. The pain is located over the anterior to lateral shoulder and frequently radiates to the lateral mid-humerus, but not below the elbow.^2,6 Patients usually complain of pain at night that is deep and aching and interferes with sleep. This pain occurs especially when the patient lies on that shoulder or sleeps with the arms overhead. The pain may be exacerbated by activities that require overhead arm use, such as brushing the hair or reaching into a cupboard. Patients also note weakness and stiffness of the shoulder that is usually secondary to pain.^2,6 Once the shoulder pain has resolved, any weakness should trigger a search for a rotator cuff tear or cervical radiculopathy.

Disuse atrophy of the shoulder musculature occurs when impingement or tendinitis symptoms are chronic (stages 2 and 3). Palpation of the rotator cuff insertion at the lateral aspect of the proximal humerus usually produces pain and tenderness. During range-of-motion maneuvers, fibrosis and scarring within the tendon can cause crepitus, but the patient should have a normal and full active and passive range of motion.⁶ Pain with an active arc of abduction, especially between 60 and 100 degrees, is consistent with rotator cuff pathology.² A sensation of catching also may be present if scar tissue is trapped beneath the acromion. Rotator cuff strength testing usually reveals mild to moderate weakness secondary to pain. The pain is usually present when resistance is applied.

The individual muscles of the rotator cuff should be isolated and tested individually, looking for pain or weakness; to isolate the supraspinatus, abduct the arm to 90 degrees and forward flex it 30 degrees with the thumb pointed down in the "empty can" position (Figure 280-5). Either symptom against resistance (continued abduction) in this position suggests inflammation or injury to the supraspinatus muscle, the most likely to be involved in the impingement syndrome.³

To isolate the infraspinatus and the teres minor, externally rotate the shoulder with the patient's arm against the body and the elbow bent to 90 degrees and the forearm in neutral position. Stabilize the elbow against the patient's waist and instruct the patient to rotate the arm outward.

To isolate the subscapularis, have the patient place the hand behind the back and attempt to push the examiner's hand away by moving the dorsum of the hand away from the back (lift-off test).

Specific maneuvers on physical examination test for signs of impingement by compressing the rotator cuff and bursa between the humeral head and coracoacromial arch. In the classic impingement maneuver of Neer, the examiner prevents scapular rotation with one hand while raising the patient's straightened arm smoothly in full forward flexion to overhead. A positive sign is pain in the arc between 70 and 120 degrees. A second test, the Hawkins impingement test (Figure 280-6), requires the examiner to position the patient's arm (shoulder) in 90 degrees of abduction and 90 degrees of elbow flexion. Rotation of the arm inwardly across the front of the patient with internal rotation of the shoulder compresses the cuff and bursa between the humeral head and coracoacromial ligament. The Neer and Hawkins tests are 75% to 89% and 91% to 92% sensitive, respectively, but specificity is much lower at 30% to 40% and 25% to 44%, respectively.⁷

DIAGNOSIS

The diagnosis is based on a history of chronic shoulder pain with a full range of motion, with possible weakness of the rotator cuff muscles and positive responses to provocative maneuvers. Radiography is used to identify other causes like fracture or degenerative joint changes. Early nonspecific radiographic signs of rotator cuff syndromes include sclerosis and subchondral cyst formation of the greater tuberosity of the humerus or sclerosis or spur formation on the anterior edge of the acromion.⁸

TREATMENT

The goals of treatment of impingement syndrome are to reduce pain and inflammation and to prevent progression of the process. Therapy starts with a conservative treatment program that should include the following:

1. Relative rest and activity modification. Advise the patient to avoid the aggravating activity and minimize all overhead activities. Although brief periods of support with a sling help, avoid complete immobilization and prescribe range-of-motion exercises (see below) three to four times daily to minimize the chance of developing adhesive capsulitis.

2. Anti-inflammatories and analgesics. Nonsteroidal anti-inflammatory agents for 7 to 21 days are key, with short-term opioid analgesics added for moderate to severe pain, and acetaminophen may aid in lesser pain syndromes.

3. Cryotherapy. Apply ice to the affected shoulder for 10 to 15 minutes three to four times daily for analgesic effects and potential reduction of inflammation and edema.

4. Range-of-motion exercises. Two simple exercises can help the patient maintain glenohumeral motion. Pendulum swings are done with the patient slightly bent at the waist with the arm hanging freely in front of the body. The arms should be swung in gentle arcs of motion in both a clockwise and counterclockwise direction to the level of pain tolerance for 5 to 10 minutes three to four times daily. The size of the arcs should increase daily as symptoms allow. Also, the patient should stand sideways an arm's length from a wall and walk the fingers up the wall to the level of pain tolerance, repeating the exercise three to four times daily.

5. Stretching and strengthening. Stretching and strengthening exercises are best carried out under the supervision of a physical therapist.

6. Corticosteroid injections. Although local corticosteroid injections into the subacromial space relieve pain, adverse effects include muscular atrophy, weakness, and further tissue degeneration. Injection directly into the tendon can lead to necrosis and rupture. Injection is not an emergency procedure and is best left to the primary care physician or orthopedist.

7. Follow-up. Ensure reassessment within 7 to 14 days with an orthopedist and/or a rehabilitation expert.

PATHOPHYSIOLOGY

Patients with rotator cuff tears present with shoulder pain after acute traumatic injury, chronic injury, or an acute extension of a chronic impingement (stage 3) of the rotator cuff. Rotator cuff tears due to chronic impingement in patients >40 years of age account for most tears. In younger patients, rotator cuff tears are seen in laborers and athletes who participate in sports that require overhead activities like tennis, swimming, and baseball.⁹ In general, healthy rotator cuff tendons are resistant to acute injury, with acute rotator cuff tears accounting for only 10% of all rotator cuff tears. These acute tears usually occur as a result of trauma, such as forced or extreme hyperabduction or hyperextension from falling on an outstretched arm, lifting a heavy object, or catching a heavy object as it falls. Glenohumeral dislocation is a common cause of acute rotator cuff tears. In patients >40 years of age with a first-time dislocation, there is a 57% incidence of acute rotator cuff tear; think of a rotator cuff tear in patients with weakness >3 weeks after an acute dislocation.⁹

In addition to being categorized by the acuteness of the injury, rotator cuff tears can be full or partial thickness, with either difficult to detect on the clinical evaluation. Partial-thickness tears are twice as common as full-thickness tears, and most commonly occur on the inferior aspect of the tendon. The type and extent of the tear have significant implications for the ultimate treatment and prognosis. The supraspinatus, due to its location within the coracoacromial arch, is the most commonly affected tendon of the rotator cuff.

CLINICAL FEATURES

The clinical features of a chronic rotator cuff tear differ from those of an acute tear. Only about half of patients with chronic rotator cuff tears can recall specific trauma or an event associated with the onset of pain, often seemingly insignificant in description. Patients more commonly report a history of gradual and progressive pain; while initially described as worse at night, the pain eventually becomes persistent. The pain may be diffuse, but is commonly localized to the lateral aspect of the upper arm. Often, initial therapy with rest, anti-inflammatory agents, and glucocorticoid injections helps. If the rotator cuff weakens, the frequency, intensity, and duration of the symptoms increase and are less responsive to the usual treatments. Shoulder dysfunction progressively worsens and interferes with work, recreation, and normal daily activities. Arm elevation, external rotation, and lifting of even light objects worsen the symptoms.

With acute injuries, such as those due to falling or catching a heavy object, the patient may report a "tearing" sensation in the shoulder followed by severe pain and inability to raise the arm. An acute rotator cuff tear produces immediate profound pain and disability, with asymmetry often present due to local swelling. Active motion is limited, with inability to abduct or externally rotate the arm against even minimal resistance. On examination, disuse atrophy is often present in patients with chronic rotator cuff tears. Palpation may produce discomfort at the lateral aspect of the upper arm or in the subacromial region. Most patients with rotator cuff tears have weakness and pain on abduction, elevation, and, most commonly, external rotation. The result of the drop arm test is positive if the patient is unable to hold or lower a fully extended arm at 90 degrees of shoulder abduction without dropping it. Crepitus and pain are usually present on range-of-motion testing.

DIAGNOSIS

It may be very difficult to distinguish a full-thickness tear from a partial-thickness tear or a rotator cuff injury from impingement syndrome. The diagnosis is primarily clinical based on a finding of rotator cuff weakness on examination in a patient with a history of chronic shoulder pain or acute shoulder pain after significant trauma. In patients with an acute injury, it may be difficult to diagnose the tear due to excessive pain from the injury. In these cases, assume a preliminary diagnosis of acute rotator cuff tear and treat conservatively, with appropriate follow-up in 1 week.

Routine shoulder radiographs occasionally give additional diagnostic information. The most specific radiographic sign for large rotator cuff tears is a narrowing of the acromiohumeral space (<7 mm).⁸ No radiographic findings are diagnostic of an acute rotator cuff tear, and the diagnosis should rely on clinical findings. MRI, US, and arthrography are the most sensitive modalities for detecting rotator cuff tears, although all tend to underestimate the extent of the tear.

TREATMENT

The basic goals of emergency care for suspected rotator cuff injuries are the same as with impingement (see above), with analgesia, support, and prevention of further dysfunction and disability. An arm sling can provide support and comfort until the acute symptoms subside. However, avoid prolonged immobilization and prescribe range-of-motion exercises three to four times daily to minimize the development of adhesive capsulitis.

Any evidence or suspicion of neurovascular compromise requires immediate orthopedic consultation. Refer all patients with an acute rotator cuff tear (with or without a history of chronic symptoms) and those with significant disability to an orthopedist for follow-up within a week. Complete rotator cuff tears usually require surgical repair, and functional results are better if repair is carried out early, before retraction, fibrosis, tendon degeneration, and muscular atrophy have occurred. Partial-thickness or chronic tears may respond to conservative measures.

PATHOPHYSIOLOGY

Calcific tendinitis is a self-limiting disorder characterized by calcium crystal deposition within one or more tendons of the rotator cuff. In time, the calcium undergoes painful spontaneous resorption with subsequent healing of the tendon. Middle-age patients are most commonly affected, and this process is rarely seen in patients >70 years of age. Females are slightly more likely to be affected than males, and calcification is often present bilaterally. Primary tendon degeneration as a result of chronic repetitive microtrauma, age, and tissue hypoxia are causes of this disorder. The supraspinatus is by far the most commonly affected tendon, with calcium deposition usually occurring near its origin on the humerus. Any of the rotator cuff tendons or the long head of the biceps may be affected.

CLINICAL FEATURES

Because calcification occurs over a period of time, patients are generally asymptomatic or have mild pain at rest or at night. Pain with abduction or a "catching" sensation may be present on movement. During the resorptive phase, incapacitating pain can occur from vascular proliferation, formation of granulation tissue, and calcium crystal extravasation into the subacromial bursa. Symptoms are usually self-limited, lasting 1 to 2 weeks in most cases. After the initially painful resorptive phase, patients can have variable levels of pain and shoulder dysfunction that may last for several months (postcalcific period). Adhesive capsulitis is the most common complication of calcific tendinitis and creates more chronic symptoms.

Symptomatic patients experience sudden onset of shoulder pain, usually at rest, and shoulder motion reproduces significant pain. The pain is often worse at night and interferes with sleep. During an acute attack with intense pain, the patient holds the arm across the body and often is reluctant to move it. A point of maximum tenderness may be palpated over the proximal humerus near the tendinous insertion of the rotator cuff. Both active and passive range of motion of the glenohumeral joint are usually limited to varying degrees. Flexion, extension, abduction, and internal and external rotation of this joint should be documented. Muscle atrophy and crepitus may also be present.

DIAGNOSIS

Obtain shoulder radiographs for patients with suspected calcific tendinitis to localize deposits and seek any signs of possible impingement. During the initial formative phase, calcium deposits are usually dense and well-defined if visualized. In patients who are experiencing intense pain in the resorptive phase, calcium deposits may appear hazy with poorly defined borders. The presence of visible calcifications is not necessarily specific for this disorder. US is unlikely to be helpful during the resorptive phase as the poorly defined calcifications produce little or no acoustic shadowing.^10,11

TREATMENT

Treatment is similar to that for impingement syndrome, and nonoperative management is successful in 90% of cases. During an acute attack, nonsteroidal anti-inflammatory agents, opioid analgesics, and ice help calm the intense pain. The shoulder may be rested using a sling for brief periods of immobilization, but avoid prolonged immobilization. Instruct patients to rest the shoulder in abduction on the back of a chair as often as is tolerable. Sleeping with a pillow beneath the axilla can also help prevent restriction of motion. Local application of heat may be used once acute symptoms have diminished. Gentle and progressive range-of-motion exercises should be emphasized and encouraged. Physical therapy is indicated in patients with more chronic cases who have significantly limited range of motion of the shoulder.

Subacromial corticosteroid injection, oral steroids, platelet-rich plasma therapy, transcutaneous electrical nerve stimulation, and therapeutic US are sometimes used, but no strong supporting evidence exists for their use. Extracorporeal shockwave therapy appears to improve success rates.¹² A recent randomized controlled trial compared US-guided needle lavage with corticosteroid injection to corticosteroid injection alone, with modestly favorable clinical and radiographic results for the US group at 1 year.¹³

DISPOSITION AND FOLLOW-UP

Calcific tendinitis is a self-limited process in the vast majority of cases. For patients with new presentation of this disease, arrange follow-up with a primary care doctor within a week. For the 10% of patients in whom nonoperative methods are unsuccessful, arthroscopic or open surgery may be indicated. Refer patients who have progression of symptoms, constant pain interfering with daily activities, or absence of improvement after conservative therapy.¹⁴

PATHOPHYSIOLOGY

Adhesive capsulitis, commonly referred to as frozen shoulder syndrome, begins as painful inflammation of the glenohumeral joint, followed by eventual fibrosis of the joint capsule and restriction of shoulder motion. Primary or idiopathic adhesive capsulitis is associated with a wide variety of unrelated conditions, including diabetes, thyroid disease, postmenopausal, pulmonary neoplasm, and autoimmune disorders. Secondary adhesive capsulitis produces similar findings, but results from a known cause, such as prolonged immobilization after trauma, surgery, stroke, or a primary inflammatory condition of the shoulder such as impingement syndrome or bicipital tendinitis. The condition resolves with conservative therapy in most patients within 1 to 2 years, although some are left with residual pain or stiffness.

Four stages of this disorder exist, although patients do not necessarily follow these stages in a linear fashion. Stage 1, around the first 2 to 3 months, presents with acute synovial inflammation with limitation of shoulder movement due to pain. Stage 2 (freezing stage), about months 3 to 9, has decreased shoulder motion from capsular thickening and scarring, and chronic pain. Stage 3 (frozen stage), months 9 to 15, is characterized by less pain, but a more fibrotic and thick capsule and more limitation in range of motion. Stage 4 (thawing stage), usually after 15 months, has minimal pain and progressive improvement in the range of motion of the shoulder.¹⁵

DIAGNOSIS

Limited active and passive range of motion is the hallmark of adhesive capsulitis. Pain is typically diffuse and aching, poorly localized, accompanied by stiffness, and often extends down the upper arm. The pain is frequently worse at night and at rest, especially in earlier stages. Disuse atrophy may be present. Impingement testing is difficult due to the restriction of motion. Occasionally, posterior glenohumeral dislocation creates restricted motion of the shoulder; exam and imaging can help detect this condition. US may demonstrate increased vascular flow, thickening of rotator cuff structures, and bulging of the supraspinatus tendon. MRI or magnetic resonance angiography findings approach 70% sensitivity and 95% specificity for the condition.¹⁵

TREATMENT

The goals of treatment are to reduce pain and restore motion and function. Avoid shoulder immobilization; if a sling is used in patients in early stage 1 who have severe pain, limit it to days to prevent increased loss of motion due to further capsular restriction. Although physical therapy is difficult in the early, more painful stages of disease, it is key along with nonsteroidal anti-inflammatory drugs, analgesics, and ice.

Although it is not an ED procedure, intra-articular steroid injection is a potential option during follow-up to improve pain and function in the short term; the long-term effects are less clear.

Refer patients to an orthopedist if ongoing symptoms exist despite good therapy (usually after >6 months) or when the diagnosis is unsure. Closed manipulation under general anesthesia, arthroscopic capsular release, and open capsular release are surgical options.

PATHOPHYSIOLOGY

Disorders of the proximal aspect of the long head of the biceps tendon include tendinopathy, subluxation or dislocation, and partial or complete tears; these occur from inflammation, instability, or trauma.¹⁶ The long head of the biceps tendon originates from the superior labrum and the supraglenoid tubercle on the scapula. As it exits the glenohumeral joint, it courses through the bicipital groove as it travels anterior and superior to the humeral head.¹⁶ Approximately 50% of the long head of the biceps tendon originates from the superior labrum. Forces applied tend to pull the labrum off the glenoid rim. Due to this anatomic association, tears of the superior labrum, known as SLAP (superior labrum anterior to posterior) lesions, are frequently found in conjunction with long head of the biceps tendon pathology. Injuries of one or the other structure may be difficult to distinguish, both clinically and operatively.

The biceps tendon may also become inflamed, may become partially displaced out of the bicipital groove, or may rupture altogether. (See chapter 271, "Shoulder and Humerus Injuries" for the approach to traumatic ruptures of the distal bicipital tendon.)

CLINICAL FEATURES

Bicipital tendinopathy may be due to inflammation (tendinitis) or collagen tears in or around the tendon (tendinosis) and may be acute or chronic. Tendinitis and tendinosis are difficult to distinguish clinically. Bicipital tendinopathy triggers intense and localized pain at the anterior aspect of the shoulder. Repetitive overhead arm motion may result in inflammation chronically or an acute SLAP lesion, particularly in athletes. Pain at rest, night pain, and pain on rotation are common. Dislocation or subluxation of the biceps tendon from the bicipital groove is painful and occurs medially or laterally, while complete dislocation is seen only medially and is associated with a subscapularis tear. Posterolateral instability is associated with a supraspinatus tear. Concurrent injury to the biceps reflection pulley is necessary for tendon dislocation in either direction.¹⁶

Partial or complete rupture is almost always proximal and is due to micro-tears and other age-related degenerative changes in this area of the tendon. In younger patients, mild trauma may cause complete rupture of the biceps tendon, which is heralded by an audible snap or pop followed by severe pain and deformity.

DIAGNOSIS

Palpation of the tendon within the bicipital groove reproduces the intense pain. Forearm supination, one of the main actions of the long head of the biceps, also reproduces pain, especially when resistance is applied. In assessing for instability, resisted forearm supination may cause palpable subluxation or a painful popping sensation as the tendon undergoes subluxation; these findings are classic but not common.

Because biceps tendon pathology is frequently associated with pathology of adjacent structures, clinical testing is often inconclusive and inaccurate.¹⁶ Many provocative tests to confirm the presence of pathology of the long head of the biceps or superior labrum have been described in the literature. Speed's test identifies tear or tendinitis of the long head of the biceps; flex the shoulder to 90 degrees with the patient's arm (elbow) fully extended and supinated. Provide downward resistance against shoulder flexion. Pain localized to the bicipital groove indicates a positive test. The Speed's test appears to have a sensitivity of 87% and a specificity of 80% for tear of the long head of the biceps.¹⁷

SLAP lesions or labral tears are complex, and a recent Cochrane review concluded that physical examination alone cannot be used as the sole basis by which to diagnose a SLAP lesion. The test most likely to help diagnose a SLAP lesion is the active compression test. To perform, have the standing patient flex his or her shoulder to 90 degrees, and then adduct 10 to 15 degrees medially and rotate fully, with elbow extended. The examiner stands behind the patient and applies a uniform downward force to the arm. This is repeated in full lateral position. A positive response is indicated by eliciting pain on the first maneuver, which is reduced or eliminated on the second maneuver; the test is 60% to 100% sensitive and 85% to 98% specific.¹⁷

In biceps tendon rupture, the classic finding is described as a "Popeye" deformity caused by distal contraction of the muscle belly. Supination is weak on muscle testing, but elbow flexion remains strong because of the presence of other intact elbow flexors (short head of the biceps and brachialis muscles).

Plain radiographs are generally unhelpful in diagnosing biceps tendon or SLAP lesions. MRI is also poor in diagnosing biceps tendon and SLAP lesions; magnetic resonance arthrography is preferable. In the hands of skilled operators, US is poorly sensitive but very specific in diagnosing disorders of the long head of the biceps. Arthroscopy is considered the gold standard, although recent studies have demonstrated poor intrarater reliability of arthroscopic diagnosis.¹⁸

TREATMENT

Manage tendinitis and subluxation with brief use of a sling as needed for support and comfort, aided by analgesics, anti-inflammatory agents, application of ice several times daily, and elevation to reduce swelling. Prescribe early mobilization with stretching exercises and follow-up within 7 to 14 days with a primary care provider.

Although not commonly administered by emergency physicians, intra-articular injections of local anesthetic and steroid can improve symptoms. Intra-articular injections can relieve bicipital symptoms but may be ineffective if adhesions or synovitis prevent dispersal into the bicipital groove. Direct injection into the bicipital groove with US guidance may be an option for specialists if previous intra-articular injections have not worked.¹⁸ Bicipital tendinitis usually resolves with conservative therapy.

Reserve orthopedic consultation for those with tendinopathy associated with instability, partial rupture, or high-grade SLAP lesion or those failing to respond to a conservative treatment regimen. Surgical options include debridement, tenotomy, or tenodesis.¹⁸ Bicipital tendon rupture often requires surgical repair, so orthopedic consultation in 24 to 48 hours is best. Patients with suspected SLAP lesions or other mechanical proximal biceps injuries generally require arthroscopic or other surgical intervention when symptomatic.

Because the glenohumeral joint is non–weight bearing, primary osteoarthritis is rare. When it does occur, presentation is similar to that of degenerative disease in other joints: the patient experiences gradual and progressive onset of pain, worse with motion and better with rest. This usually occurs concurrently with degenerative disease of the acromioclavicular joint.

Secondary osteoarthritis is more common and is usually associated with a previous fracture, recurrent dislocations, or an underlying rheumatologic, metabolic, or endocrinologic disorder. ED care of both primary and secondary arthritis relies on analgesics, anti-inflammatory agents, and gentle exercises to preserve range of motion.

Although disorders of the rotator cuff and other intrinsic structures of the shoulder are the most common cause of shoulder pain, extrinsic conditions outside the shoulder complex can refer pain to the shoulder. The differential diagnosis includes disorders of the cervical spine, brachial plexus injuries, axillary artery thrombosis, suprascapular nerve injury, thoracic outlet syndrome, Pancoast's tumor, and miscellaneous thoraco-abdominal disorders.

The neck is the most common source of pain referred to the shoulder. Degenerative disease of the cervical spine, degenerative disk disease, and herniated nucleus pulposus can all refer pain to the shoulder. A patient with a C5-C6 herniated disk may present with pain very similar to that due to rotator cuff disease. Careful and thorough examination of the cervical spine and a complete neurovascular examination should be included in the evaluation of any patient with shoulder pain. (See chapter 279, "Neck and Back Pain").

Brachial plexus injury can cause pain referred to the shoulder and can produce weakness and atrophy in the muscles of the shoulder within weeks of injury. Radiographic evaluation of the cervical spine should be included in the ED evaluation of patients with suspected brachial plexus injury or involvement. Brachial plexus neuritis is uncommon but can be very painful. Its etiology is unknown, although inflammatory, postimmunization, and viral origins have been proposed. Inflammation of the brachial plexus can lead to weakness and atrophy of the muscles of the shoulder complex within weeks following the onset of pain.¹⁹ Brachial plexus neuritis is usually self-limiting. Referral to a neurologist should be arranged if this disorder is suspected.

The most serious vascular injury that can cause shoulder pain is acute thrombosis of the axillary artery. Repetitive mechanical trauma or explosive stress from lifting heavy objects can compress and contuse the intimal lining of the axillary artery, predisposing the artery to thrombosis.

Compression of the suprascapular nerve can cause shoulder pain. This nerve originates from the brachial plexus distal C5-C6 nerve roots and courses posteriorly to the suprascapular notch. It can become entrapped beneath the transverse ligament at the level of the suprascapular notch. Traction injuries from explosive movements can also injure the nerve. On examination, active external rotation typically reveals infraspinatus atrophy and associated weakness. The initial treatment is conservative. Electromyography and nerve conduction velocity studies will reveal the extent and location of nerve injury. Surgery for decompression is considered if conservative measures fail.

Compression of the brachial plexus and blood vessels proximal to the shoulder, the thoracic outlet syndrome, can cause shoulder pain. Women in the childbearing years are affected three times more commonly than men. The medial trunk of the brachial plexus is most commonly involved, and the symptoms usually include pain that radiates through the shoulder to the medial forearm and occasionally to the small and ring fingers. Patients also complain of numbness and tingling of the fingers and a weak grip. Patients can usually identify motions that reproduce the symptoms. Plain radiographic evaluation is often nondiagnostic, although some will have evidence of a prior clavicular fracture with malunion or the presence of a cervical rib band that compress the brachial plexus. Conservative measures include activity modification, education, postural exercises, nonsteroidal anti-inflammatory drugs, and physical therapy. Referral to the primary care provider is important to allow for a thorough evaluation to differentiate between neurogenic, arterial, or venous thoracic outlet syndrome.^20,21

Pancoast's tumor may compress the brachial plexus against the chest wall and cause shoulder pain. The patient may experience local or radicular shoulder pain or a sense of fullness in the supraclavicular fossa.

Finally, myocardial ischemia and infarction, pneumonia, pulmonary embolism, or any disorder that irritates the diaphragm can also cause referred shoulder pain. Abdominal disorders that can cause shoulder pain include biliary tract disease, splenic injury or inflammation, perforated viscus, and ruptured ectopic pregnancy.

Acknowledgment: The authors gratefully acknowledge the contributions of Dr. Benjamin Harrison, coauthor of this chapter in the previous editions.