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Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e

Chapter 280: Shoulder Pain David Della-Giustina; David Hile

ANATOMY

The shoulder is designed for mobility in all directional planes, but stability is less than other joints. To meetthe many demands placed on it, the shoulder uses three bones, four joints, and a specialized set of so�tissues consisting of muscles, tendons, ligaments, and bursae. The most common causes of nontraumaticshoulder pain in descending order of frequency are rotator cu� 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 bodyplus three bony extensions: the glenoid, the coracoid, and the acromion.

The four joints of the shoulder are the glenohumeral, acromioclavicular, sternoclavicular, andscapulothoracic. 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 threecomponents. The first is the glenoid labrum, which is a fibrous ring of tissue encircling the glenoid cavity. Theglenoid labrum increases the surface contact area of the humeral head within the relatively shallow glenoidfossa. The second component consists of three glenohumeral ligaments, which aid stability by reinforcingthe joint capsule. Finally, four specialized muscles, known as the rotator cu�, encompass the glenohumeraljoint and provide stability during motion.

The sternoclavicular and acromioclavicular joints together contribute to glenohumeral motion, but theirprimary function is to suspend and stabilize the shoulder girdle. Rotation at the acromioclavicular joint andelevation at the sternoclavicular joint allow complete arm elevation. The scapulothoracic joint represents thearticulation of the scapula on the posterior wall of the thorax. Scapular motion is essential for overallshoulder 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 independentelevator of the arm. Along with the pectoralis, the deltoid is the primary source of movement of the upperextremity.

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The rotator cu� 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 theproximal humerus. The rotator cu� muscles also contribute to the power of the upper extremity, providing30% 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 beneaththe acromion, inserting onto the great tuberosity of the humeral head. It initiates arm elevation and abductsthe shoulder. It also balances the power of the deltoid, keeping the humerus centered in the glenoid duringdeltoid contraction. The infraspinatus originates on the posterior scapula just inferior to the scapular spine. Itinserts 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 infraspinatusand inserts on the posterior aspect of the humerus. It works with the infraspinatus to provide externalrotation (Figure 280-1). The subscapularis is the only rotator cu� muscle that arises from the anterior aspectof the scapula. It attaches to the lesser tuberosity of the humeral head and provides internal rotation of thearm (Figure 280-2).

FIGURE 280-1.

Posterior view of the shoulder illustrating rotator cu� muscles.

FIGURE 280-2.

Anterior view of the shoulder illustrating the supraspinatus muscle and the long head of the biceps.

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The long head of the biceps tendon, although not part of the rotator cu�, assists in rotator cu� function. Thelong head of the biceps tendon courses superiorly in the bicipital groove of the humerus between the greaterand lesser tuberosities, passes between the subscapularis and supraspinatus tendons, and penetrates theglenohumeral joint to insert on the labrum (Figure 280-2). During arm elevation, the tendon of the long headof 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 eightbursae in the shoulder complex, only the extra-articular subacromial bursa is clinically significant. Its roofadheres to the undersurface of the deltoid, and its floor to the underlying rotator cu�. The bursa is lubricatedby 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 thecoracoacromial ligament that forms the anterior roof of the arch (Figure 280-3). The humeral head providesthe floor of the arch. This arch defines the space within which the tendons of the rotator cu�, the tendon ofthe long head of the biceps, and the subacromial bursa must function.

FIGURE 280-3.

Lateral view of the shoulder illustrating the coracoacromial arch with the rotator cu� and subacromial bursa.

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IMPINGEMENT SYNDROME (SUBACROMIAL BURSITIS, ROTATOR CUFFTENDINITIS, SUPRASPINATUS TENDINITIS, PAINFUL ARC SYNDROME)

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 cu�, and biceps tendon that result in aloss of the normal gliding mechanism between the rotator cu� and related so� tissues within thecoracoacromial arch. Impingement syndrome is the encompassing term used for the conditions of

subacromial bursitis, rotator cu� tendinitis, supraspinatus tendinitis, and painful arc syndrome.2,3,4,5

FIGURE 280-4.

Impingement of the subacromial bursa and rotator cu�.

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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 cu� occur. Although possible at anyage, 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 byactivity 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 rotatorcu� creates fibrosis and thickening of the tendons of the rotator cu� and bursa. This stage is typically seen inpatients between the ages of 25 and 40, and the prolonged duration (weeks to months) or recurrence ofsymptoms is useful in making this diagnosis. During this stage, patients complain of a recurrent or chronicaching pain with daily activities, pain with vigorous activity, and night pain (caused by irritation triggered bya relaxed supporting muscle tone).

Continued overuse can lead to stage 3 with rotator cu� tears, rupture of the long head of the biceps, andsubacromial spurs. Patients at this stage have progressive symptoms and disability, and they o�en requiresurgical decompression of the subacromial space.

CLINICAL FEATURES

The primary symptom with impingement syndrome is pain, developing insidiously over a period of weeks tomonths. 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 andinterferes with sleep. This pain occurs especially when the patient lies on that shoulder or sleeps with thearms overhead. The pain may be exacerbated by activities that require overhead arm use, such as brushingthe hair or reaching into a cupboard. Patients also note weakness and sti�ness of the shoulder that is usually

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secondary to pain.2,6 Once the shoulder pain has resolved, any weakness should trigger a search for a rotatorcu� 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 cu� insertion at the lateral aspect of the proximal humerus usuallyproduces 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 Painwith an active arc of abduction, especially between 60 and 100 degrees, is consistent with rotator cu�

pathology.2 A sensation of catching also may be present if scar tissue is trapped beneath the acromion.Rotator cu� strength testing usually reveals mild to moderate weakness secondary to pain. The pain isusually present when resistance is applied.

The individual muscles of the rotator cu� should be isolated and tested individually, looking for pain orweakness; to isolate the supraspinatus, abduct the arm to 90 degrees and forward flex it 30 degrees with thethumb 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

FIGURE 280-5.

The "empty can" position, which isolates the supraspinatus tendon. Pain or weakness against resistance inthis position suggests injury to the supraspinatus muscle.

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To isolate the infraspinatus and the teres minor, externally rotate the shoulder with the patient's arm againstthe body and the elbow bent to 90 degrees and the forearm in neutral position. Stabilize the elbow againstthe 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 theexaminer's hand away by moving the dorsum of the hand away from the back (li�-o� test).

Specific maneuvers on physical examination test for signs of impingement by compressing the rotator cu�and bursa between the humeral head and coracoacromial arch. In the classic impingement maneuver ofNeer, the examiner prevents scapular rotation with one hand while raising the patient's straightened armsmoothly in full forward flexion to overhead. A positive sign is pain in the arc between 70 and 120 degrees. Asecond test, the Hawkins impingement test (Figure 280-6), requires the examiner to position the patient'sarm (shoulder) in 90 degrees of abduction and 90 degrees of elbow flexion. Rotation of the arm inwardlyacross the front of the patient with internal rotation of the shoulder compresses the cu� and bursa betweenthe 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

FIGURE 280-6.

Hawkins impingement test. The examiner positions the patient's shoulder at 90 degrees of abduction and 90degrees of elbow flexion. The examiner then rotates the shoulder internally and brings the patient's armacross the front of the patient.

DIAGNOSIS

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The diagnosis is based on a history of chronic shoulder pain with a full range of motion, with possibleweakness of the rotator cu� muscles and positive responses to provocative maneuvers. Radiography is usedto identify other causes like fracture or degenerative joint changes. Early nonspecific radiographic signs ofrotator cu� 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 preventprogression of the process. Therapy starts with a conservative treatment program that should include thefollowing:

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

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

3. Cryotherapy. Apply ice to the a�ected shoulder for 10 to 15 minutes three to four times daily for analgesice�ects 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 frontof the body. The arms should be swung in gentle arcs of motion in both a clockwise and counterclockwisedirection to the level of pain tolerance for 5 to 10 minutes three to four times daily. The size of the arcsshould increase daily as symptoms allow. Also, the patient should stand sideways an arm's length from awall and walk the fingers up the wall to the level of pain tolerance, repeating the exercise three to fourtimes daily.

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

6. Corticosteroid injections. Although local corticosteroid injections into the subacromial space relieve pain,adverse e�ects include muscular atrophy, weakness, and further tissue degeneration. Injection directlyinto the tendon can lead to necrosis and rupture. Injection is not an emergency procedure and is best le�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.

ROTATOR CUFF TEARS

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PATHOPHYSIOLOGY

Patients with rotator cu� tears present with shoulder pain a�er acute traumatic injury, chronic injury, or anacute extension of a chronic impingement (stage 3) of the rotator cu�. Rotator cu� tears due to chronicimpingement in patients >40 years of age account for most tears. In younger patients, rotator cu� tears areseen in laborers and athletes who participate in sports that require overhead activities like tennis, swimming,

and baseball.9 In general, healthy rotator cu� tendons are resistant to acute injury, with acute rotator cu�tears accounting for only 10% of all rotator cu� 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, li�ing aheavy object, or catching a heavy object as it falls. Glenohumeral dislocation is a common cause of acuterotator cu� tears. In patients >40 years of age with a first-time dislocation, there is a 57% incidence of acute

rotator cu� tear; think of a rotator cu� tear in patients with weakness >3 weeks a�er an acute dislocation.9

In addition to being categorized by the acuteness of the injury, rotator cu� tears can be full or partialthickness, with either di�icult to detect on the clinical evaluation. Partial-thickness tears are twice ascommon as full-thickness tears, and most commonly occur on the inferior aspect of the tendon. The typeand extent of the tear have significant implications for the ultimate treatment and prognosis. Thesupraspinatus, due to its location within the coracoacromial arch, is the most commonly a�ected tendon ofthe rotator cu�.

CLINICAL FEATURES

The clinical features of a chronic rotator cu� tear di�er from those of an acute tear. Only about half ofpatients with chronic rotator cu� tears can recall specific trauma or an event associated with the onset ofpain, o�en seemingly insignificant in description. Patients more commonly report a history of gradual andprogressive pain; while initially described as worse at night, the pain eventually becomes persistent. Thepain may be di�use, but is commonly localized to the lateral aspect of the upper arm. O�en, initial therapywith rest, anti-inflammatory agents, and glucocorticoid injections helps. If the rotator cu� weakens, thefrequency, 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 li�ing 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 cu� tearproduces immediate profound pain and disability, with asymmetry o�en present due to local swelling. Activemotion is limited, with inability to abduct or externally rotate the arm against even minimal resistance. Onexamination, disuse atrophy is o�en present in patients with chronic rotator cu� tears. Palpation mayproduce discomfort at the lateral aspect of the upper arm or in the subacromial region. Most patients withrotator cu� 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

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degrees of shoulder abduction without dropping it. Crepitus and pain are usually present on range-of-motiontesting.

DIAGNOSIS

It may be very di�icult to distinguish a full-thickness tear from a partial-thickness tear or a rotator cu� injuryfrom impingement syndrome. The diagnosis is primarily clinical based on a finding of rotator cu� weaknesson examination in a patient with a history of chronic shoulder pain or acute shoulder pain a�er significanttrauma. In patients with an acute injury, it may be di�icult to diagnose the tear due to excessive pain fromthe injury. In these cases, assume a preliminary diagnosis of acute rotator cu� 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 cu� tears is a narrowing of the acromiohumeral space (<7 mm).8 Noradiographic findings are diagnostic of an acute rotator cu� tear, and the diagnosis should rely on clinicalfindings. MRI, US, and arthrography are the most sensitive modalities for detecting rotator cu� tears,although all tend to underestimate the extent of the tear.

TREATMENT

The basic goals of emergency care for suspected rotator cu� injuries are the same as with impingement (seeabove), with analgesia, support, and prevention of further dysfunction and disability. An arm sling canprovide support and comfort until the acute symptoms subside. However, avoid prolonged immobilizationand prescribe range-of-motion exercises three to four times daily to minimize the development of adhesivecapsulitis.

Any evidence or suspicion of neurovascular compromise requires immediate orthopedic consultation. Referall patients with an acute rotator cu� tear (with or without a history of chronic symptoms) and those withsignificant disability to an orthopedist for follow-up within a week. Complete rotator cu� tears usuallyrequire 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 mayrespond to conservative measures.

CALCIFIC TENDINITIS

PATHOPHYSIOLOGY

Calcific tendinitis is a self-limiting disorder characterized by calcium crystal deposition within one or moretendons of the rotator cu�. In time, the calcium undergoes painful spontaneous resorption with subsequenthealing of the tendon. Middle-age patients are most commonly a�ected, and this process is rarely seen inpatients >70 years of age. Females are slightly more likely to be a�ected than males, and calcification is o�enpresent bilaterally. Primary tendon degeneration as a result of chronic repetitive microtrauma, age, and

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tissue hypoxia are causes of this disorder. The supraspinatus is by far the most commonly a�ected tendon,with calcium deposition usually occurring near its origin on the humerus. Any of the rotator cu� tendons orthe long head of the biceps may be a�ected.

CLINICAL FEATURES

Because calcification occurs over a period of time, patients are generally asymptomatic or have mild pain atrest or at night. Pain with abduction or a "catching" sensation may be present on movement. During theresorptive 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 to2 weeks in most cases. A�er the initially painful resorptive phase, patients can have variable levels of painand shoulder dysfunction that may last for several months (postcalcific period). Adhesive capsulitis is themost common complication of calcific tendinitis and creates more chronic symptoms.

Symptomatic patients experience sudden onset of shoulder pain, usually at rest, and shoulder motionreproduces significant pain. The pain is o�en worse at night and interferes with sleep. During an acute attackwith intense pain, the patient holds the arm across the body and o�en is reluctant to move it. A point ofmaximum tenderness may be palpated over the proximal humerus near the tendinous insertion of therotator cu�. Both active and passive range of motion of the glenohumeral joint are usually limited to varyingdegrees. Flexion, extension, abduction, and internal and external rotation of this joint should bedocumented. Muscle atrophy and crepitus may also be present.

DIAGNOSIS

Obtain shoulder radiographs for patients with suspected calcific tendinitis to localize deposits and seek anysigns of possible impingement. During the initial formative phase, calcium deposits are usually dense andwell-defined if visualized. In patients who are experiencing intense pain in the resorptive phase, calciumdeposits may appear hazy with poorly defined borders. The presence of visible calcifications is notnecessarily 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 calmthe intense pain. The shoulder may be rested using a sling for brief periods of immobilization, but avoidprolonged immobilization. Instruct patients to rest the shoulder in abduction on the back of a chair as o�enas is tolerable. Sleeping with a pillow beneath the axilla can also help prevent restriction of motion. Localapplication 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 morechronic cases who have significantly limited range of motion of the shoulder.

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Subacromial corticosteroid injection, oral steroids, platelet-rich plasma therapy, transcutaneous electricalnerve 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 controlledtrial 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 ofthis disease, arrange follow-up with a primary care doctor within a week. For the 10% of patients in whomnonoperative methods are unsuccessful, arthroscopic or open surgery may be indicated. Refer patients whohave progression of symptoms, constant pain interfering with daily activities, or absence of improvement

a�er conservative therapy.14

ADHESIVE CAPSULITIS

PATHOPHYSIOLOGY

Adhesive capsulitis, commonly referred to as frozen shoulder syndrome, begins as painful inflammation ofthe 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, includingdiabetes, thyroid disease, postmenopausal, pulmonary neoplasm, and autoimmune disorders. Secondaryadhesive capsulitis produces similar findings, but results from a known cause, such as prolongedimmobilization a�er trauma, surgery, stroke, or a primary inflammatory condition of the shoulder such asimpingement syndrome or bicipital tendinitis. The condition resolves with conservative therapy in mostpatients within 1 to 2 years, although some are le� with residual pain or sti�ness.

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 shouldermovement due to pain. Stage 2 (freezing stage), about months 3 to 9, has decreased shoulder motion fromcapsular thickening and scarring, and chronic pain. Stage 3 (frozen stage), months 9 to 15, is characterized byless pain, but a more fibrotic and thick capsule and more limitation in range of motion. Stage 4 (thawingstage), usually a�er 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 di�use andaching, poorly localized, accompanied by sti�ness, and o�en extends down the upper arm. The pain isfrequently worse at night and at rest, especially in earlier stages. Disuse atrophy may be present.Impingement testing is di�icult due to the restriction of motion. Occasionally, posterior glenohumeral

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dislocation creates restricted motion of the shoulder; exam and imaging can help detect this condition. USmay demonstrate increased vascular flow, thickening of rotator cu� structures, and bulging of thesupraspinatus 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; ifa sling is used in patients in early stage 1 who have severe pain, limit it to days to prevent increased loss ofmotion due to further capsular restriction. Although physical therapy is di�icult in the early, more painfulstages 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 toimprove pain and function in the short term; the long-term e�ects are less clear.

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

DISORDERS OF THE BICEPS TENDON

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 longhead 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 superiorlabrum. Forces applied tend to pull the labrum o� the glenoid rim. Due to this anatomic association, tears ofthe superior labrum, known as SLAP (superior labrum anterior to posterior) lesions, are frequently found inconjunction with long head of the biceps tendon pathology. Injuries of one or the other structure may bedi�icult to distinguish, both clinically and operatively.

The biceps tendon may also become inflamed, may become partially displaced out of the bicipital groove, ormay rupture altogether. (See chapter 271, "Shoulder and Humerus Injuries" for the approach to traumaticruptures 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 di�icult to distinguish clinically.Bicipital tendinopathy triggers intense and localized pain at the anterior aspect of the shoulder. Repetitive

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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 tendonfrom the bicipital groove is painful and occurs medially or laterally, while complete dislocation is seen onlymedially and is associated with a subscapularis tear. Posterolateral instability is associated with asupraspinatus 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-relateddegenerative changes in this area of the tendon. In younger patients, mild trauma may cause completerupture of the biceps tendon, which is heralded by an audible snap or pop followed by severe pain anddeformity.

DIAGNOSIS

Palpation of the tendon within the bicipital groove reproduces the intense pain. Forearm supination, one ofthe 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 poppingsensation 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 o�en inconclusive and inaccurate.16 Many provocative tests to confirm the presence of pathology ofthe long head of the biceps or superior labrum have been described in the literature. Speed's test identifiestear 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 thebicipital 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 examinationalone cannot be used as the sole basis by which to diagnose a SLAP lesion. The test most likely to helpdiagnose a SLAP lesion is the active compression test. To perform, have the standing patient flex his or hershoulder to 90 degrees, and then adduct 10 to 15 degrees medially and rotate fully, with elbow extended. Theexaminer stands behind the patient and applies a uniform downward force to the arm. This is repeated in fulllateral 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 distalcontraction of the muscle belly. Supination is weak on muscle testing, but elbow flexion remains strongbecause 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 indiagnosing biceps tendon and SLAP lesions; magnetic resonance arthrography is preferable. In the hands ofskilled operators, US is poorly sensitive but very specific in diagnosing disorders of the long head of the

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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 byanalgesics, 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 careprovider.

Although not commonly administered by emergency physicians, intra-articular injections of local anestheticand steroid can improve symptoms. Intra-articular injections can relieve bicipital symptoms but may beine�ective if adhesions or synovitis prevent dispersal into the bicipital groove. Direct injection into thebicipital 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, orhigh-grade SLAP lesion or those failing to respond to a conservative treatment regimen. Surgical options

include debridement, tenotomy, or tenodesis.18 Bicipital tendon rupture o�en requires surgical repair, soorthopedic consultation in 24 to 48 hours is best. Patients with suspected SLAP lesions or other mechanicalproximal biceps injuries generally require arthroscopic or other surgical intervention when symptomatic.

OSTEOARTHRITIS

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 andprogressive onset of pain, worse with motion and better with rest. This usually occurs concurrently withdegenerative disease of the acromioclavicular joint.

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

OTHER CAUSES OF SHOULDER PAIN

Although disorders of the rotator cu� and other intrinsic structures of the shoulder are the most commoncause of shoulder pain, extrinsic conditions outside the shoulder complex can refer pain to the shoulder. Thedi�erential diagnosis includes disorders of the cervical spine, brachial plexus injuries, axillary arterythrombosis, suprascapular nerve injury, thoracic outlet syndrome, Pancoast's tumor, and miscellaneousthoraco-abdominal disorders.

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The neck is the most common source of pain referred to the shoulder. Degenerative disease of the cervicalspine, degenerative disk disease, and herniated nucleus pulposus can all refer pain to the shoulder. A patientwith a C5-C6 herniated disk may present with pain very similar to that due to rotator cu� disease. Careful andthorough examination of the cervical spine and a complete neurovascular examination should be included inthe 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 themuscles of the shoulder within weeks of injury. Radiographic evaluation of the cervical spine should beincluded in the ED evaluation of patients with suspected brachial plexus injury or involvement. Brachialplexus 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 issuspected.

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

Compression of the suprascapular nerve can cause shoulder pain. This nerve originates from the brachialplexus distal C5-C6 nerve roots and courses posteriorly to the suprascapular notch. It can become entrappedbeneath the transverse ligament at the level of the suprascapular notch. Traction injuries from explosivemovements can also injure the nerve. On examination, active external rotation typically reveals infraspinatusatrophy and associated weakness. The initial treatment is conservative. Electromyography and nerveconduction velocity studies will reveal the extent and location of nerve injury. Surgery for decompression isconsidered if conservative measures fail.

Compression of the brachial plexus and blood vessels proximal to the shoulder, the thoracic outletsyndrome, can cause shoulder pain. Women in the childbearing years are a�ected three times morecommonly than men. The medial trunk of the brachial plexus is most commonly involved, and the symptomsusually include pain that radiates through the shoulder to the medial forearm and occasionally to the smalland ring fingers. Patients also complain of numbness and tingling of the fingers and a weak grip. Patients canusually identify motions that reproduce the symptoms. Plain radiographic evaluation is o�en nondiagnostic,although some will have evidence of a prior clavicular fracture with malunion or the presence of a cervical ribband that compress the brachial plexus. Conservative measures include activity modification, education,postural exercises, nonsteroidal anti-inflammatory drugs, and physical therapy. Referral to the primary careprovider is important to allow for a thorough evaluation to di�erentiate 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. Thepatient may experience local or radicular shoulder pain or a sense of fullness in the supraclavicular fossa.

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

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

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USEFUL WEB RESOURCES

Nicholas Institute of Sports Medicine and Athletic Trauma—http://www.nismat.org/clinicians/physical-exam/evaluation-of-the-shoulder

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