Upper extremity bursitis

Author: Keith L. Salzman, Janus D. Butcher
Date: Nov 1, 1997

Bursal inflammation is a frequent cause of upper extremity pain. Bursae may be injured through several processes, including autoimmune diseases, crystal deposition, infection, hemorrhage or, most commonly, through overuse or repetitive microtrauma. These injuries are often quite disabling and can pose a significant diagnostic and therapeutic challenge for the clinician.

The three upper extremity bursae that are most commonly involved are the subacromial (subdeltoid) bursa, the olecranon bursa and the subscapular bursa. We previously presented an overview of the etiology, pathophysiology, clinical presentation and treatment of bursitis in a review of lower extremity bursitis (Am Fam Physician 1996;53:2317-24). This article focuses on specific considerations for upper extremity bursar injuries.

Subacromial (Subdeltoid) Bursitis

The subacromial bursa is a synovial-lined sac separating the superior surface of the supraspinatus tendon from the overlying coracoacromial arch and deep surface of the deltoid muscle (Figure 1). The primary function of this bursa is to facilitate the motion of the supraspinatus tendon beneath the superior structures. This bursa may extend beyond the lateral edge of the acromion beneath the deltoid muscle, where it is referred to as the subdeltoid bursa.


Inflammation of the subacromial bursa usually is a result of injury to adjacent structures. Most often it is the rotator cuff, specifically the supraspinatus tendon, that is damaged by acute macrotrauma or repetitive overuse (microtrauma). This latter condition is commonly referred to as the impingement syndrome. Primary inflammation of the subacromial bursa is much less common but may arise from autoimmune inflammatory conditions, crystal deposition and, rarely, infection.

In patients with subacromial pain that is due to the impingement syndrome, it is often difficult to differentiate between the symptoms of subacromial bursitis and the underlying rotator cuff injury. The relationship between rotator cuff injuries and bursitis was detailed in Neer's[1] classic descriptions of impingement lesions. The impingement syndrome was described as a series of stages beginning with acute supraspinatus tendinitis as the initial injury (stage 1), followed by bursar thickening, fibrosis and cuff fraying (stage 2) and, finally, tear of the rotator cuff tendon (stage 3). Classically, the impingement syndrome was described as bony compression of the supraspinatus tendon between the acromion above and the lateral humerus below.[1]

It is now known that this process may involve a combination of factors, including repetitive overload of the poorly vascularized tendon, soft tissue or bony impingement, and instability of the glenohumeral joint with secondary impingement. The bursa becomes involved in later stages of supraspinatus tendinitis and is frequently associated with a partial- or complete-thickness tear of the supraspinatus tendon. In one series,[2] subacromial bursar inflammation was found in seven of 12 patients undergoing surgery for chronic impingement syndrome. Another report[3] describes bursar involvement in 19 of 50 patients treated with acromioplasty for chronic shoulder pain. More recent studies comparing ultrasonographic evaluation of bursar effusion and findings on shoulder arthroscopy have supported this relationship in tears of the rotator cuff.[4]


The impingement syndrome is the most common cause of shoulder pain in the primary care setting. Often these symptoms are attributed simply to bursitis but, as described above, the etiology is more complex. Subacromial bursitis and rotator cuff tendinitis typically present with lateral or anterior shoulder pain. Patients only occasionally report a single macrotraumatic event leading to persistent pain. More commonly, the onset of pain is insidious and no specific injury is recalled. Overhead lifting or reaching activities are uncomfortable, and the pain is often worse at night, interrupting sleep.

Physical examination reveals a reduced active range of motion with decreased elevation, intermal rotation and abduction, primarily because of pain. The most painful arc of motion is between 70 and 120 degrees of abduction. Tenderness is found laterally below the acromion, anteriorly at the insertion of the supraspinatus tendon on the greater tuberosity and, occasionally, along the supraspinatus muscle belly beneath the trapezius. Strength testing may reveal weakness with internal and external rotation, a finding that demonstrates an important factor in the etiology of these injuries: functional instability due to rotator cuff weakness.

The impingement signs are usually positive (Figure 2). The Neer's sign is performed by forcibly forward flexing the internally rotated arm maximally above 90 degrees. The Hawkin's impingement sign refers to forced internal rotation of the arm performed during forward elevation to 90 degrees. Both tests are considered positive if they produce pain.


Isolated testing of the supraspinatus muscle will also elicit pain. To test the supraspinatus muscle, the patient abducts the arms to 90 degrees with the elbows extended and the arms internally rotated. The arms are placed 30 degrees anteriorly (in the coronal plane), and the patient resists as the examiner forces the arms downward. This is often referred to as the "empty beer can" sign.

The lidocaine impingement test can be performed to confirm the location of the injury. From 6 to 8 mL of 1 percent lidocaine (Xylocaine) are injected into the subacromial space, and the impingement signs are repeated. If a reduction in pain occurs, the impingement test is considered to be positive, and subacromial tendinitis or bursitis is suggested.

Radiographic studies are often helpful in the evaluation of subacromial pain. Injury of the rotator cuff tendon is suggested by several radiographic findings, including the presence of a curved or hooked acromion, calcified supraspinatus tendon, osteopenia of the greater tuberosity of the humerus, and an acromial-humeral distance of less than 5 mm. The presence of fibrocartilaginous bodies (rice bodies) in the bursa is suggestive of an autoimmune disorder such as rheumatoid arthritis.[5] Magnetic resonance imaging (MN) can aid in confirming the presence of rotator cuff injuries and in imaging the bursa. However, its usefulness is limited both by its high cost and the high rate of nonspecific findings not related to rotator cuff injury.[6] As a result, MRI should be reserved for use in cases suspicious for rotator cuff tear or septic bursitis.


Since the association between rotator cuff injury and subacromial bursitis is strong, treatment should be directed toward both entities (Table 1). The exceptions to this are autoimmune systemic conditions such as rheumatoid arthritis and the rare instance of septic bursitis, which will be discussed separately below. The treatment plan for subacromial pain (impingement) should address both pain management and facilitation of tissue healing through rehabilitative exercise or surgery.

TABLE 1 Differential Diagnosis and Treatment of Subacromia/Subdeltoid Bursitis

Etiology Physical examination Laboratory findingsAutoimmune Fluctuant subdeltoid Elevated ESR inflammatory mass Positive ANA, disorders Erythema, tenderness positive RFSeptic/ Fluctuant subdeltoid Aspirate Gram infectious mass stain/culture causes Erythema, tendernessCrystal Anterolateral Aspiration: deposition tenderness apatite crystals Positive impingement signsTrauma Anterior/lateral None (rotator cuff tenderness injury) Positive impingement signs Supraspinatus challengeEtiology Radiographic findings TreatmentAutoimmune Joint destruction NSAIDs inflammatory Corticosteroids disordersSeptic/ Bursal effusion Surgical drainage infectious (MRI, ultrasound) Culture-directed causes antibiotic therapyCrystal Intrabursal rice NSAIDs deposition bodies Corticosteroid injectionTrauma Hooked acromion PRICEMM (rotator cuff Tendon calcification Functional injury) Decreased rehabilitation acromiohumeral Surgery distance MRI: supraspinatus tendon tear

Findings of a more recent prospective comparison of aspiration versus aspiration-steroid injection[24] support the use of local steroid injection. Forty-five patients with olecranon bursitis were randomized into one of four treatment groups: aspiration with intrabursal methylprednisolone acetate (20 ma) and oral naproxen (Naprosyn); aspiration with intrabursal methylprednisolone and oral placebo; oral naproxen alone, and oral placebo alone. Aspiration and injections were performed with a 22-gauge needle using a lateral approach, and all patients were treated with local compression wraps. The methylprednisolone groups showed a statistically significant decrease in the amount of swelling and the number of repeat aspirations at both the one-week and six-month follow-up visits. Of greater interest is the lack of skin atrophy or development of septic bursitis in any of the methylprednisolone-treated groups. The authors theorized that the lack of complications may have been related to the use of a smaller bore needle and a lateral approach.

A patient information handout on shoulder pain, written by the authors of this article, is provided on page 1811.


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KEITH L. SALZMAN, MAJ, MC, USA is a faculty member in the family medicine residency program at Tripler Army Medical Center in Honolulu. He received his medical degree from the Mayo Medical School, Rochester, Minn., and completed a residency in family medicine at Dwight D. Eisenhower Army Medical Center, Ft. Gordon, Ga.

WADE A. LILLEGARD, M.D. is a faculty member Of the Duluth (Minn.) Center for Sports Medicine. He graduated from the Uniformed services university of Health sciences, Bestheda, Md., and completed a residency in family medicine at Martin Army community Hospital, Fort Benning, Ga. He also completed a primary care sports medicine fellowship at Michigan state university College of Human Medicine, East Lansing.

JANUS D. BUTCHER, MAJ, MC, USA is a faculty member in the family medicine residency program at Dwight D. Eisenhower Army Medical Center, Fort Gordon, Ga. He received his medical degree from the university of Minnesota-Duluth School of Medicine and completed a residency in family medicine at Madigan Army Medical Center, Tacoma, Wash. He also completed a fellowship in primary care sports medicine at the Uniformed services university of Health sciences.

Address correspondence to Janus D. Butcher, Maj, MC, USA, Department of Family Practice, Eisenhower Army Medical Center, Augusta, GA 30905-5650.

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