Most often, tendon injury is caused by chronic overuse resulting in degenerative changes.^2,³ The classic inflammatory signs of pain, warmth, erythema, and swelling may sometimes be experienced acutely, although tendinitis is no longer thought to be an inflammatory disorder.⁴ Bursae may become inflamed for many reasons: chronic friction, trauma, crystal deposition, infection, and systemic diseases (rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, tuberculosis, and gout). Because tendons frequently cross over bursae, it is not uncommon for bursitis to be secondary to overlying tendonitis (e.g., supraspinatus tendinitis, subacromial bursitis).

Tendonitis

The signs and symptoms of tendinitis can be quite variable. Pain is the most common complaint of patients with joint problems seen in the ED. Particular attention should be paid to the location of the pain; it can be articular (within the joint capsule), as in septic arthritis, or periarticular (outside the joint capsule), as in tendinitis or bursitis (Table 86.1).

Table 86.1 Clinical Features of Articular versus Periarticular Joint Pain

CLINICAL FEATURE	ARTICULAR	PERIARTICULAR
Associated conditions	Septic or other arthropathies	Tendinitis and bursitis
Range of motion	Decreased	Preserved
Pain	With passive and active motion	Only with certain active movements
Fever	Yes	No*
Trauma	Fractures	Repetitive use or stress
Risk factors	Rheumatoid and psoriatic arthritis, osteoarthritis, crystal arthropathy	Corticosteroid or fluoroquinolone use, connective tissue disease
Association with rest	Morning stiffness improves throughout the day	Night pain prevents sleep

^* Exceptions are septic bursitis and suppurative tenosynovitis.

Bursitis

Inflammation of a bursa may be infectious or traumatic, degenerative, or due to underlying systemic disease.⁵ Risk factors for the development of bursitis are acute trauma, repetitive injury to the painful area, infections, tuberculosis, gout, pseudogout, uremia, and rheumatoid arthritis. The diagnosis is made clinically based on tenderness at a bursal site, swelling of a superficial bursa, and localized pain with motion and at rest. Regional loss of active motion may occur as a result of swelling; however, range of motion should not be affected in patients with aseptic bursitis (see the Red Flags box on tendinopathy and bursitis).

Red Flags

Tendinopathy and Bursitis

Any joint effusion with systemic symptoms is septic arthritis until proved otherwise.

Any injury in a patient with a history of trauma is considered a fracture until proved otherwise.

Pain with passive motion indicates joint involvement; further investigation for an inflammatory or infectious cause is needed.

A history of steroid injection into a large tendon greatly increases the risk for rupture.

Steroid injections or systemic steroids increase the risk for infection.

Fluoroquinolone use increases the risk for tendonitis and tendon rupture.

Presenting Signs and Symptoms

Shoulder

Supraspinatus Tendinitis/Impingement Syndrome

Because of its complex structure and extensive range of motion, the shoulder is a joint predisposed to overuse injuries. The muscles of the rotator cuff (supraspinatus, infraspinatus, teres minor, subscapularis) and the glenohumeral ligaments serve to stabilize the joint. Impingement of these tendons occurs because of their position between the humeral head and acromion, which predisposes to chronic tendinosis ^6,⁷ (Table 86.2). Impingement syndrome is the number one cause of shoulder pain. It occurs in three progressive stages that worsen over time. Testing and staging of impingement syndrome are reviewed in Table 86.3.

Table 86.2 Shoulder Tendinopathies

Table 86.3 Impingement Syndrome of the Supraspinatus Tendon

In addition to the classic tests for impingement, the examiner should isolate and test individual muscles of the rotator cuff. The empty beer can position tests the supraspinatus by applying downward resistance to an arm in 90 degrees of abduction and 30 degrees of flexion with the thumb pointed downward. Applying resistance to external rotation when the elbow is against the patient’s body and bent at 90 degrees tests the infraspinatus and teres minor. The subscapularis is tested with the arm in the same position and applying resistance to internal rotation.

Subacromial Bursitis

The subacromial bursa lies under the acromion and coracoacromial ligament, to which it is attached. This bursa separates the ligament from the supraspinatus muscle and rotator cuff. Subacromial bursitis is thus thought to be an extension of supraspinatus tendinitis and typically follows this disorder’s stages of impingement. Pain and tenderness are localized to the lateral aspect of the shoulder, and signs of impingement are noted on physical examination (see Table 86.3).

Elbow

Lateral and Medial Epicondylitis

The lateral and medial epicondyles are commonly injured as a result of repetitive use (Table 86.4). Pain often begins as a dull ache that increases with the inciting activity. Approximately 50% of tennis players will experience lateral epicondylitis, although less than 5% of those with the syndrome play tennis. Radiographs may be helpful in atypical or prolonged cases to exclude rare pathologic conditions such as tumors.⁸

Table 86.4 Elbow Tendinopathies

Olecranon Bursitis

Because of its superficial location at the posterior tip of the elbow, the olecranon bursa is vulnerable to injury. When traumatized, the resulting bursal hematoma causes pain and swelling mimicking acute bursitis. Infection is frequent and most often occurs locally as a result of puncture wounds or lacerations. If fever is present, septic bursitis must be considered and septic arthritis excluded.

Wrist and Hand

The wrist and hand are composed of several tendons that pass through thick, fibrous retinacular tunnels. Overuse syndromes are thought to result from degenerative changes in the synovial lining between these tendons and the retinaculum (Table 86.5).

Table 86.5 Wrist and Hand Tendinopathies

The differential diagnosis of wrist and hand tendinopathy also includes osteoarthritis of the carpometacarpal joint, rheumatoid or psoriatic arthritis of the flexor or extensor tendons, gonococcal tenosynovitis, and suppurative tenosynovitis. It is therefore important to review the clinical history for trauma, systemic symptoms, fever, penile or vaginal discharge, or rash (see the Red Flags box on suppurative tenosynovitis).

Red Flags

Suppurative Tenosynovitis

Infection of the closed synovial sheaths of the flexors (rarely extensors), often of the fingers and hand

Usually caused by trauma, with the type of bacteria depending on the traumatic exposure (bite wound, puncture, skin flora)

Kanavel signs: tenderness over the flexor sheath, symmetric swelling of the digit, slightly flexed finger at rest, pain with passive extension of the finger

Additional signs: local erythema, edema, lymphangitic streaking, fever, leukocytosis

Treatment with broad-spectrum antibiotics, admission to the hospital, emergency surgical evaluation for incision and drainage

Prophylaxis of all bite wounds recommended to prevent flexor tenosynovitis

Hip

Trochanteric Bursitis

Patients with trochanteric bursitis are generally middle-aged or older women who complain of acute or chronic pain over the bursal area and lateral aspect of the thigh. The pain is increased when lying on the hip or walking down or climbing stairs and is classically worse at night. The pain associated with superficial bursitis can be reproduced by adduction and that of deep trochanteric bursitis by abduction. Approximately 50% of patients have pain with sequential flexion, abduction, external rotation, and extension of the hip while the contralateral knee is held in flexion (Patrick-Fabere test). Internal rotation does not usually provoke symptoms. The hip joint itself appears normal on examination, and no pain is elicited with flexion or extension.

Ischial Bursitis

Ischial bursitis develops secondary to trauma or sitting on a hard surface (weaver’s bottom). Sometimes the pain radiates down the back of the thigh and mimics sciatic nerve inflammation. The pain can be reproduced by applying pressure over the ischial tuberosity by sitting, standing on tiptoes, or bending forward.

Knee

Ankle

Achilles Tendinitis

The Achilles tendon can be injured as a result of direct trauma, overuse, and medications such as steroids or fluoroquinolones ¹¹ (Table 86.6; also see the Red Flags box on fluoroquinolones and tendinopathy). It can also become inflamed as part of a systemic disease (ankylosing spondylitis, Reiter syndrome, gout, pseudogout). However, most causes of Achilles tendinitis are thought to be multifactorial. Additionally, the vascular supply creates a watershed area approximately 2 to 6 cm above the calcaneal insertion and is thought to be responsible for the clinical symptoms and pathologic disruption at this site. Tendon rupture must be ruled out. Diagnosis and treatment of Achilles tendon rupture are discussed further in Chapter 85.

Table 86.6 Ankle Tendinopathies

Red Flags

Fluoroquinolones and Tendinopathy

The Food and Drug Administration has issued a black box warning for all fluoroquinolone antibiotics because of the increased risk for tendinopathy and tendon rupture.

Risks are increased in patients older than 60 years, those taking corticosteroids, and transplant recipients.

Patients prescribed fluoroquinolones should be advised to stop the medication at the first sign of pain, swelling, or inflammation in a tendon area and to avoid exercise and use of the area.

Signs of tendon rupture include an audible snap or pop, immediate bruising, and loss of motor function or inability to bear weight in the area.

Initial conservative treatment includes pain control, splinting in plantar flexion, and referral to orthopedics for stretching, eccentric load strength training, and correction of limb misalignment with orthotics. Surgical referral is urgent if there is any concern for tendon rupture.¹²

Calcaneal Bursitis

Two bursae are found at the insertion of the Achilles tendon. The superficial bursa lies between the skin and the tendon. It may become inflamed secondary to Achilles tendinitis or from repetitive friction or overuse. The deep bursa lies between the tendon and calcaneus and is rarely affected. Pain with range of motion and tenderness anterior to the Achilles tendon will be noted.

Differential Diagnosis

The differential diagnosis of tendonitis and aseptic bursitis is related to the clinical features accompanying the patient’s joint pain (see Table 86.1). Febrile patients need evaluation for septic bursitis and septic joints. Additional differential diagnostic considerations include inflammatory arthritis and gout. If multiple joints are involved and the swelling is symmetric, viral infection, drug-induced reaction, and osteoarthritis should be considered. If the joint swelling is asymmetric, rheumatoid arthritis, lupus, and serum sickness should be considered. If a characteristic rash is present, rheumatologic diseases, Reiter syndrome, Lyme disease, and dermatomyositis should be considered. If the pain is migratory, one should consider gonococcal disease and rubella. If the pain occurred after trauma and a joint effusion is present, hemarthrosis is a possibility. If an audible “pop” is heard, tendon rupture should be considered. If no joint effusion is present, one should look for radiographic evidence of fracture.

Diagnostic Testing

Patients with bursitis who have local signs of inflammation or any systemic symptoms should be evaluated for septic bursitis (see the Red Flags box on septic bursitis). Some distinguishing characteristics of septic bursitis are rapid onset, marked warmth, erythema, and extremely tense and painful bursae. The most commonly infected bursae are those most superficial: the olecranon and the prepatellar and superficial infrapatellar bursae. Bursae are most often directly inoculated with Staphylococcus aureus as a result of subcutaneous trauma. Hematogenous spread of infection is rare. If a deep bursa becomes infected, it is probably due to contiguous cellulitis or septic arthritis.⁵

Red Flags

Septic Bursitis

Erythema, edema, pain, or adjacent cellulitis over a bursa is a possible indication of septic bursitis.

Patients with septic bursitis may have fever, leukocytosis, an elevated erythrocyte sedimentation rate, or neutrophilic bandemia, although systemic findings are not universal and are more common with deep bursa infection.

Joint mobility may be preserved if no direct joint involvement is present.

Any swollen bursa with signs of infection should be aspirated and sent for culture and Gram stain.

Eighty percent of cases of bacterial septic bursitis are due to Staphylococcus aureus; the rest are due mostly to β-hemolytic streptococci.

Antibiotic coverage should cover staphylococcal and streptococcal species, preferably guided by Gram stain results.

Empiric choices for outpatients include dicloxacillin and clindamycin (with or without trimethoprim-sulfamethoxazole for patients at risk for methicillin-resistant S. aureus.

Empiric intravenous antibiotic choices include cefazolin or vancomycin.

The duration of therapy is between 1 and 4 weeks, depending on culture results and response to treatment.

Any patient with severe inflammation, systemic signs, diabetes, or immunosuppression should be admitted for intravenous antibiotics and consultation with orthopedics for incision and drainage.

Gram stain, culture, crystal analysis, and a bursal white blood cell (WBC) count should be obtained. Because systemic leukocytosis is neither sensitive nor specific, a routine complete blood count can be omitted. A bursal fluid WBC count higher than 5000/mm³ suggests bursal fluid infection; however, this may not be clear-cut because of overlap in the WBC count of bursa fluid in septic versus aseptic cases (synovial fluid analysis is discussed in more detail in Chapter 107). Therefore, if infection is suspected, regardless of the Gram stain results, treatment with antistaphylococcal antibiotics should be instituted pending culture results.

Imaging Studies

A diagnosis of tendinitis or bursitis is generally made on clinical grounds, but radiologic studies are sometimes required to confirm the diagnosis by ruling out other causes of pain. Plain radiographs help distinguish extraarticular from articular sources of pain.¹³ In acute injury, radiographs are essential to exclude an avulsion fracture. Ultrasonography is useful in the evaluation of joint effusions and lesions involving tendons, ligaments, and skeletal muscles. It can be very helpful in guiding difficult joint aspirations in the ED and is particularly useful in imaging of the shoulder region.¹⁴ Ultrasound has been shown to be more sensitive than magnetic resonance imaging and is now considered the “gold standard” for evaluating tendon involvement with concomitant trauma or rheumatic diseases.

Treatment

Most patients seen in the ED with tendinopathy can be managed conservatively by resting the affected region, administering adequate pain medication, and referral to orthopedics or physical therapy for biomechanical rehabilitation and gradual eccentric load exercises (Box 86.1). Aseptic bursitis can be managed conservatively with joint protection, modification of activity, and pain control. Exceptions are olecranon bursitis and prepatellar bursitis, which have a moderate risk of being infected, most likely with S. aureus. These bursae require needle aspiration and treatment with antibiotics until culture results are negative. Documentation should support the clinical suspicion of infection (see the Documentation box).

Box 86.1 Treatment of Tendinopathy and Aseptic Bursitis

Rest

Ice for 24 to 48 hours after trauma

Immobilization of the involved tendon

Aspiration of the swollen bursa

Circumferential compression band for the swollen bursa

Oral analgesics tailored to the patient

Documentation