Bursitis

Bursae are flattened sacs that serve as protective cushions between bones and overlapping muscles (deep bursae) or between bones and tendons or skin (superficial bursae). These synovial-lined sacs are filled with minimal amounts of fluid to facilitate movement during muscle contraction. Deep bursae (eg, subacromial and iliopsoas bursae) are located in the fascia. Superficial bursae (eg, olecranon and prepatellar bursae) are located in the subcutaneous tissue.

There are two types of bursae: constant and adventitial. Both types can be involved in acute or chronic bursitis. Constant bursae have the following characteristics:

• They form during embryologic development
• They are lined with endothelial cells
• They are located between bones and tendons or skin
• They contain synovial cells that secrete a lubricating fluid rich in collagen and proteoglycans

Adventitial bursae (eg, those that develop over a bunion or osteochondroma) have the following characteristics:

• They form later in life in response to repeated trauma or constant friction and pressure
• They lack endothelial cells
• They do not contain synovial fluid

All of the approximately 160 bursae in the human body are potentially susceptible to injury. The three upper-extremity bursae that are most commonly affected by bursitis are the subacromial, subscapular, and olecranon bursae.[4]

The subacromial bursa separates the superior surface of the supraspinatus tendon from the overlying coracoacromial arch and the deltoid muscle. It lies between the acromion and the rotator cuff and cushions the coracoacromial ligament from the supraspinatus muscle. When the arm is resting at the side, the bursa protrudes laterally from beneath the acromion; when the arm is abducted, it rolls medially beneath the bone. See the image below.

Subscapular bursae are found between the anterior surface of the scapula and the posterior chest wall. The two commonly affected bursae are located superomedially between the serratus anterior and the chest wall. See the image below.

Several olecranon bursae can become inflamed: the superficial olecranon bursa, subtendinous olecranon bursa, or intratendinous olecranon bursa. The former is the most commonly involved as it is more superficial, lying between the attachment of the triceps to the olecranon and the skin.

Various lower-extremity bursae can also be affected by bursitis. The ones most commonly involved are in the hip, the knee, and the ankle.[5, 6, 7]

In the hip, the ischiogluteal bursa lies deep to the gluteus maximus over the ischial tuberosity. The iliopsoas bursa, the largest bursa in the body, lies between the iliopsoas tendon and the lesser trochanter, extending upward into the iliac fossa beneath the iliacus. The trochanteric bursa has superficial and deep components, with the superficial bursa lying between the tensor fascia latae and the skin and the deep bursa located between the greater trochanter and the tensor fasciae latae.

In the knee, the following bursae are commonly affected by bursitis[6] :

• The medial collateral ligament bursa
• The anserine (pes anserinus) bursa (see the image below)
• The prepatellar bursa (located anteriorly over the patella, between patella and skin)
• The infrapatellar bursa (containing a superficial component lying between the patellar ligament and the skin and a deep component lying between the patellar ligament and the proximal anterior tibia)
• The popliteal bursae, or Baker cysts (located in the posterior joint capsule of the knee)

In the ankle, two bursae are found at the level of insertion of the Achilles tendon. The superficial one is located between the skin and the tendon, and the deep one is located between the calcaneus and the tendon. The latter is more commonly affected by bursitis. There is also the subcutaneous bursa of the medial malleolus.

Inflammation of the bursa causes synovial cells to multiply and thereby increases collagen formation and fluid production. A more permeable capillary membrane allows entrance of high protein fluid. The bursal lining may be replaced by granulation tissue followed by fibrous tissue. The bursa becomes filled with fluid, which is often rich in fibrin, and the fluid can become hemorrhagic.[8] One study suggests that this process may be mediated by cytokines, metalloproteases, and cyclooxygenases.

In septic arthritis, local trauma can inoculate bacteria into the bursa, which triggers the inflammatory process. Hematogenous seeding is less common due to the relatively poor blood supply to the bursae.[9]

There are three phases of bursitis: acute, recurrent, and chronic.[10] During the acute phase of bursitis, local inflammation occurs and the synovial fluid is thickened, and movement becomes painful as a result. Chronic bursitis leads to persistent inflammation with continual pain and can lead to weakening of the overlying ligaments and tendons and, ultimately, rupture of the tendons. Because of the possible adverse effects of chronic bursitis on overlying structures, bursitis and tendinitis may occur together; the differential diagnosis should include both of these diagnoses.

Upper-extremity bursitis

Subacromial bursitis

The subacromial bursa facilitates movement of the supraspinatus tendon and becomes inflamed secondary to repetitive overuse injury of this tendon. Subacromial bursitis is often coexistent with supraspinatus tendinitis and partial- or complete-thickness tears of the supraspinatus tendon (1 of the 4 tendons comprising the rotator cuff).[11]

Subscapular bursitis

Subscapular bursae become inflamed as a result of abnormal bony structures or soft-tissue changes that affect the movement of the scapula over the posterior chest wall.

Olecranon bursitis

The more superficial of the 2 olecranon bursae commonly involved in bursitis is predisposed to direct trauma or cumulative microtrauma from activities requiring frequent elbow motion (eg, swimming, skiing, gymnastics, and weightlifting). This type of bursitis is often recurrent.[12]

Lower-extremity bursitis

Bursitis of hip

Ischiogluteal bursitis is associated with sedentary occupations and is caused by direct stress on the bursa (hence the nickname “weaver’s bottom”). Patients have pain with sitting and walking and have localized tenderness over the ischial tuberosity. Physical examination often reveals pain with passive hip flexion and resisted hip extension.

Iliopsoas bursitis arises when a defect develops in the anterior part of the hip joint capsule, allowing communication of the joint with the bursa. It is often associated with hip pathology (eg, rheumatoid arthritis or osteoarthritis) or recreational injury (eg, running). Infection of the iliopsoas bursa is rare.

Greater trochanter bursitis is common in overweight middle-aged women and is associated with acute trauma, overuse, and mechanical factors. The clinical presentation is of deep, aching lateral hip pain that may radiate into the buttocks or lateral knee. Pain is worse with activity and stretching and may be worse at night, especially when the patient lies on the affected side. Palpation over the greater trochanter elicits severe tenderness. Physical examination reveals pain with resisted hip abduction and external rotation.[13, 14, 15, 16]

Bursitis of knee

The medial collateral ligament bursa is most commonly injured secondary to a twisting injury with external tibial rotation. Medial joint line pain occurs and may limit knee extension. This may be confused with a meniscal tear on physical examination.

Anserine (pes anserinus) bursitis can be caused by trauma, anatomic derangement, overuse, and in association with medial compartmental osteoarthritis. Clinically, patients complain of pain and tenderness over the anteromedial knee that is worse with knee flexion. This condition may be confused with medial meniscal pathology.[17, 18]

Prepatellar bursitis, also known as housemaid’s knee, is associated with trauma or with repetitive kneeling over an extended period. The prepatellar bursa is also a common site for septic (infectious) bursitis, a diagnosis that should be considered when there is skin injury, erythema, warmth, or severe tenderness over the patella. In patients with septic prepatellar bursitis, the patella is not palpable, and knee flexion is painful.

Popliteal bursae (Baker or popliteal cysts) can become enlarged due to degenerative changes of the knee, trauma, soft tissue injuries, or arthritis and are associated with local swelling and pain on walking, jumping, and squatting. Magnetic resonance imaging (MRI) or ultrasonography can differentiate an isolated bursitis from intra-articular injury (see also Baker Cyst).

Bursitis of ankle

Retrocalcaneal bursitis can be caused by local trauma from poorly designed shoes, overuse (eg, in athletes), or conditions causing inflammatory arthritis. Patients complain of posterolateral heel pain and may have a posterior heel prominence (known as the Haglund deformity or a “pump bump”), as well as local swelling and tenderness over the Achilles tendon. Pain is increased by squeezing the bursa from side to side and anterior to the Achilles. Rest and ice in the acute period can reduce inflammation, while stretching (eg, physical therapy), a heel lift or open-back shoes can alleviate pressure on the bursa.[19]

Bursitis has many causes, including autoimmune disorders, crystal deposition (gout and pseudogout), infectious diseases, traumatic events, and hemorrhagic disorders, as well as being secondary to overuse. Repetitive injury within the bursa results in local vasodilatation and increased vascular permeability, which stimulate the inflammatory cascade. Subdeltoid and subacromial bursitis have been reported after vaccination, when poor technique results in direct injection of the vaccine into the bursa.[20, 21, 22]

The following systemic diseases have also been associated with bursitis:

• Rheumatoid arthritis
• Ankylosing spondylitis
• Reactive arthritis
• Psoriatic arthritis
• Scleroderma
• Systemic lupus erythematosus
• Pancreatitis
• Whipple disease
• Oxalosis
• Uremia
• Hypertrophic pulmonary osteoarthropathy
• Idiopathic hypereosinophilic syndrome

In addition, generalized hypermobility has been associated with bursitis and other soft-tissue disorders. Some rheumatic conditions, such as gout, can predispose patients to bursitis.

Septic (infectious) bursitis is most common in superficial bursae. In the majority (50-70%) of cases, it results from direct introduction of microorganisms through traumatic injury or through contiguous spread from cellulitis. Less commonly, infection of deep bursae is due to contiguous septic arthritis or bacteremia (10% of cases).

The most common causative organism is Staphylococcus aureus (80% of cases), followed by streptococci.[23, 24] However, many other organisms have been implicated in septic bursitis, including mycobacteria (both tuberculous and nontuberculous strains), fungi (Candida), and algae (Prototheca wickerhamii).[25] There have also been cases of olecranon bursitis from Brucella melitensis.[26]

Factors predisposing to infection include diabetes mellitus, corticosteroid therapy, uremia, alcoholism, skin disease, and trauma, among others. A history of noninfectious inflammation of the bursa also increases the risk of septic bursitis.

Bursitis accounts for 0.4% of all visits to primary care clinics. The most common locations of bursitis involve the subacromial, olecranon, ischial, trochanteric, and prepatellar bursae.

The incidence of bursitis is higher in athletes, reaching levels as high as 10% in runners. Approximately 85% of cases of septic superficial bursitis occur in men. A French study aimed at assessing the prevalence of knee bursitis in the working population found that most cases occurred in men whose occupations involved heavy workloads and frequent kneeling.[27]

Mortality in patients with bursitis is very low. The prognosis is good, with the vast majority of patients receiving outpatient follow-up and treatment.

A prospective study of 60 patients with trochanteric bursitis found that poor clinical outcomes correlated with obesity, smoking, emotional stress, fibromyalgia, and hypothyroidism. In contrast, better overall physical function was associated with the use of fewer corticosteroid infiltrations, a shorter length of time between symptom onset and surgery, being a nonsmoker, and the absence of prior lumbosacral fusion.[28]

Patients with bursitis may report the following:

• Localized tenderness
• Decreased range of motion or pain with movement
• Erythema or edema (seen in superficial bursitis)
• History of repetitive movement (eg, frequent kneeling leading to prepatellar or infrapatellar bursitis)
• History of inflammatory disease (eg, rheumatoid arthritis, systemic lupus erythematosus)
• History of trauma

On physical examination, patients have tenderness at the site of the inflamed bursa. If the bursa is superficial, physical examination findings are significant for localized tenderness, warmth, edema, and erythema of the skin.

Reduced active range of motion with preserved passive range of motion is suggestive of bursitis, but the differential diagnosis includes tendinitis and muscle injury. A decrease in both active and passive range of motion is more suggestive of other musculoskeletal disorders. In patients with chronic bursitis, the affected limb may show disuse atrophy and weakness. Tendons may also be weakened and tender.

Although septic bursitis is not diagnosed solely on the basis of clinical signs, certain signs tend to favor the diagnosis of septic over sterile inflammatory bursitis. In particular, patients with septic bursitis may have fever, bursal warmth, tenderness that is more severe than in nonseptic bursitis, and associated peribursal cellulitis. Joint motion is typically preserved in septic bursitis, whereas other types of bursitis are associated with limited range of motion.

Subacromial bursitis

Subacromial bursitis is frequently associated with supraspinatus tendinitis because inflammation extends from one structure to the other. Repetitive activities with an elevated arm most frequently cause inflammation of the bursae. Examples of this include frequent pitching of a baseball or lifting luggage overhead. Less commonly, a primary process, such as rheumatoid arthritis, gout, or tuberculosis, may lead to bursitis.

Patients often exhibit tenderness over the greater tuberosity. Difficulty in abduction may occur, specifically from 70° to 100°.

Olecranon bursitis

Trauma of the skin and surrounding tissues makes the olecranon a frequent location for infectious bursitis. The risk of septic bursitis increases in patients with chronic disease. Because of the higher likelihood of infection, some physicians encourage aspiration and analysis of the bursa even when tenderness and erythema are minimal.

Chronic stress from repetitive forward-leaning positions with pressure on the elbows is seen in patients on long-term hemodialysis (dialysis elbow), in patients with chronic obstructive lung disease, in students (student's elbow), and in those whose occupation involves laying down carpet. Another term "lunger elbow" has been suggested to describe this affliction.

The most common nontraumatic cause of olecranon bursitis is gout, followed by pseudogout, rheumatoid arthritis, and uremia.

When inflamed, the bursa is evident as a fluctuant bulge posterior to the olecranon process (see the images below). Pain and tenderness over the bursa may be increased in extreme flexion as tension increases.

Iliopsoas bursitis

Pain from iliopsoas bursitis radiates down the anteromedial side of the thigh to the knee and is increased on flexion, adduction, and internal rotation of the hip. Typically, the pain worsens slowly over weeks or months; it may be the only symptom present. Tenderness may occur anteriorly below the middle of the inguinal ligament and lateral to the femoral artery. Occasionally, a palpable mass or visible edema may be found lateral to the femoral vessels. Pulsations from the femoral artery are sometimes transmitted through this mass.

Rarely, retroperitoneal extension can cause an abdominal or pelvic mass that gives rise to compressive syndromes in the groin (eg, femoral vein compression or femoral neuropathy) or pelvis (eg, medial displacement of pelvic structures or superior displacement of abdominal structures).[29] A classic triad of a palpable mass, extrinsic pressure on adjacent structures, and radiographic changes of advanced arthritis has been described, but was determined not to be sensitive for early disease. Diagnostic imaging may assist with diagnosis.

Greater trochanter bursitis

Patients with greater trochanter bursitis are predominantly women (female-to-male ratio, 2-4:1) in their fourth to sixth decade of life. Runners and ballet dancers may develop deep trochanteric bursitis from overuse injury. The disorder is also associated with rheumatoid or osteoarthritis of the hips, lumbosacral disease, and leg-length discrepancies.

Patients experience chronic, intermittent, aching pain over the lateral hip. In 40% of cases, this radiates down to the lateral thigh. Walking or lying on the affected side exacerbates the pain. In the seated position, local tenderness is present over the greater trochanter or more posteriorly for deep bursa.

Pain can be reproduced by hip adduction (superficial bursitis) or resisted active abduction (deep bursitis). More than one half of patients have pain on FABERE testing (flexion, abduction, external rotation, extension of the hip with the contralateral knee flexed). Range of motion of the hip joint itself should not be affected.

Ischiogluteal bursitis

In ischiogluteal bursitis, inflammation commonly arises as a result of trauma, prolonged sitting on a hard surface (so-called weaver’s bottom), or prolonged sitting in the same position (spinal cord injury). Pain may radiate down the back of the thigh and mimic sciatic nerve inflammation. However, in ischiogluteal bursitis, pain can be reproduced by applying pressure over the ischial tuberosity.

Prepatellar bursitis

In prepatellar bursitis, inflammation arises secondary to trauma or constant friction between the skin and the patella, most commonly when frequent forward kneeling is performed. Previously referred to as housemaid's knee, it now is seen regularly in many other occupations, including carpet laying (carpet-layer knee), coal mining (beat knee), roofing, gardening, and plumbing. Bursitis may also develop 7-10 days after a single blow, such as a fall. Rheumatoid arthritis and gout may also be the cause.

Prepatellar bursitis is often visualized as fluctuant, well-circumscribed warm edema over the lower pole of the patella. Knee flexion causes increased tension over the bursa and increased pain. The knee joint itself, however, is normal.

The superficial location of the prepatellar bursa allows easy introduction of microorganisms and predisposes to septic arthritis. Therefore, aspiration of fluid to rule out infection is highly recommended if any clinical suspicion is present.

Infrapatellar bursitis

Superficial infrapatellar bursitis (clergyman knee) is located more distally than prepatellar bursitis and is often caused by frequent kneeling in an upright position. It can also be seen in gout or syphilis. The differential diagnosis includes Osgood-Schlatter disease. The deep infrapatellar bursa is less frequently inflamed.

Clinically, the patient has pain with flexion and extension at the extremes of the range of motion. Edema is located on both sides of the patellar tendon and is associated with tenderness.

Anserine (pes anserinus) bursitis

The anserine bursa separates the insertions of the sartorius, gracilis, and semitendinosus tendons from the tibial plateau. It is so named because the edematous bursa, restrained by these three tendons, gives the appearance of a goose’s foot (pes anserinus). See the image below.

An abnormal pull on any of the 3 tendons or an abnormal gait predisposes to repetitive friction and to bursitis. Patients with anserine bursitis are commonly obese older women with a history of osteoarthritis of the knees. An association has also been described between this bursitis and type 2 diabetes mellitus. Other risk factors include long-distance running, valgus knee alignment, and excess external rotation of the lower leg.

Unlike prepatellar bursitis, anserine bursitis is almost never septic. The differential diagnosis includes medial collateral ligament strain and osteoarthritis of the medial compartment of the knee. It is helpful to ensure that the medial collateral ligament is intact, by performing a valgus stress maneuver.

Tenderness is present on the medial aspect of the knee 5 cm below the joint margin at the site of the tibial tubercle. Neither swelling nor warmth is present. Pain radiates along the medial joint line to the inner thigh and calf. Pain is exacerbated with stair climbing and extremes of flexion or extension. Anserine bursitis may occur bilaterally.

Calcaneal bursitis

Either the retrocalcaneal or subcutaneous calcaneal bursa can become inflamed in patients with heel spurs or in patients with poor-fitting shoes (eg, high heels). Inflammation can occur secondary to Achilles tendinitis, especially in young athletes. Patients exhibit tenderness to palpation of the bursa on either side of the Achilles tendon. They have pain with movement, which is worsened with dorsiflexion due to the increased pressure placed on the insertion of the Achilles tendon.

Routine laboratory blood work is generally not helpful in the diagnosis of noninfectious bursitis. In cases of septic bursitis, however, the leukocyte count and erythrocyte sedimentation rate (ESR) may be mildly to moderately elevated. Blood cultures may be drawn if infection of deep bursae is a concern. ESR, antinuclear antibody (ANA), rheumatoid factor (RF), and anti–citric citrullinated peptide (anti-CCP) tests should all be ordered in cases where autoimmune disease is suspected, because these inflammatory disorders can trigger bursitis.

Aspiration and analysis of bursal fluid should be done to rule out infectious or rheumatic causes; they may also be therapeutic. Bursal fluid should be sent for crystal analysis, cell count with differential, gram stain, and aerobic/anaerobic bacterial culture. Fungal and mycobacterial testing should be sent if there is suggestive history or clinical suspicion. Physicians should be more inclined to perform bursal fluid aspiration in the most frequently infected bursae—the olecranon (see the image below), prepatellar, and infrapatellar bursae.

Nonseptic bursitis has cell counts lower than 2000/µL, with a predominance of mononuclear cells. Septic bursitis may have cell counts exceeding 70,000/µL, with a predominance of polymorphonuclear leukocytes (PMNs). The white blood cell (WBC) count in septic bursitis is typically lower than that in septic arthritis. A WBC count of 5000-20,000/µL or higher may be considered indicative of infection.

Gram stain and culture are performed to identify any pathogens. These results can guide the modification of antibiotics in cases of bacterial infection. The most common organism cultured is the gram-positive coccus penicillinase-producing Staphylococcus aureus.[23]

The accuracy of Gram staining varies considerably, with sensitivities between 15-100%. Therefore, fluid that has a high WBC count but negative Gram stain is still suspicious for infection and should be managed accordingly.

Elevated protein level and reduced glucose level (or a low bursal-to-serum glucose ratio) are associated with infection but are not sufficiently sensitive or specific to be used in isolation. Bursal fluid culture is the conclusive test for diagnosis. Culture in liquid medium has been shown to be superior to culture on solid medium.[30]

With chronic or recurrent bursitis, samples should be sent for acid-fast staining and cultured on special media for mycobacteria, fungi, algae, and Brucella.

Fluid should also be examined for crystals. Monosodium urate crystals are seen in gout; calcium pyrophosphate crystals are seen in pseudogout; cholesterol crystals are seen in rheumatoid chylous bursitis and in a variety of chronic effusions.

Arthrocentesis should be performed if joint involvement is suspected.

Plain radiography usually is not helpful in the diagnosis of bursitis but may be useful for identifying underlying bony pathology (eg, fractures, arthritis, osteophytes, or dislocations) that may trigger bursal inflammation. They may also show joint effusions. In chronic bursitis, the bursal walls or nearby tendons may be calcified and radiopaque.

Bone scanning is not a sensitive test for bursitis, but it may be done in cases in which the diagnosis is unclear to rule out other causes of pain.

Because of the characteristic clinical presentation of bursitis, magnetic resonance imaging (MRI) and computed tomography (CT) are usually unnecessary. MRI can be useful for delineating the anatomy of the entire joint (including adjacent soft tissues) and depicting bursal or prebursal fluid and associated abscesses[31] ; if needed, it is a very sensitive test for identification of bursitis. MRI is also helpful in ruling out suspected solid tumors and defining pathology for possible surgical excision.

Ultrasonography is useful for further imaging of the bursa when the diagnosis is uncertain. For diagnostic aspiration or treatment injections, ultrasonography may be performed to elucidate the structures and to guide procedures. The accuracy of ultrasound-guided injections has increased; however, studies of the efficacy of ultrasound-guided versus blinded injections provide variable results.[32, 33] In addition, ultrasound studies distinguish solid from cystic masses and are helpful in detecting Baker cysts (popliteal bursitis) when there are extensive joint deformities.[12, 34] Baker cysts are often discovered incidentally when lower-extremity Doppler studies are done to rule out deep vein thrombosis.

Most patients with bursitis are treated conservatively to reduce inflammation. Conservative treatment includes the following[15] :

• Rest
• Cold and heat treatments
• Elevation
• Nonsteroidal anti-inflammatory drugs (NSAIDs)
• Bursal aspiration
• Intrabursal steroid injections (with or without local anesthetic agents)

Patients with suspected septic bursitis should be treated with antibiotics while awaiting culture results. Superficial septic bursitis can be treated with oral outpatient therapy. Those with systemic symptoms or who are immunocompromised may require admission for intravenous (IV) antibiotic therapy.

Surgical excision of bursae may be required for chronic or frequently recurrent bursitis. Surgery is reserved as a last resort for patients in whom conservative treatment fails. The operation varies according to site.

Most patients respond well to conservative management. Patients who do not respond to nonoperative treatment or who have signs of tendinous or ligamentous injury require further evaluation. Consultation with a general or orthopedic surgeon or a rheumatologist may be helpful.

With regard to resumption of activities, patients should let pain be their guide.

Conservative treatment involves control of pain and inflammation, which may be guided by the PRICEMM acronym, as follows:

• Protect - Use padding, braces, or changes in technique
• Rest - Avoid activities that exacerbate pain
• Ice - Cryotherapy can relieve pain and decrease inflammation
• Compression - Elastic dressings can ease pain, as in olecranon bursitis
• Elevation - Raise the affected limb above the level of the heart
• Modalities - Employ electrical stimulation, ultrasonography, or phonophoresis
• Medications - Administer nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, or corticosteroid injections

Physical measures

The affected area should be placed at rest. Because of the risk of adhesive capsulitis, shoulders should not be immobilized for more than a few days. After immobilization, patients should begin graduated range-of-motion exercises. Patients who have bursitis secondary to overuse should be educated about the importance of regular periods of rest and possible alternative activities to prevent recurrence.

Applying cold treatments for 20 minutes every several hours may be of value in the first 24-48 hours. Such treatments may be followed by heat treatments. Elevation is useful, particularly in lower-limb bursitis. Consider site-specific therapy (eg, cushions for ischial bursitis; well-fitted, padded shoes for calcaneal bursitis).

A randomized comparative clinical trial by Homayouni et al in 56 patients with pes anserinus tendino-bursitis concluded that kinesiotaping of the tender area is more effective than 10 days of naproxen (250 mg three times daily) plus daily physical therapy for reducing pain and swelling. Kinesiotaping, using a space-correction (lifting) technique, was repeated three times in 1 week.[35]

NSAIDs

NSAIDs are used to reduce inflammation and relieve pain. In a multicenter, double-blind, parallel study involving 372 patients with acute (≤72 hours) traumatic bursitis or tendinitis of the shoulder, 90% of patients treated with diclofenac 50 mg two or three times daily improved over 14 days, with 40-50% demonstrating at least moderate improvement.[36]

A randomized trial by Kim et al in 133 patients with olecranon bursitis treated with compression bandaging and NSAIDs, aspiration, or aspiration with steroid injections found no differences in the proportion of patients whose bursitis resolved by week 4. Although treatment with steroid injection after aspiration was associated with the earliest resolution, the authors acknowledge the risk of complications with that method, along with the possibility of recurrence; thus, they suggest that “compression bandaging and a short course of NSAIDs may offer the most appropriate balance of safety and efficacy”.[37]

Topical NSAIDs have been used for reducing pain due to chronic musculoskeletal conditions; this may be complicated by mild skin reactions or other local adverse effects, but it reduces the risk of gastrointestinal adverse effects.[38] Some NSAIDs are commercially available in topical form, and any NSAID can be prepared for topical administration by a compounding pharmacy.

Intrabursal corticosteroid injections

Corticosteroid injections can be helpful if the patient does not respond to other treatment within 7-14 days. Various steroids (eg, hydrocortisone, prednisolone, methylprednisolone, triamcinolone, betamethasone, and dexamethasone) have been used in this setting, but no single agent has been found to be demonstrably superior. Steroids can be mixed in the same syringe with lidocaine or bupivacaine.

Corticosteroid injections can be performed either in the emergency department (ED) or in an outpatient setting.[39, 40] A 1.5-4 inch, 20-gauge spinal needle may be used as a probe to determine the points of maximal tenderness in the affected bursa. Typically, a mix of corticosteroid and local anesthetic is injected into each tender site. The corticosteroid dose should be 20 mg or less per lesion, and no more than a total of 40 mg of corticosteroid should be used.[11, 13, 41]

The potential complications of intrabursal injections include the following:

• Infection
• Bleeding
• Allergy to injected agents
• Local subcutaneous atrophy (Methylprednisolone is associated with the lowest incidence)
• Postinjection flare/pain (usually starts within hours and may last up to 72 hours)
• Tendon rupture (major tendons should not be injected)

Intrabursal steroid injections (with or without local anesthetics) should not be performed if infection is suspected. In overuse injuries, injections should not replace cessation or modification of the offending activity.

In a randomized study of 42 patients with olecranon bursitis who were assigned after bursal aspiration to 1 of 4 treatment groups (intrabursal methylprednisolone 20 mg plus naproxen 1 g/day for 10 days, intrabursal methylprednisolone without naproxen, naproxen only, or placebo), steroid injection was more successful in decreasing edema and preventing recurrence than naproxen or placebo was.[42]

In a systematic review of 29 studies involving a total of 1278 patients with olecranon bursitis, Sayegh and Strauch found that treatment of aseptic bursitis with corticosteroids was associated with significantly increased rates of overall complications and skin atrophy. Patients with aseptic bursitis had a significantly higher overall complication rate than those with septic bursitis. Compared with nonsurgical management, surgical management was significantly less likely to result in clinical resolution of septic or aseptic bursitis, and it was associated with significantly higher rates of overall complications, persistent drainage, and bursal infection.[43]

A study comparing the short- and long-term effectiveness of betamethasone injections (6, 12, or 24 mg with 4 mL of 1% lidocaine) for trochanteric bursitis reported that improvement of pain was achieved at 1, 6, and 26 weeks in 77%, 69%, and 61% of patients, respectively.[44] Higher doses of steroids were significantly more effective.

Ultrasound (US) can be used to guide aspiration and injection.[45] However, Mitchell et al reported that US-guided injection of the trochanteric bursa provides 2-week and 6-month outcomes similar to those of injection guided by anatomic landmarks, but is considerably more expensive. These authors advise that anatomic landmark-guided injection remains the method of choice, but should be routinely performed using a sufficiently long needle (at least 2 in [50.8 mm]), with US guidance reserved for cases of extreme obesity or injection failure.[33]

In a study of 25 cases of postarthroplasty trochanteric bursitis requiring corticosteroid injection, Farmer et al found that corticosteroid injections were effective therapy and that nonoperative management may be more likely to fail in young patients and patients with leg-length discrepancies.[46] Of the 25 hips, 11 required multiple corticosteroid injections, and symptoms resolved in 20 cases.

An 8-week placebo-controlled study of acromial injections demonstrated that steroids brought about a decrease in pain and an improvement in function as compared with placebo.[47] Furthermore, the study showed no significant differences between higher (40 mg) and lower (20 mg) doses of triamcinolone acetonide. Therefore, in general, lower doses of steroids should be used initially.

Other injected agents

Experiences with platelet-rich therapy (PRT) injections of soft-tissue injuries (ligament, muscle, and tendon tears or tendinopathies) are increasingly being published.[48] A Cochrane review cited insufficient evidence to support the use PRT and a need for standardization of platelet-rich plasma preparations.[49]

Isolated case reports describe management of recurrent non-septic bursitis.with aspiration followed by injection of a sclerosing agent (eg, polidocanol).[50]

In cases in which septic bursitis is suspected, the bursa should be aspirated. The skin over the bursa is sterilized, and the area is anesthetized with lidocaine via a 27-gauge needle. A sterile 20- or 22-gauge needle is then introduced into the bursa. Fluid is aspirated and sent for analysis to identify any infectious organisms or crystals.

Staphylococcus aureus is the most common pathogen in septic bursitis, accounting for more than 80% of cases. Streptococcal species (mostly group A hemolytic streptococci) account for 5-20% of cases. Other gram-positive, gram-negative, and anaerobic infections are rare. Mycobacterial, fungal, algal, and spirochetal infections are even rarer and tend to occur in unusual clinical settings (especially in patients who are predisposed to infection).

After aspiration and fluid analysis, antibiotic therapy is driven by the severity of the bursitis, the patient's clinical status (eg, toxic, febrile), underlying prostheses, history of methicillin-resistant S aureus (MRSA) or MRSA colonization, allergies, and ability to tolerate oral antibiotics. Based on these factors, there are various options, which include but are not limited to oxacillin (or a penicillinase-resistant penicillin), cefazolin, clindamycin, doxycycline, trimethoprim-sulfamethoxazole, ciprofloxacin, and rifampin. In severe cases or immunocompromised patients, admission for parenteral vancomycin therapy may be the appropriate treatment.

In a study involving 82 patients with severe septic bursitis, Martinez-Taboada et al concluded that in patients with severe septic bursitis but without extensive cellulitis, aspiration plus IV cloxacillin may be sufficient treatment, whereas in patients with more severe cases of septic bursitis, aspiration along with cloxacillin plus gentamicin may be appropriate in the majority.[51]

The duration of antibiotic treatment varies with the patient and the clinical situation. Patients with uncomplicated septic bursitis who present within 7 days of infection should be treated with a minimum 10-day course.[52] Outpatient treatment is effective in 40-50% of patients with mild to moderate infections. A 4-week course is advisable, using high doses of sensitivity-directed antibiotics. Aspiration should be repeated every 1-3 days while antibiotics are being administered. Antibiotics should be continued for 5 days past sterilization of bursal fluid as seen by aspiration. Aspiration also helps to decrease the bacterial load and to promote comfort.

Immunocompromised patients require at least 15 days of treatment. Deep bursae infections have higher associations with bacteremia and call for more aggressive and prolonged antibiotic therapy. In particularly severe cases, hospitalization is required, with 1 week of parenteral antibiotics followed by 30 days of oral antibiotics. Surgical drainage or debridement is often necessary.

Treatment of tuberculous bursitis involves full excision of the bursa and surrounding tissue with concomitant antituberculous therapy for 6-12 months. Infection with atypical mycobacteria may be successfully treated with conservative drainage and appropriate antibiotics. Brucella bursitis is treated with excision of bursae and administration of tetracycline with or without rifampin.

In general, bursitis is not treated surgically. However, there are some cases in which surgical interventions such as the following are appropriate:

• Incision and drainage
• Excision of chronically inflamed bursae
• Removal of underlying bony prominences

As a rule, surgical intervention is reserved for the following situations[53] :

• Failure of needle aspiration to drain the bursa adequately
• Bursa site inaccessible to repeated needle aspirations
• Abscess, necrosis, or sinus formation
• Need for exploration to assess the extent of infection of adjacent structures
• Recurrent or refractory disease after conservative treatment

Surgical release may be indicated when adhesive bursitis develops that severely limits joint motion. During surgery, the adhered bursa is removed, and the contiguous tissues are released.[54, 55, 19, 56]

In the upper extremity, subscapular bursitis can be caused by bony exostoses, and surgery may be needed to reduce these structures. In addition, the association of subacromial bursitis with rotator cuff impingement and tears is high, and surgical repair of the tear may be indicated. Singh and Bain describe a technique for treatment of olecranon spurs in which the spur is dissected out and excised in its entirety under endoscopic vision; this technique results in less morbidity compared with open excision and avoids an incision in the sensitive skin over the olecranon.[57]

In the lower extremity, Baker cysts (popliteal bursitis) are often removed surgically. Before open excision, arthroscopy should be performed to evaluate for intra-articular conditions. Most cysts are approached posteromedially through a hockey-stick incision.

For treatment of recalcitrant trochanteric bursitis, Pretell et al described distal “Z” lengthening of the fascia lata in 13 hips and found that 12 of the 13 patients reported good results.[58] According to the authors, this technique is less aggressive, can be performed with local anesthesia, and is associated with little morbidity and disability. The mean operating time for the procedure was 15 minutes, and one seroma was reported as a complication.

Lohrer and Nauck, in a prospective study of 89 athletes who underwent surgery for recalcitrant retrocalcaneal bursitis or recalcitrant midportion Achilles tendinopathy, found that clinical severity scores improved significantly at 6 and 12 months following surgery, and that improvements were similar among patients who did or did not undergo tendon repair.[59]

Endscopic procedures

A small case series from Australia found endoscopic bursectomy to be safe and effective as therapy for infectious prepatellar bursitis and suggested that it reduced the duration of hospitalization and hastened return to work as compared with conventional open surgical treatment.[60]

A systematic review from The Netherlands found that for surgical treatment of chronic retrocalcaneal bursitis, endoscopic approaches appear to yield better results than open approaches; however, more evidence is needed to establish the optimal surgical approach.[19]

A Korean review of endoscopic resection in 30 patients with olecranon bursitis (15 of them septic) reported excellent outcomes without recurrence or joint motion limitation in both septic and aseptic cases. Average follow-up was 21.1 months.[61]

A series of 27 endoscopic bursectomies for recalcitrant septic bursitis (14 cases of olecranon bursitis and 13 cases of prepatellar bursitis) reported good results, with no wound healing complications and only 1 minor recurrence.[62]

The goals of pharmacotherapy are to reduce morbidity and prevent complications. Medications used include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and topical anesthetics.

Class Summary

Nonsteroidal anti-inflammatory drugs (NSAIDs) are most commonly used for relief of mild to moderately severe pain. Although the pain-relieving effects tend to be patient-specific, ibuprofen is usually used for initial therapy. All NSAIDs now have a black box warning for increased cardiovascular risk, even with short-term use, with naproxen having the least risk. Some NSAIDs are commercially available in topical form, and any NSAID can be prepared for topical administration by a compounding pharmacy.

Ibuprofen (Ibu, Addaprin, Advil, Motrin, Caldolor)

Ibuprofen is the drug of choice for mild to moderately severe pain. It inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Naproxen (Anaprox DS, Naprelan, Naprosyn, EC-Naprosyn, Aleve)

Naproxen is used for relief of mild to moderately severe pain. It inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase (COX), an enzyme responsible for prostaglandin synthesis. It is also available in topical form.

Ketoprofen (Frotek, Ketophene Radiopaq)

Ketoprofen is used for the relief of mild to moderate pain and inflammation. It works via COX inhibition. Small doses are indicated initially in patients with small body size, elderly patients, and persons with renal or liver disease. Doses of over 75 mg do not increase therapeutic effects. Administer high doses with caution, and closely observe the patient for response. This agent is also available in topical form.

Flurbiprofen

Flurbiprofen may inhibit COX, thereby inhibiting prostaglandin biosynthesis. These effects may result in analgesic, antipyretic, and anti-inflammatory activities.

Diclofenac (Voltaren XR, Cataflam, Cambia, Zipsor, Zorvolex)

This is one of a series of phenylacetic acids that has demonstrated anti-inflammatory and analgesic properties in pharmacological studies. It is believed to inhibit the COX enzyme, which is essential in the biosynthesis of prostaglandins. Diclofenac can cause hepatotoxicity; hence, liver enzymes should be monitored in the first 8 weeks of treatment. It is absorbed rapidly; metabolism occurs in the liver by demethylation, deacetylation, and glucuronide conjugation. The delayed-release, enteric-coated form is diclofenac sodium, and the immediate-release form is diclofenac potassium. While all NSAIDs have the potential for hepatotoxicity, diclofenac has the greatest risk.

Tolmetin

Tolmetin inhibits prostaglandin synthesis by decreasing the activity of the COX enzyme, which in turn, decreases the formation of prostaglandin precursors.

Celecoxib (Celebrex)

Celecoxib inhibits primarily COX-2. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, the incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions, may be decreased when compared with nonselective NSAIDs. Seek the lowest dose for each patient.

Indomethacin (Indocin, Tivorbex)

Indomethacin is used for relief of mild to moderate pain; it inhibits inflammatory reactions and pain by decreasing the activity of COX, which results in a decrease of prostaglandin synthesis.

Meloxicam (Mobic, Vivlodex)

Meloxicam decreases the activity of COX, which in turn, inhibits prostaglandin synthesis. These effects decrease the formation of inflammatory mediators.

Diclofenac topical (Flector Transdermal Patch, Voltaren Gel, Pennsaid topical)

Diclofenac is designated chemically as 2-[(2,6-dichlorophenyl) amino] benzeneacetic acid, monosodium salt, with an empirical formula of C14 H10 Cl2 NO2 NA. It is one of a series of phenylacetic acids that has demonstrated anti-inflammatory and analgesic properties in pharmacological studies. It is believed to inhibit the COX enzyme, which is essential in the biosynthesis of prostaglandins. Diclofenac can cause hepatotoxicity; hence, liver enzymes should be monitored in the first 8 weeks of treatment.

Class Summary

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, they modify the body’s immune response to diverse stimuli.

Hydrocortisone (Solu-Cortef, Cortef)

Hydrocortisone decreases inflammation by suppressing migration of polymorphonuclear leukocytes (PMNs) and reversing increased capillary permeability.

Methylprednisolone (Depo-Medrol, Medrol, Solu-Medrol)

Methylprednisolone decreases inflammation by suppressing migration of PMNs and reducing capillary permeability.

Dexamethasone (Decadron, DoubleDex)

Dexamethasone is used for various inflammatory diseases. It decreases inflammation by suppressing migration of PMNs and reducing capillary permeability.

Class Summary

Anesthetics are used to induce local analgesia.

Lidocaine 1-2% (Xylocaine, Eha, Tranzarel, Astero)

Lidocaine is a local anesthetic used to reduce pain resulting from inflammatory reactions associated with bursitis.