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Bursitis
Updated: Dec 18, 2018
Author: Kristine M Lohr, MD, MS; Chief Editor: Herbert S Diamond, MD

Overview

Practice Essentials
Bursitis is defined as inflammation of a bursa. Humans have approximately 160 bursae. These are saclike structures between
skin and bone or between tendons, ligaments, and bone. The bursae are lined by synovial tissue, which produces fluid that
lubricates and reduces friction between these structures.

Bursitis occurs when the synovial lining becomes thickened and produces excessive fluid, leading to localized swelling and pain.
[1, 2, 3] The following bursae are most commonly affected:

Subacromial
Olecranon
Trochanteric
Prepatellar
Infrapatellar

Symptoms of bursitis may include the following:

Localized tenderness
Pain (aggravated by movement of the specific joint, tendon, or both)
Edema
Erythema
Reduced movement

Routine laboratory blood work is generally not helpful in the diagnosis of noninfectious bursitis but is appropriate when septic
bursitis or underlying autoimmune disease is suspected. Aspiration and analysis of bursal fluid should be done to rule out
infectious or rheumatic causes and may also be therapeutic.

MRI is usually unnecessary but if needed is very sensitive for identification of bursitis, and can rule out suspected solid tumors
and define pathology for possible surgical excision. Ultrasonography is useful for further imaging of the bursa when the
diagnosis is uncertain, and can guide diagnostic aspiration or therapeutic injections.

Conservative treatment to reduce inflammation is used for most patients with bursitis and includes the following:

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. Surgical excision of
bursae may be required as a last resort for chronic or frequently recurrent bursitis.

See the following for discussion of bursitis at specific sites:

Prepatellar Bursitis
Olecranon Bursitis
Retrocalcaneal Bursitis

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Calcaneal Bursitis
Trochanteric Bursitis
Pes Anserine Bursitis
Hip Tendonitis and Bursitis

For patient education resources, see the Arthritis Center, as well as Bursitis.

Anatomy
Bursae are flattened sacs that serve as protective buffers 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 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

Examples include those that develop over a bunion and osteochondroma

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 2 commonly
affected bursae are located superomedially between the serratus anterior and the chest wall. See the image below.

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Shoulder anatomy muscle, anterior view.

Two olecranon bursae can become inflamed; one lies between the tendon of the triceps and the posterior ligament of the elbow
and the olecranon, whereas the other 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, bursae commonly affected by bursitis include 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), and the popliteal bursae, or Baker cysts (located in the
posterior joint capsule of the knee).[6]

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Location of anserine (pes anserinus) bursa on medial knee. MCL=medial collateral ligament.

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 the one more commonly
affected by bursitis.

Pathophysiology
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 usually causes inoculation of bacteria into the bursa, which triggers the inflammatory process.

There are three phases of bursitis: acute, recurrent, and chronic.[9] 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 continual pain and can
cause weakening of 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).[10]

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
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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.[11, 12, 13]

Olecranon bursitis, shown here with elbow flexed. Image courtesy of UMDNJ-New Jersey Medical School,
www.DoctorFoye.com, and www.TailboneDoctor.com.

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.[14, 15, 16, 17]

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 is not usually associated with overuse but may occur in patients 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.[18, 19]

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 cysts) 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 is generally caused by local trauma from poorly designed shoes. Patients complain of posterolateral heel
pain and may have a posterior heel prominence (“pump bump”), as well as local swelling and tenderness over the Achilles

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tendon. Pain is increased by squeezing the bursa from side to side and anterior to the Achilles. A heel lift and open-back shoes
help alleviate pressure.[20]

Etiology
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.[21]

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, bursitis and other soft-tissue disorders have been associated with generalized hypermobility. 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 (50-70% of cases). 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. However, many
other organisms have been implicated in septic bursitis, including mycobacteria (both tuberculous and nontuberculous strains),
fungi (Candida), and algae (Prototheca wickerhamii).[22] Factors predisposing to infection include diabetes mellitus, steroid
therapy, uremia, alcoholism, skin disease, and trauma. A history of noninfectious inflammation of the bursa also increases the
risk of septic bursitis.

Epidemiology and Prognosis

Bursitis accounts for 0.4% of all visits to primary care clinics. The most common locations of bursitis are the subdeltoid,
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 male workers whose occupations involved heavy workloads and frequent kneeling.[23]

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

Presentation

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History
Patients with bursitis have a history that may include 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

Physical Examination
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 those who have a history of 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 (so-called dialysis elbow), in patients with chronic obstructive lung disease, in students, and in those whose
occupation involves laying down carpet. The 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.

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Acute infectious bursitis upon presentation to emergency department. Image courtesy of Christopher Kabrhel, MD.

Infectious bursitis. Image courtesy of Christopher Kabrhel, MD.

Iliopsoas bursitis

Pain from iliopsoas bursitis radiates down the anteromedial side of the thigh to the knee and is increased on extension,
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.

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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). A classic triad of a palpable mass, extrinsic pressure on adjacent structures, and
radiographic changes of advanced arthritis was described, but this triad has been determined not to be sensitive for early
disease. Diagnostic imaging may assist with diagnosis.

Greater trochanter bursitis

Patients with greater trochanter bursitis are predominately women (male-to-female ratio, 1:2-4) in their fourth to sixth decade of
life. Runners and ballet dancers may develop deep trochanteric bursitis from overuse injury. The disease is also associated with
rheumatoid arthritis of the hips, 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 Patrick-Fabere testing (sequential 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 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 of
bursitis.

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 exhibits 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.

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Location of anserine (pes anserinus) bursa on medial knee. MCL=medial collateral ligament.

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 diabetes mellitus type 2. 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

The calcaneal bursa can become inflamed in patients with heel spurs or in patients with poor-fitting shoes (eg, high heels).
Inflammation can occur secondarily from Achilles tendinitis, especially in young athletes.

Patients exhibit tenderness to palpation of the bursa anterior to the Achilles tendon on both the medial and lateral aspects. They
have pain with movement, which is worsened with dorsiflexion.

DDx

Diagnostic Considerations
Because of the possible adverse effects of chronic bursitis on overlying structures, bursitis and tendinitis may occur together;
accordingly, the differential diagnosis should include both of these diagnoses.

In addition to the conditions listed in the differential diagnosis, other problems to be considered include the following:

Septic arthritis

Ligamentous injury

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Fracture

Osteoarthritis

Differential Diagnoses
Cellulitis

Gout and Pseudogout

Rheumatoid Arthritis (RA)

Soft Tissue Knee Injury

Tendonitis

Workup

Workup

Blood Studies
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.

Joint Aspiration and Fluid Analysis

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 drawn for monosodium urate crystal determination, cell count with differential, Gram stain, and culture.
Physicians should be more inclined to perform bursal fluid aspiration in the most frequently infected bursae—namely, the
olecranon (see the image below), prepatellar, and infrapatellar bursae.

Olecranon bursitis: aspiration of hemorrhagic effusion. Image courtesy of UMDNJ-New Jersey Medical School,
www.DoctorFoye.com, and www.TailboneDoctor.com.

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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 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. The accuracy of Gram staining varies considerably, with
sensitivities between 15% and 100%. Therefore, fluid that has a high WBC count but is negative on Gram staining is still
considered suspicious for infection.

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

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, Bone Scanning, MRI, and CT

Plain radiography usually is not helpful in the diagnosis of bursitis but may be useful for identifying osteophytes or other
underlying bony pathology (eg, fractures or dislocations) that may be triggering the 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[24] ; 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
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
controversial results.[25, 26] In addition, ultrasound studies distinguish solid from cystic masses and are helpful in detecting
Baker cysts (popliteal bursitis) when there are extensive joint deformities.[11, 27] Baker cysts are often discovered incidentally
when lower-extremity Doppler studies are done to rule out deep vein thrombosis.

Treatment

Approach Considerations
Most patients with bursitis are treated conservatively to reduce inflammation. Conservative treatment includes rest, cold and
heat treatments, elevation, administration of nonsteroidal anti-inflammatory drugs (NSAIDs), bursal aspiration, and intrabursal
steroid injections (with or without local anesthetic agents).[16]

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

P rotect - Use padding, braces, or changes in technique

R est - Avoid activities that exacerbate pain

I ce - Cryotherapy can relieve pain and decrease inflammation

C ompression - Elastic dressings can ease pain, as in olecranon bursitis

E levation - Raise the affected limb above the level of the heart

M odalities – Employ electrical stimulation, ultrasonography, or phonophoresis

M edications – 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-fitting padded shoes for calcaneal bursitis).

A randomized comparative clinical trial by Homayouni and colleagues 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 space-correction (lifting) technique, was repeated three
times in 1 week.[28]

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.[29]

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 earliest resolution, the authors note the risk of
complications with that method and the possibility of recurrence, and so suggest that “compression bandaging and a short
course of NSAIDs may offer the most appropriate balance of safety and efficacy”.[30]

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.

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Corticosteroid injections can be performed either in the emergency department (ED) or in an outpatient setting.[31, 32] A 1.5- to
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.[10, 14, 33]

The potential complications of intrabursal injections include the following:

Infection

Bleeding

Allergy to injected agents

Local subcutaneous atrophy (Methylprednisolone is associated with the least frequent development of local
subcutaneous atrophy.)

Postinjection flare or pain – Postinjection flares usually start within hours and may last up to 72 hours; postinjection pain
may last several 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.[34]

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. Compared with patients with septic bursitis, those with aseptic bursitis had a significantly higher overall
complication rate. Compared with nonsurgical management, surgical management was significantly less likely to clinically
resolve septic or aseptic bursitis, and it was associated with significantly higher rates of overall complications, persistent
drainage, and bursal infection.[35]

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.[36] Higher doses of steroids were significantly more effective.

Ultrasound (US) can be used to guide aspiration and injection.[37] 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.[26]

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.[38] 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.[39] 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;
tendinopathies) are increasingly being published.[40] A Cochrane review cited insufficient evidence to support the use PRT and
a need for standardization of platelet-rich plasma preparations.[41]

Isolated case reports describe management of recurrent non-septic bursitis.with aspiration followed by injection of a sclerosing
agent (eg, polidocanol).[42]

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Antibiotic Therapy
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 20- or 22-gauge needle is then introduced sterilely into the bursa. Fluid
is aspirated and sent for analysis to identify any infectious organisms or crystals present.

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 those who are predisposed to infection).

If bursitis is found to be secondary to infection after aspiration and fluid analysis, treatment should be initiated with antibiotics.
[43] An appropriate antistaphylococcal antibiotic should be started empirically. This should be a penicillinase-resistant penicillin,
such as oxacillin, or a first-generation cephalosporin, such as cefazolin. In penicillin-allergic patients or in carriers of methicillin-
resistant S aureus (MRSA), vancomycin is an appropriate alternative 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.[11]

The duration of antibiotic treatment varies with the patient and the clinical situation. Uncomplicated septic bursitis presenting
within 7 days of infection should be treated with a minimum 10-day course.[44] 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 a longer course of treatment, at least 15 days. 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 bursae and surrounding affected tissue with concomitant
antituberculous therapy for 6-12 months. Atypical mycobacteria occasionally 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.

Surgical Drainage and Excision

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[45] :

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

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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.[46, 47, 20, 48]

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.[49]

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.

Pretell et al described distal “Z” lengthening of the fascia lata in 13 hips and reported that 12 of the 13 patients reported good
results.[50] 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.[51]

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.[52]

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.[20]

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.[53]

Medication

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

Nonsteroidal Anti-inflammatory Drugs

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 the black
box warning for increased cardiovascular risk, even with short-term use, with naproxen having the least risk. Topical NSAIDs
available in the US have also been used[54] . Compounding pharmacies can also compound any NSAID into a topical form.

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.
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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, which is 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. 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 cyclooxygenase, 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 enzyme cyclooxygenase, 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 enzyme cyclooxygenase, which, in turn, decreases the
formation of prostaglandin precursors. The pediatric dosage is 20 mg/kg/d PO divided tid/qid initially, then 15-30 mg/kg/d, not to
exceed 30 mg/kg/d

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. The adult dosage is 100-200 mg PO bid; the pediatric dosage has not been established
for patients younger than 2 years and is 50 mg PO bid for patients 2 years or older whose weight is at least 10 kg but up to 25
kg, and is 100 mg PO bid for patients 2 years or older whose weight is more than 25 kg.

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 cyclo-oxygenase, 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 enzyme cyclooxygenase, which is essential in the

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biosynthesis of prostaglandins. Diclofenac can cause hepatotoxicity; hence, liver enzymes should be monitored in the first 8
weeks of treatment.

Corticosteroids

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.

Anesthetics, Topical

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.

Questions & Answers

Overview

What is bursitis?

What are bursae most commonly affected by bursitis?

What are symptoms of bursitis?

Which lab tests are performed in the diagnosis of bursitis?

What is included in conservative treatment for bursitis?

What is the clinical anatomy of bursae relative to bursitis?

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Which bursae that are most commonly affected by bursitis?

What is the pathophysiology of bursitis?

What is the pathophysiology of subacromial bursitis?

What is the pathophysiology of subscapular bursitis?

What is the pathophysiology of olecranon bursitis?

What is the pathophysiology of bursitis of hip?

What is the pathophysiology of bursitis of knee?

What is the pathophysiology of bursitis of ankle?

What causes bursitis?

Which systemic diseases associated with bursitis?

What causes septic (infectious) bursitis?

What is the prevalence and prognosis of bursitis?

Presentation

What are the signs and symptoms of bursitis?

Which physical findings are characteristic of subacromial bursitis?

Which findings are characteristic of bursitis?

Which physical findings are characteristic of olecranon bursitis?

Which physical findings are characteristic of iliopsoas bursitis?

Which physical findings are characteristic of greater trochanter bursitis?

Which physical findings are characteristic of ischiogluteal bursitis?

Which physical findings are characteristic of prepatellar bursitis?

Which physical findings are characteristic of infrapatellar bursitis?

Which physical findings are characteristic of anserine (pes anserinus) bursitis?

Which physical findings are characteristic of calcaneal bursitis?

DDX

Which conditions should be included in the differential diagnoses of bursitis?

What are the differential diagnoses for Bursitis?

Workup

What is the role of blood studies in the workup of bursitis?

What is the role of joint aspiration and fluid analysis in the workup of bursitis?

What is the role of imaging studies in the workup of bursitis?

What is the role of ultrasonography in the workup of bursitis?

Treatment

What are the treatment options for bursitis?

What is the role of NSAIDs in the treatment of bursitis?

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What is included in conservative treatment in bursitis?

What is the role of intrabursal corticosteroid injections in the treatment of bursitis?

What are potential complications of intrabursal injections for treatment of bursitis?

What is the efficacy of intrabursal injections for the treatment of bursitis?

What are is the role of antibiotic therapy in the treatment of bursitis?

What is the role of surgery in the treatment of bursitis?

What is the role of endoscopic procedures in the treatment of bursitis?

Medications

What are the goals of drug treatment for bursitis?

Which medications in the drug class Anesthetics, Topical are used in the treatment of Bursitis?

Which medications in the drug class Corticosteroids are used in the treatment of Bursitis?

Which medications in the drug class Nonsteroidal Anti-inflammatory Drugs are used in the treatment of Bursitis?

Contributor Information and Disclosures

Author

Kristine M Lohr, MD, MS Professor, Department of Internal Medicine, Interim Chief, Division of Rheumatology, Director,
Rheumatology Training Program, University of Kentucky College of Medicine

Kristine M Lohr, MD, MS is a member of the following medical societies: American College of Physicians, American College of
Rheumatology

Disclosure: Nothing to disclose.

Coauthor(s)

Alita Gonsalves, MD Physiatrist, Private Practice, Vero Orthopaedics and Neurology; Former Staff Physician, Department of
Physical Medicine and Rehabilitation, New York Presbyterian Hospital

Alita Gonsalves, MD is a member of the following medical societies: American Academy of Physical Medicine and
Rehabilitation, Physiatric Association of Spine, Sports and Occupational Rehabilitation

Disclosure: Nothing to disclose.

Leon Root, MD Professor of Clinical Surgery, Department of Orthopedics, Weill Medical College of Cornell University; Founder
and Director, Pediatric Outreach Program; Emeritus Chief of Osteogenesis Imperfecta Clinic, Attending Orthopedic Surgeon,
Medical Director of Rehabilitation, Emeritus Chief of Pediatric Orthopedics, The Hospital for Special Surgery

Leon Root, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American
Orthopaedic Association, New York Academy of Medicine, American Academy of Cerebral Palsy and Developmental Medicine,
Pediatric Orthopaedic Society of North America

Disclosure: Nothing to disclose.

Janet Kay Talbot-Stern, MD, FACEM, FCEM Emergency Medicine VMO, Ryde and Bankstown Hospitals, Australia Locum
Consultant, St Thomas Hospital, UK

Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD Visiting Professor of Medicine, Division of Rheumatology, State University of New York Downstate
Medical Center; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

https://emedicine.medscape.com/article/2145588-print 20/23
4/11/2020 https://emedicine.medscape.com/article/2145588-print

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians,
American College of Rheumatology, American Medical Association, Phi Beta Kappa

Disclosure: Nothing to disclose.

Acknowledgements

Ian D Dickey, MD, FRCSC Adjunct Professor, Department of Chemical and Biological Engineering, University of Maine;
Consulting Staff, Adult Reconstruction, Orthopedic Oncology, Department of Orthopedics, Eastern Maine Medical Center

Ian D Dickey, MD, FRCSC is a member of the following medical societies: American Academy of Orthopaedic Surgeons, British
Columbia Medical Association, Canadian Medical Association, and Royal College of Physicians and Surgeons of Canada

Disclosure: Stryker Orthopaedics Consulting fee Consulting; Cadence Honoraria Speaking and teaching

Gino A Farina, MD, FACEP, FAAEM Associate Professor of Clinical Emergency Medicine, Albert Einstein College of Medicine;
Program Director, Department of Emergency Medicine, Long Island Jewish Medical Center

Gino A Farina, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency
Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Mark Louden, MD Assistant Professor of Clinical Medicine, Division of Emergency Medicine, Department of Medicine, University
of Miami, Leonard M Miller School of Medicine

Mark Louden, MD is a member of the following medical societies: American Academy of Emergency Medicine and American
College of Emergency Physicians

Disclosure: Nothing to disclose.

Heidi M Stephens, MD, MBA Associate Professor, Department of Surgery, Division of Orthopedic Surgery, University of South
Florida College of Medicine; Courtesy Joint Associate Professor, Department of Environmental and Occupational Health,
University of South Florida College of Public Health

Heidi M Stephens, MD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of
Orthopaedic Surgeons, American Medical Association, American Orthopaedic Foot and Ankle Society, and Florida Medical
Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy;
Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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