Version July 2025
INTRODUCTION —
A bursa is a lubricated, fluid-filled sac or pouch adjacent to or in between soft tissues. The purpose of the bursa is to reduce friction between nearby structures, such as bones, joints, tendons, and skin. Bursitis can develop when bursae become irritated or inflamed and can present acutely with pain and swelling, or more chronically with functional limitations due to joint contractures. A wide range of conditions can cause bursitis, including infection (septic bursitis), chronic overuse/trauma, gout, rheumatoid arthritis (RA), or, rarely, systemic sclerosis.
This topic provides an overview of bursitis including clinical presentation, diagnostic evaluation, and treatment. Septic bursitis and knee bursitis are discussed in more detail elsewhere (see "Septic bursitis" and "Knee bursitis"). Greater trochanteric pain syndrome (formerly known as trochanteric bursitis) is also discussed separately. (See "Greater trochanteric pain syndrome (formerly trochanteric bursitis)".)
OVERVIEW OF BURSITIS —
A bursa (bursae in plural) is a lubricated, fluid-filled sac or pouch of serous membrane adjacent to or in between hard or soft tissues, such as bones and tendons. Normally, bursae are considered potential spaces, not actual or realized spaces. The bursal walls are lined internally by synovial membrane, which secretes a thin film of lubricating fluid. We use the term "bursitis" when there is irritation or inflammation of one or more bursae. In this setting, the collapsed bursa becomes a realized or actual space due to inflammation of the synovial lining and a subsequent increase in the amount of intrabursal fluid.
It is estimated that about 160 bursae are present in the adult body. The bursae serve to reduce friction and tension between bones, joints, tendons, and/or skin.
Bursae are usually classified according to their location as well as whether they develop before or after birth:
●Location
•Superficial – Bursae are considered superficial or subcutaneous when they are located in the subcutaneous tissue between skin and bone. Examples include the olecranon, prepatellar, superficial infrapatellar, and Achilles bursae.
•Deep – Bursae are classified as deep when located between adjacent muscles or between bone and nearby muscles and/or tendons. This category includes bursae that are subtendinous, submuscular, and subfascial [1]. Examples of deep bursae include the subacromial, deep infrapatellar, semimembranosus, trochanteric, and anserine bursae.
●Time of development
•Native – Bursae that are present at birth are described as native. These bursae are typically synovial or adjacent to joints.
•Non-native or adventitious – Bursae can develop after birth due to mechanical stress, which is described as non-native or adventitious [2]. As an example, the gastrocnemius-semimembranosus bursa, commonly known as the popliteal bursa, is thought to be a non-native bursa [3]. Data are limited to describe precisely when various bursae develop. However, the olecranon bursa is absent in most children under the age of seven and presumably develops later during childhood [4].
In addition, bursae may be categorized based on their constancy (ie, whether or not they are appreciable on imaging in the absence of associated pathology). Constantly present bursae are apparent on imaging whether or not there is associated inflammation; this category includes the retrocalcaneal and deep infrapatellar bursae. Other bursae are only seen on imaging when they are inflamed, as occurs with olecranon and prepatellar bursae. Finally, some bursae are seen intermittently on imaging even when there are associated symptoms, as is the case with trochanteric, pes anserine, and subacromial bursae.
Studies describing bursitis affecting the last category of bursae (ie, those intermittently present on imaging despite associated symptoms) can be challenging to interpret since it is unclear what reflects bursitis versus nearby tendonitis. As an example, "trochanteric bursitis" is only associated with clinically symptomatic bursitis on imaging in a minority of cases [5]; instead, symptoms are thought to reflect tendinosis of the gluteus medius and/or minimus tendons, prompting a change in nomenclature to "greater trochanteric pain syndrome" (GTPS). Physical therapy is often helpful for GTPS, which likely reflects improvement in tendinosis rather than bursitis. (See "Greater trochanteric pain syndrome (formerly trochanteric bursitis)".)
EPIDEMIOLOGY —
The most common types of bursitis are prepatellar, olecranon, and retrocalcaneal [6]. While accurate prevalence and incidence data for bursitis are lacking, bursitis is typically more frequent in adults as compared with children and occurs equally in males and females. (See "Knee bursitis", section on 'Epidemiology'.)
ETIOLOGY —
Bursitis develops usually in response to trauma, chronic overuse, infection (also known as septic bursitis), or certain systemic rheumatic diseases (eg, gout, rheumatoid arthritis [RA]):
●Mechanical causes – Mechanical causes of bursitis include trauma, prolonged pressure (eg, leaning on the elbow, kneeling), overuse, and strenuous activity. Mechanical imbalance can cause bursitis locally or in more distant locations (eg, patients with knee pain may develop greater trochanteric pain syndrome in the contralateral hip) [7].
●Infection – Infection is responsible for roughly one-third of bursitis cases. Septic bursitis usually presents acutely and most commonly affects superficial bursae [8]. Staphylococcus aureus is the most common pathogen, accounting for 80 percent of cases in olecranon or prepatellar bursitis [8]. However, there are rare cases of atypical organisms like fungi causing subacute or chronic bursitis [9]. Superficial bursae are affected more often as infection primarily spreads from nearby cellulitis or direct inoculation through trauma [10,11]. Uncommonly, septic bursitis may be caused by nearby septic arthritis or hematogenous spread in patients with bacteremia. (See "Septic bursitis".)
●Crystalline arthropathies – Bursitis can be the initial presentation of gout [12,13] and is also commonly seen as a complication of chronic tophaceous gout. Calcific bursitis in association with the deposition of calcium hydroxyapatite crystals has also been described, particularly in the subacromial bursa [14]. (See "Gout: Clinical manifestations and diagnosis", section on 'Typical clinical manifestations' and "Gout: Clinical manifestations and diagnosis", section on 'Tophaceous gout'.)
●Inflammatory arthritis – Bursitis has been described in many types of inflammatory arthritides, including RA [15,16], juvenile idiopathic arthritis (JIA) [17], and systemic sclerosis [18]. In particular, intermetatarsal bursitis has been described as a potential precursor to RA [15]. (See "Clinical manifestations of rheumatoid arthritis".)
●Polymyalgia rheumatica – Subacromial and trochanteric bursitis are part of the classification criteria for polymyalgia rheumatica (PMR) [19]. PMR classically causes bilateral shoulder and hip pain and stiffness and is associated with elevated inflammatory markers (erythrocyte sedimentation rate [ESR] and C-reactive protein [CRP]). It may cause progressive, debilitating, and diffuse bursitides in the shoulder and pelvic girdle regions. Ultrasound may be helpful in identifying multifocal bursitis related to PMR [19]. (See "Clinical manifestations and diagnosis of polymyalgia rheumatica".)
●Osteoarthritis – Osteoarthritis is highly associated with bursitis, likely due to skeletal malalignment, altered body mechanics, and a subsequent increase in pressure around certain bursae. As examples, iliopsoas bursitis is associated with osteoarthritis of the hip [20] and greater trochanteric pain syndrome is associated with osteoarthritis of the hip and spine [21].
The most common causes of bursitis vary by age. As an example, adults with popliteal cysts have intraarticular pathology 70 percent of the time, while children rarely do [22].
It is important to recognize that causes of bursitis are not mutually exclusive (eg, patients may have a concurrent septic and gouty bursitis). However, there are very limited published data on such cases, and they are presumably quite rare.
CLINICAL PRESENTATION —
The most common signs of bursitis are pain, swelling, and tenderness near a joint. Patients may also complain of stiffness.
The clinical presentation of bursitis varies depending on whether it is acute or chronic:
●Acute bursitis – Patients with acute bursitis typically develop pain and functional limitations over the course of days. When acute bursitis is related to a systemic condition like crystalline arthropathy or inflammatory arthritis, patients may have systemic symptoms and multiple affected joints and/or bursae. Acute bursitis is most often caused by trauma, infection, or crystalline disease.
●Chronic bursitis – Patients with chronic bursitis often present with symptoms that have been present for weeks to months. Chronic bursitis can present with pain, although in some cases, pain is minimal because the bursa has had time to expand and accommodate the increased intrabursal fluid and associated pressure. Chronic bursitis is most often related to overuse, mechanical pressure, or inflammatory arthritis.
The clinical presentation of bursitis may be confused with other soft tissue and joint disorders, including tendonitis, arthritis, and muscle injury. (See 'Differential diagnosis' below and "Overview of soft tissue musculoskeletal disorders".)
DIAGNOSTIC EVALUATION —
Obtaining a thorough history and physical examination is critical in the evaluation of patients with suspected bursitis and may be sufficient to make the diagnosis in certain scenarios (eg, chronic bursitis with low concern for infection) (algorithm 1). Bursal aspiration may be required when sepsis, crystalline disease (eg, gout), or autoimmune disease (eg, rheumatoid arthritis [RA]) are suspected. Various imaging modalities may be helpful when there is a history of trauma, a need for image-guided bursal aspiration (eg, deep bursae near important anatomical structures), suspected deep bursitis (eg, the iliopsoas bursitis), and/or a possibility of alternative, time-sensitive diagnoses.
History — Obtaining a through history is useful in differentiating between acute and chronic bursitis and in elucidating the cause of bursitis. Helpful historical features include the following:
●Onset of symptoms
●Location of pain and alleviating or exacerbating factors
●Visible changes to the affected area, such as swelling and redness
●Recent trauma or pressure on the affected area
●Repetitive motions affecting the bursa, including occupational history
●History of associated conditions, including crystalline arthropathy and inflammatory arthritis
●Risk factors for septic bursitis, such as recent cellulitis or intravenous drug use
●Associated symptoms, such as fever and arthralgia
Physical examination — We perform a detailed musculoskeletal and skin examination looking for evidence of bursitis as well as potentially associated conditions (eg, tophi (picture 1 and picture 2) to suggest chronic gout, rheumatoid nodules (picture 3) or other joint involvement to suggest RA).
Common physical examination findings in bursitis differ based on the chronicity of the presentation as well as the depth of the affected bursa(e):
●Acute bursitis – Obvious signs of inflammation may be evident upon physical examination for patients with acute bursitis of superficial bursae, including swelling, warmth, and erythema of the overlying skin. However, acute bursitis of deep bursae is seldom associated with visible changes on examination. Careful examination of the skin may reveal evidence of trauma that may have caused hemorrhagic or septic bursitis. There is usually tenderness over the affected area, although this is less common in chronic and deep bursitis.
Active range of motion of a joint adjacent to the involved bursa typically exacerbates pain. By contrast, passive range of motion and joint extension usually do not worsen pain unless the affected bursa becomes compressed. As an example, patients with acute olecranon bursitis can often fully extend their elbow without difficulty, while full active or passive flexion of the elbow is uncomfortable. Similarly, patients with acute prepatellar bursitis are typically most comfortable with their knee in full extension, whereas active or passive knee flexion worsens the pain. This pattern is in contrast to that found in patients with acute arthritis, who often have less pain when holding the affected joint in partial flexion to reduce intraarticular pressure, and more pain with joint extension.
Some symptoms and examination findings occur more commonly with certain causes of acute bursitis. As an example, while fever can be seen with bursitis related to infection or crystalline arthropathy, only 20 percent of patients with septic bursitis manifest fever [23]. In addition, a lack of focal warmth of the skin overlying the affected bursae substantially reduces suspicion for septic bursitis, while increased warmth is typically seen in septic bursitis and, less commonly, in bursitis related to other inflammatory causes (eg, gout, RA). In an observational study of 46 patients with olecranon bursitis, all 11 cases of septic bursitis had focal warmth of the affected area, compared with only half of the 35 nonseptic cases [24].
●Chronic bursitis – Patients with chronic bursitis of superficial bursae may have bursal swelling and bursal wall thickening that can be palpated on examination. Local warmth and overlying erythema are usually less marked than in an acute process. Patients with chronic bursitis can have pain with movements that compress the affected bursae, as in acute bursitis. However, for superficial bursae, pain is typically less than expected given the degree of swelling.
When to aspirate — Aspiration of an inflamed bursa is indicated whenever there is a question of septic bursitis or bursitis secondary to crystalline arthropathy or autoimmune disease (algorithm 1). The procedure can be both diagnostic and therapeutic since it relieves intrabursal pressure. Aspiration of a superficial bursa can be performed in the primary care and urgent care setting, if the clinician feels comfortable, and is also performed routinely in rheumatology and orthopedic surgery clinics. (See "Septic bursitis", section on 'Obtaining bursal samples'.)
●Image-guided aspiration – When available, ultrasonography prior to or with aspiration can help identify potential loculations and the optimal place for needle insertion. Ultrasonography or computed tomography (CT) guidance are more important to guide aspiration when the affected bursa is deep, relatively inaccessible, and/or near other important structures (eg, a major artery or nerve). Otherwise, experienced providers may use palpation alone to guide aspiration of easily accessible bursae. More information on using musculoskeletal ultrasound for aspiration is provided separately. (See "Musculoskeletal ultrasonography: Guided injection, aspiration, and biopsy of joints and related structures".)
●Evaluation of bursal fluid – We grossly examine bursa fluid samples for evidence of inflammation, such as cloudiness or purulence. If the fluid appears grossly inflammatory, we send formal laboratory testing including a Gram stain, bacterial culture (aerobic and anaerobic), white blood cell (WBC) count with differential, and assessment for crystals by polarizing light microscopy.
When bursitis is not caused by infection [25], crystalline arthropathy [26], or autoimmune disease [27], fluid is typically bland (WBC count <500/mm3) and nonbloody. When interpreting the synovial fluid cell count, it is important to recognize that cell counts tend to be substantially lower in bursal samples compared with intraarticular samples. As an example, most series report synovial fluid WBC count of <2,000/mm3 in 10 to 20 percent of septic bursitis cases, which would be quite rare in septic arthritis [28]. In bursitis related to gout, monosodium urate crystals may be visible microscopically or grossly (as chalky particulate matter). Laboratory analysis of bursal fluid is discussed in more detail elsewhere. (See "Septic bursitis", section on 'Obtaining bursal samples'.)
When to image — Most patients can be diagnosed with bursitis through the above evaluation including history, physical examination, and potential aspiration. However, imaging is sometimes indicated in certain clinical scenarios including the following (algorithm 1):
●Guiding aspiration – As discussed above, ultrasound or CT may be helpful to guide aspiration, especially when it is difficult to guide the needle with palpation alone (eg, deep bursae, bursae that are close to major nerves or vessels) or in the case of loculations. (See 'When to aspirate' above.)
●Trauma – When there is a history of trauma, we obtain radiographs of the affected area to look for nearby fractures and foreign bodies. Notably, bursae are not radio-opaque so will not be visualized directly.
●Suspected deep bursitis – Deeper bursae (eg, the iliopsoas bursa) are more difficult to palpate, which often limits the sensitivity and specificity of the physical examination. Imaging may therefore be helpful to confirm a diagnosis of bursitis and/or exclude alternative diagnoses.
●Time-sensitive conditions – Bursitis in certain locations may mimic other conditions where timely diagnosis and treatment are imperative. As an example, early septic arthritis of the hip may present similarly to iliopsoas bursitis and often requires timely surgical intervention. The optimal modality and potential use of contrast depends on the differential diagnosis being considered.
The best imaging modalities to directly visualize bursae include ultrasonography and magnetic resonance imaging (MRI):
●Ultrasound – Ultrasound has the advantage of being able to dynamically evaluate the bursa and nearby joint by incorporating specific active and passive range of motion techniques, which affords a better understanding of the relationship between structures than static imaging. The use of ultrasound power Doppler can identify increased blood flow around an abnormal bursa. Ultrasound can also be used to guide aspiration. More information on the use of musculoskeletal ultrasound, including applications for bursitis, is provided separately. (See "Musculoskeletal ultrasonography: Nomenclature, technical considerations, and basic principles of use" and "Musculoskeletal ultrasonography: Clinical applications", section on 'Bursae'.)
●MRI – MRI may be more useful than ultrasound for deep bursitis and bursae without good ultrasound windows due to overlying bone (eg, the scapulothoracic bursa). More information on the uses of MRI in imaging painful joints and contraindications to this modality (eg, indwelling metal hardware) are discussed separately. (See "Imaging techniques for evaluation of the painful joint", section on 'Magnetic resonance imaging'.)
Other imaging modalities such as radiography and CT are used less often. Bursae are not radio-opaque and therefore are not well visualized on radiographs. However, radiography can reveal soft tissue swelling, bursal calcifications or tophi, and intrabursal gas (eg, related to aspiration or certain types of septic bursitis). CT may sometimes be used to guide aspiration when ultrasonography is not available.
DIAGNOSIS —
The diagnosis of bursitis is made clinically based on a suggestive history and consistent physical examination. Key clinical features of bursitis depend on the cause, location, and chronicity but often include tenderness, pain with movements that increase bursal pressure (often joint flexion), swelling of superficial bursae, and overlying warmth. Aspiration should be performed if there is a suspected underlying infection, microcrystalline disorder (eg gout), or autoimmune disease (eg, rheumatoid arthritis [RA]). Bursal fluid should be nonbloody and bland (white blood cell [WBC] count <500/mm3) in cases of bursitis that are not caused by infection, gout, or autoimmune disease.
DIFFERENTIAL DIAGNOSIS —
The differential diagnosis of bursitis includes arthritis, tendonitis, muscle injury, fracture, cellulitis and other soft tissue infections, benign and cancerous soft tissue tumors, calcific deposits, gouty tophi, and rheumatoid nodules. Submuscular or deep bursitis may be especially difficult to differentiate from other musculoskeletal issues due to the lack of visible and/or palpable swelling on examination.
●Inflammatory arthritis – Patients with acute arthritis often have less pain when holding the affected joint in partial flexion to reduce intraarticular pressure, and more pain with joint extension. By contrast, patients with bursitis often feel more pain with joint flexion that compresses the bursa. Patients with various types of inflammatory arthritis may develop related bursitis or other clinical manifestations that mimic bursitis (eg, arthritis, enthesitis). (See "Evaluation of the adult with polyarticular pain".)
●Tendinopathy – Patients with tendonitis will have pain with movements that stretch or load the tendon and may have visible thickening of superficial tendons (eg, the Achilles tendon). (See "Tendinopathy: Overview of pathophysiology, epidemiology, and presentation".)
●Enthesitis – Enthesitis happens when there is irritation at the insertion sites of tendons and ligaments onto bone (figure 1). There should be focal tenderness over the insertion site, as well as worsening pain with stretching or loading of the associated ligament or tendon. The presence of enthesitis raises concern for possible underlying spondylarthritis. (See "Overview of soft tissue musculoskeletal disorders", section on 'Enthesitis'.)
●Fracture – Bone fractures may be confused with bursitis or co-occur with bursitis. As examples, subacute presentations of stress fractures may be mistakenly diagnosed as bursitis, and acute fractures and hemorrhagic bursitis can co-occur in the setting of trauma.
●Rheumatoid nodules – Subcutaneous rheumatoid nodules are firm, nontender nodules that are typically 1 to 2 cm in diameter (picture 3) and are seen in patients with rheumatoid arthritis (RA). They have a predisposition to form over areas of pressure or repeated trauma, such as the olecranon process and extensor surfaces. Rheumatoid nodules can be mistaken for bursitis or may co-occur in patients with bursitis related to RA. (See "Rheumatoid nodules".)
●Tophaceous gout – Tophi consist of monosodium urate crystals that have been deposited in bursae, tendons, or other soft tissues. They may be painful during gout flares but are otherwise nontender. An inflamed tophus can mimic bursitis or accompany bursitis related to gout. (See "Gout: Clinical manifestations and diagnosis", section on 'Tophaceous gout'.)
TREATMENT —
The primary treatment goal for patients with bursitis is reducing pain and therefore improving mobility in hopes of reducing the risk of developing complications such as joint contractures or muscle weakness. It is also important to address any contributing factors, such as joint overuse, mechanical imbalance, or systemic rheumatic diseases. The treatment of septic bursitis is discussed separately. (See "Septic bursitis", section on 'Treatment'.)
Initial therapy for all patients — Patients with bursitis may benefit from relative rest, bursa protection, cold compresses, and analgesia.
●Relative rest, rehabilitative exercise, and joint protection – Avoiding repetitive movements of and pressure over the affected bursa can help speed improvement. Depending on the location of the affected bursae, patients may benefit from various assistive devices to help protect the joint from irritation, such as cushions, pads, splints, braces, and/or custom-fit orthotics. As an example, we typically use a compression bandage to treat olecranon bursitis. (See 'Olecranon bursitis' below.)
When patients have bursitis due to chronic repetitive microtrauma, we also provide education about bursa protection. Some patients may benefit from physical therapy, especially for shoulder bursitis. (See "Overview of joint protection" and "Joint protection program for the upper limb" and "Joint protection program for the lower limb".)
●Cold compresses – Using cold compresses with ice may help temporarily relieve pain from bursitis. Typically, compresses may be applied for 15 minutes every few hours, taking care to avoid frostbite. The use of ice for superficial and deep bursitis is similar to its use for soft tissue musculoskeletal injuries, which is described in detail elsewhere. (See "Initial management of soft tissue musculoskeletal injuries", section on 'Ice (cryotherapy)'.)
●Analgesic and antiinflammatory medications – We frequently prescribe a short course of nonsteroidal antiinflammatory drugs (NSAIDs) to reduce pain and inflammation from bursitis. For patients with a contraindication to systemic NSAIDs, topical NSAIDs may be an alternative. Less commonly, oral glucocorticoids may be required to treat bursitis related to a systemic disease and/or when patients cannot take NSAIDs.
•NSAIDs for most patients – In patients who do not have a contraindication to NSAIDs, we typically provide a one- to two-week course of NSAIDs to help reduce inflammation and pain. As an example, ibuprofen may be given at doses of 600 to 800 mg three times daily, or naproxen may be given at doses of 375 to 500 mg twice daily, as summarized in the table (table 1). Cyclooxygenase 2 (COX-2) selective NSAIDs may be preferable for patients who are at higher risk of gastroduodenal toxicity. Additionally, some patients with a relative contraindication to systemic NSAIDs may still be a candidate for topical NSAIDs (eg, diclofenac gel) given the limited systemic absorption of these forms. (See "Overview of COX-2 selective NSAIDs".)
Indications for prophylaxis for gastrointestinal complications of NSAIDs, as well as other potential adverse effects of and contraindications to NSAIDs, are discussed in detail elsewhere. (See "Nonselective NSAIDs: Overview of adverse effects" and "NSAIDs: Adverse cardiovascular effects" and "NSAIDs (including aspirin): Primary prevention of gastroduodenal toxicity".)
Data to support the use of NSAIDs in the treatment of bursitis are very limited. In a trial of 306 patients with acute shoulder tendinitis or bursitis, those who were randomized to take naproxen (500 mg twice daily) or celecoxib (400 mg once, followed by 200 mg twice daily) experienced greater improvements in pain after 7 days compared with those taking placebo [29]; however, this may reflect improvement in tendonitis rather than bursitis. In another trial that randomly assigned patients with nonseptic olecranon bursitis to naproxen or placebo, the rates of improvement in bursal swelling and the likelihood of recurrence were similar between the two groups [30].
●Indications for oral glucocorticoids – While not commonly used, oral glucocorticoids may be indicated for certain groups of patients with a contraindication to the use of NSAIDs and/or those who have other clinical manifestations of a related systemic condition (eg, a flare of polyarticular gout or inflammatory arthritis). In the case of gouty bursitis, we typically use 0.5 to 1 mg/kg daily of prednisone or its equivalent for 5 to 14 days, depending on the severity of the bursitis. Ideally, the patient should receive the lowest dose of glucocorticoids that relieves symptoms for the shortest duration possible. Contraindications, adverse effects, and monitoring of systemic glucocorticoids are described in detail elsewhere. (See "Overview of the pharmacologic use of glucocorticoids" and "Major adverse effects of systemic glucocorticoids".)
●Treatment of underlying systemic disease – Patients with bursitis due to an underlying systemic disease (eg, gout, RA) require targeted therapy for their related condition. Treatment of related systemic diseases is addressed separately in the respective disease-specific treatment topics.
Intrabursal glucocorticoid injections — Our approach to using intrabursal glucocorticoid injections depends on the location of the affected bursae:
●Deep bursitis – For patients with bursitis in a deep location, we often offer an intrabursal glucocorticoid injection as an adjunct to the other components of initial therapy. This may be beneficial therapeutically and diagnostically (ie, when trying to distinguish bursitis from other conditions that do not respond to glucocorticoids). Evidence to support this approach is very limited, but in the authors' experience it may be useful when NSAIDs and other more conservative measures only offer partial relief of symptoms. The potential use of intrabursal glucocorticoid injections in several specific types of deep bursitis is discussed in more detail separately:
•Subacromial/subdeltoid bursitis (see 'Subacromial/subdeltoid bursitis' below)
•Retrocalcaneal bursitis (see 'Retrocalcaneal bursitis' below)
•Greater trochanteric pain syndrome (formerly trochanteric bursitis) (see "Greater trochanteric pain syndrome (formerly trochanteric bursitis)", section on 'Oral NSAIDs or glucocorticoid injection')
•Pes anserinus pain syndrome (formerly anserine bursitis) (see "Knee bursitis", section on 'Persistent symptoms')
●Superficial bursitis – Using intrabursal glucocorticoid injections to treat superficial bursitis is somewhat controversial due to a potential increased risk of complications such as infection, skin atrophy, and formation of a sinus tract overlying the bursae. While they are rarely used as first-line therapy for superficial bursitis, they are sometimes offered after counseling patients about such risks for superficial bursitis in certain locations. (See 'Olecranon bursitis' below and "Knee bursitis".)
Intrabursal glucocorticoid injections are not given when there is a concern for potential septic bursitis.
●Technique – The procedure for an intrabursal glucocorticoid injection is similar to the one used for bursal aspiration, as are the indications for the potential use of imaging to guide needle placement. (See 'When to aspirate' above.)
Using either palpation or imaging to guide needle placement, we use a 25 gauge needle to both aspirate and inject the affected bursa. If the bursa is deep and/or we expect its contents to be particularly viscus (eg, pus), we use a larger gauge needle (ie, at least 22 gauge). We choose the needle length depending on the depth of the bursa being targeted (eg, 1.5-inch for superficial bursae, 3-inch for deeper bursae). The approach to bursal injection should avoid lines of tension; as an example, for olecranon or prepatellar bursitis, we direct the needle from the side rather than in an anterior to posterior direction. Avoiding lines of tension and the use of a small caliber needle may reduce the chance of creating a non-healing sinus tract that could require a subsequent bursectomy [30,31].
The dosing of glucocorticoids for intrabursal injections mirrors the dosing used for intraarticular injections, but the data to support specific doses and the frequency of injections are extremely limited [32]. Dosing of intrabursal glucocorticoid injections is described in more detail separately. (See "Intraarticular and soft tissue injections: What agent(s) to inject and how frequently?".)
●Complications – Potential complications from glucocorticoid injection include infection, bleeding, creation of a nonhealing sinus tract, skin or subcutaneous atrophy, damage to nearby structures, postinjection flare, vasovagal reactions, and exacerbation of hyperglycemia and of heart failure [33]. They are similar to potential complications from intraarticular glucocorticoid injections, which are described in detail separately; however, there may be a higher risk of infection, nonhealing sinus tract, and subcutaneous atrophy from injection of the superficial bursa. (See "Joint aspiration and injection in adults: Complications".)
Postinjection flare may present with localized pain, swelling, and redness at the injection site within the first 24 hours after the procedure. It can be challenging to distinguish this from iatrogenic septic bursitis, and it may be necessary to repeat aspiration for further evaluation and administer empiric antibiotics. Key distinguishing features of postinjection flare are that symptoms start sooner (usually within 24 hours of injection, compared with a later onset after 24 hours of iatrogenic septic arthritis) and spontaneously improve, typically within 48 hours. (See "Joint aspiration and injection in adults: Complications", section on 'Postinjection flare'.)
Patients may also experience generalized or facial flushing, which can mimic an allergic reaction but lacks other classic signs and symptoms of drug allergy such as hives and pruritus (table 2). (See "Joint aspiration and injection in adults: Complications", section on 'Facial flushing'.)
Surgery in selected patients — Surgical intervention is rarely indicated for bursitis. However, it may be considered in certain situations, including the following:
●Recurrent septic bursitis (see "Septic bursitis", section on 'Bursal drainage')
●Chronic bursitis of superficial bursae (eg, olecranon bursitis) in patients without rheumatoid arthritis (RA)
●Large tophaceous bursa deposits, especially when there is subsequent formation of a sinus tract between the skin and the bursa [34,35]
Bursectomy may be done as an open procedure or, in some cases, endoscopically (eg, olecranon bursitis) [36-38]. Generally, we avoid bursectomy for olecranon bursitis in patients with RA due to an increased rate of complications (see 'Olecranon bursitis' below).
SPECIFIC BURSITIS SYNDROMES
Shoulder — Shoulder bursitis is a common problem, including bursitis that affects the subacromial/subdeltoid and subscapular bursae. It can occur concomitant with other shoulder conditions such as adhesive capsulitis and rotator cuff tears. (See "Frozen shoulder (adhesive capsulitis)" and "Presentation and diagnosis of rotator cuff tears".)
Subacromial/subdeltoid bursitis — The subacromial/subdeltoid bursa is bordered inferiorly by the supraspinatus muscle and superiorly by the acromion, coracoid, coracoacromial ligament, and deltoid muscle (figure 2). Subacromial bursitis is most often caused by recurrent overuse, trauma, subacromial impingement, calcific tendinopathy, infection, inflammatory arthritis, and polymyalgia rheumatica (PMR). It is equally common in older and younger individuals.
Pain from subacromial/subdeltoid bursitis usually is localized to the anterolateral aspect of the shoulder. The skin overlying the bursa may be warm, swollen, and, in rare cases, erythematous. Pain can be elicited by abducting the arm to 80 degrees, which causes the acromion to compress the inferior aspect of the bursa.
Our general approach to patients with suspected subacromial/subdeltoid bursitis is as follows:
●Evaluate for rotator cuff tendinopathy and/or tear – If clinical history or shoulder examination suggests the possibility of a complete rotator cuff tear, additional imaging should be considered (eg, ultrasound or MRI) to determine if surgical intervention is an option. (See "Presentation and diagnosis of rotator cuff tears".)
●Initial management – In addition to the measures outlined above for the initial treatment of bursitis, patients with subacromial/subdeltoid bursitis may benefit from glucocorticoid injections and physical therapy. (See 'Initial therapy for all patients' above.)
•Glucocorticoid injection – We typically offer a glucocorticoid injection to most patients with suspected subacromial bursitis. These injections can provide symptomatic relief as well as further diagnostic clarity.
Data to support the use of glucocorticoid injections in subacromial/subdeltoid bursitis are limited and also challenging to interpret. This is because studies frequently conflate true subacromial bursitis with rotator cuff tendinosis, and these conditions frequently cooccur; as many as 90 percent of patients with a symptomatic subacromial bursa effusion may also have a rotator cuff tear [39]. The matter is made more complicated by the presence of subacromial bursa fluid in just over three percent of asymptomatic, ostensibly healthy shoulders [40], which may lead to a misdiagnosis of subacromial bursitis.
With these limitations in mind, a meta-analysis including 20 trials found that image-guided injections for shoulder pain were superior to blind ones in some outcomes (eg, pain, shoulder functionality) but not others (eg, disability, adverse effects) [41]. A subsequent trial randomly assigned 111 patients with chronic subacromial bursitis to receive one of three interventions: two subdeltoid glucocorticoid injections, eight weeks of physical therapy, or both [42]. While those who received glucocorticoids had improved short-term symptom relief compared with those who only received physical therapy, this was at the cost of a higher risk of symptom recurrence (36, 8, and 17 percent in the groups receiving glucocorticoids alone, physical therapy alone, or combination therapy, respectively). In addition, one study that randomly assigned 136 patients with subacromial bursitis to receive a low-volume injection (1 mL of triamcinolone acetonide) or a high-volume one (1 mL of triamcinolone acetonide plus 9 mL of anesthetic agents) found that patients in the latter group were more likely to experience early pain recovery [43].
•Physical therapy – A physical therapy program can be helpful to maintain a normal range of motion and improve shoulder biomechanics. Pain control prior to physical therapy allows for full participation.
Subscapular bursitis — There are a number of bursae that facilitate gliding movement of the scapulothoracic joint. The two major anatomical bursae are the supraserratus bursa (also known as the subscapularis bursa) and the infraserratus bursa (also known as the scapulothoracic bursa).
●Supraserratus (subscapularis) bursitis – The supraserratus bursa is found between the subscapularis muscle and serratus anterior of the chest wall (image 1) [44]. It is debatable whether it is a separate pouch or connected to the subscapularis recess, which is part of the glenohumeral joint capsule. Bursitis here causes pain along the inside border of the shoulder blade and upper back. Patients may complain of pain and ache in the shoulder which is worse with raising the arm or lying on the affected side. It is most commonly caused by overuse (eg, reaching, lifting, and throwing) but can also be caused by trauma or inflammatory arthritis. Alternative diagnoses that may cause similar symptoms include chondromatosis (proliferative disease of synovium with cartilage metaplasia that results in multiple articular loose bodies) and osteochondromas [45]. The diagnosis can usually be made clinically but, in cases of diagnostic uncertainty, MRI is the optimal imaging modality. The management of supraserratus bursitis is the same as the approach outlined above. (See 'Initial therapy for all patients' above.)
●Infraserratus (scapulothoracic) bursitis – The infraserratus bursa provides a stable surface for the concave contour of the anterior scapular to glide over the convex surface of the thoracic cage during shoulder motion. Infraserratus bursitis results from overuse of the shoulder girdle and may also be related to osseous lesions, non-osseus lesions (eg, a soft tissue mass), scapular dyskinesis (ie, abnormal positioning of the scapula), and postural defects. The degree of shoulder pain from infraserratus bursitis varies from mild soreness to debilitating pain. With continued irritation, recurrent and refractory fibrosis of the bursa leads to a snapping sensation, known as chronic painful snapping scapula or snapping scapula syndrome [46]. This syndrome is characterized by audible crepitus, popping, or clicking with arm movements and may be asymptomatic or cause significant pain and disability [47]. As with supraserratus bursitis, the diagnosis is usually made clinically but in cases of diagnostic uncertainty can be confirmed by MRI.
For patients with infraserratus bursitis related to non-osseous lesions or scapular dyskinesis, we usually offer local glucocorticoid injection and physical therapy. When the condition is caused by osseous lesions, surgery may be necessary; often this involves an open or endoscopic bursal excision with partial scapulectomy of the region of superomedial impingement [48]. Otherwise, management is as outlined above. (See 'Initial therapy for all patients' above.)
Olecranon bursitis — The olecranon bursa is superficial to the olecranon and is prone to infection and trauma due to its location and lack of vascularity (figure 3). It is one of the two most common superficial bursitides and is often caused by repetitive trauma, followed by gout, RA, and infection [49].
Classic examination findings that are diagnostic of olecranon bursitis include very obvious swelling at the olecranon process (picture 4) and preserved range of motion in the elbow. Elbow range of motion is only limited in cases of very severe swelling. The presence of underlying RA or gout is suggested by adjacent rheumatoid nodules (picture 3) or intrabursal tophi, respectively. Providers should maintain a high level of suspicion for septic bursitis and consider bursal aspiration. Systemic features suggestive of infection, such as fever, may not be present in most individuals, regardless of the competence of their immune system; however, local surface heat should substantially raise the level of suspicion for bacterial infection. (See 'Diagnostic evaluation' above.)
Management of olecranon bursitis is consistent with the approach outlined above, with the addition of adjunctive orthoses, bursal drainage, and (rarely) surgical removal (see 'Initial therapy for all patients' above):
●Orthosis – Shielding the olecranon bursa with an orthosis or compression bandage and pad can be helpful to reduce pain, protect the bursa from trauma while it is enlarged, and prevent fluid from reaccumulating after bursal aspiration. An orthosis is typically a hard shell with soft padding inside that allows for full range of motion; it can be custom fit by occupational therapists when available.
●Drainage – Bursal aspiration is frequently indicated for patients with olecranon bursitis to exclude bursitis related to infection and/or crystalline arthropathy (see 'When to aspirate' above). In addition to its diagnostic utility, aspiration may be therapeutic by decompressing the bursal sac and therefore relieving pain. However, an orthosis should be placed immediately after to reduce risk of reaccumulation of fluid and abrasive microtrauma. We avoid repeated aspiration due to the high likelihood of reaccumulation of fluid and low but important risk of iatrogenic septic bursitis.
●Avoidance of intrabursal glucocorticoids – As discussed above, there is some controversy around the safety of administering intrabursal glucocorticoids for superficial bursitis. For patients with olecranon bursitis, we first try conservative measures; however, if patients fail to improve after one to two weeks, then we discuss the potential risks of the procedure and offer a glucocorticoid injection, while monitoring closely for infection. (See 'Intrabursal glucocorticoid injections' above.)
In a systematic review of four studies for nonseptic olecranon bursitis, one observational study found a 12 percent infection risk, while the two controlled trials that included a total of 48 patients who were randomly assigned to receive intrabursal glucocorticoids did not identify any infectious complications [33]. The authors speculated that the protocolized injection technique, which avoided injection over the bony prominence of the olecranon, may have been responsible for the lack of infection in the randomized controlled studies. Glucocorticoid injections generally led to an earlier and more complete resolution of pain and swelling compared with other types of interventions; however, the rate of symptom resolution and bursa tenderness level were similar between the groups.
●Surgical removal in chronic olecranon bursitis – Rarely, patients with chronic olecranon bursitis may benefit from an arthroscopic bursectomy; however, we avoid surgical intervention for patients with underlying RA due to a lower likelihood of effectiveness and higher rate of complications.
The specific indications for surgical removal are not well defined and supportive data are very limited [50]. In a retrospective study of 21 patients with chronic, noninfectious olecranon bursitis, surgical treatment led to resolution of symptoms in 94 percent of the 16 patients who did not have associated RA; by contrast, only 40 percent of the five patients with associated RA experienced similar improvements [51]. Another retrospective review of 191 adults who underwent olecranon bursa excision found that those with comorbid RA and diabetes mellitus had higher rates of revision and flap surgery [52].
Hip and pelvis — Inflammation of various bursae may cause hip pain, including the ischiogluteal, iliopsoas, and trochanteric bursae.
Ischiogluteal bursitis — The ischiogluteal (ischial) bursa is located between the ischial tuberosity and the gluteus maximus muscle (figure 4). Associated bursitis may present with pain in the upper thigh or gluteal region following repeated movement of the gluteus maximus muscle and/or prolonged sitting (thus leading to this condition being known as "weaver's bottom"). It is therefore associated with a wide range of activities and situations, including cycling, horseback riding, canoeing, tractor driving, and prolonged sitting in paraplegic patients. Ischiogluteal bursitis can cause symptoms suggestive of sciatica due to its proximity to the sciatic nerve; however, pain with sitting tends to be less focal and prominent when sciatica is due to other causes (eg, herniated lumbar disc).
Our general approach to patients with suspected ischiogluteal bursitis is as follows:
●Imaging to assess for alternative diagnoses – Depending on the location of pain and associated symptoms, imaging of the hip joint, lumbar spine, and/or pelvis may be required to rule out alternative diagnoses. The diagnosis of ischiogluteal bursitis can be made on MRI based on the characteristic location and cystic appearance [53]. MRI is also usually sufficient to evaluate for alternative diagnoses, including causes of sciatica, sacroiliitis, pelvic enthesitis, neoplasms, hematomas, and focal infections. Other imaging modalities are suboptimal for evaluation of ischiogluteal bursitis as they may not be sensitive enough to detect these alternative diagnoses. (See 'When to image' above.)
●Treatment – Treatment of ischial bursitis is similar to that for other types of bursitis, including protecting the bursa (eg, a "donut" pillow), modifying activity, controlling pain, and sometimes injecting intrabursal glucocorticoids. When intrabursal glucocorticoid injections are used, we use ultrasound guidance to avoid injury to the adjacent tissues, including the sciatic nerve. (See 'Initial therapy for all patients' above.)
Iliopsoas bursitis — The iliopsoas bursa is the largest synovial bursa in the body and is located between the iliopsoas muscle and the anterior capsule of the hip, adjacent to the thinnest and most vulnerable portion of the anterior capsule. Iliopsoas bursitis is characterized by distention of the bursa due to fluid or hypertrophic synovium and is usually associated with disease of the hip joint. Patients typically present with hip pain and notable swelling, which can rarely appear as an inguinal mass. Iliopsoas bursitis can also arise due to excessive friction between involved anatomic parts in snapping hip syndrome, where the iliopsoas tendon snaps over a hypertrophied iliacus muscle onto the pubic bone and produces a palpable and/or audible snap [54].
The main causes of iliopsoas bursitis are acute trauma, overuse, and RA, and it can also be seen in patients with advanced hip OA [55]. Activities that can be associated with overuse include heavy lifting (ie, the hip is forcefully hyperextended due to a sudden backward thrust of the body) and sports such as strength training, rowing, uphill running, and track and field. There is often coexistence of other iliopsoas-related conditions such as tendinitis [56]; the term "psoas syndrome" has been used to collectively describe these entities.
Our general approach to patients with suspected iliopsoas bursitis is as follows:
●Imaging to assess for alternative diagnoses – Imaging is usually required to exclude alternative diagnoses, especially when there is mass effect from swelling as can be seen with hernias, lymphadenopathy, and neoplasms. This area is particularly amenable to ultrasound imaging. However, MRI may be required if there is suspicion for possible avascular necrosis of the femoral head.
●Treatment – The treatment of patients with iliopsoas bursitis is consistent with the general approach outlined above. (See 'Treatment' above.)
Greater trochanteric pain syndrome — Greater trochanteric pain syndrome (formerly known as trochanteric bursitis) is a common cause of lateral hip pain. The primary pathology is thought to be tendinopathy of the gluteus medius or minimus muscles in most cases, although sometimes there is associated bursitis (figure 5). The diagnosis and management of this condition is discussed in more detail elsewhere. (See "Greater trochanteric pain syndrome (formerly trochanteric bursitis)".)
Knee — There is a wide variety of types of bursitis around the knee, most commonly including prepatellar, superficial infrapatellar, and pes anserine bursitis (also known as pes anserine syndrome). More detail on the diagnosis and management of knee bursitis is provided separately. (See "Knee bursitis".)
Ankle — Retrocalcaneal bursitis is the most common form of ankle bursitis and is sometimes confused with subcutaneous calcaneal bursitis. Less common forms of ankle bursitis include inflammation of the Gruberi bursa and subcutaneous bursae of the lateral and medial malleolus.
Retrocalcaneal bursitis — The retrocalcaneal (subtendinous) bursa lies between the calcaneus and the calcaneal (Achilles) tendon insertion (figure 6). Retrocalcaneal bursitis usually presents with a painful, swollen heel that is tender to the touch. Pain is worsened by dorsiflexion of the foot and by standing on tiptoe. Retrocalcaneal bursitis can co-occur with or be mistaken for plantar fasciitis, as they share common inciting factors (eg, overuse through running and jumping, spondyloarthritis and other rheumatic diseases) and symptoms (heel pain). Diagnosis and management of plantar fasciitis is described separately. (See "Plantar fasciitis".)
Retrocalcaneal bursitis is highly associated with calcaneal tendinopathy, Haglund's deformity (a bony enlargement of the calcaneus) [57], enthesopathy in the setting of a spondyloarthritis, and other forms of inflammatory arthritis [58]. The risk of developing retrocalcaneal bursitis in runners is increased by having a flattened contour of the calcaneal tuberosity; thickening of the calcaneal tendon and a smaller bursal surface area are additional contributory factors [59].
In addition to the general measures described above, management of patients with retrocalcaneal bursitis may include the following: (See 'Treatment' above.)
●Patients with retrocalcaneal bursitis may benefit from modifications to their shoes (eg, using a heel lift and a cushion in the heel area), relative rest and avoidance of inciting activities, and light Achilles tendon stretching exercises (picture 5 and picture 6).
●Intrabursal glucocorticoid injections may be helpful for patients with retrocalcaneal bursitis who do not respond to these measures but carry a risk of Achilles tendon rupture, even when done with imaging guidance (eg, ultrasonography or fluoroscopy). In a retrospective study of 218 patients with retrocalcaneal bursitis who had image-guided intrabursal glucocorticoid injections, 63 percent of patients who had short-term follow-up (between one and four weeks) experienced a good or excellent improvement in pain; however, four patients (1.8 percent) had Achilles tendon ruptures following acute ankle injuries in the two to eight weeks following the injection [60]. If injection is necessary, we use the lowest effective dose of corticosteroid (eg, 10 mg of triamcinolone acetonide) and instruct the patient to wear a controlled ankle movement (CAM) walking boot for two weeks after the injection in order to minimize the risk of tendon rupture.
Other ankle bursae — In addition to retrocalcaneal bursitis, other types of bursitis can affect the ankle. Symptoms may mimic stress fractures, osteoarthritis, and/or sprains. Soft tissue imaging with ultrasound or MRI may be indicated to evaluate for alternative causes of pain when the physical examination is insufficient to establish a diagnosis. (See 'When to image' above.)
●Subcutaneous calcaneal bursitis – The subcutaneous calcaneal bursa (ie, pre-Achilles bursa) is located between the skin and the Achilles tendon and serves to reduce friction between these two structures (figure 6). Subcutaneous calcaneal bursitis can sometimes be confused with retrocalcaneal bursitis due to inconsistencies in the medical and lay literature. This form of bursitis is mainly due to ill-fitting shoes (eg, high heels, tight athletic shoes) causing friction at the back at the heel. Management is similar to that of retrocalcaneal bursitis. (See 'Retrocalcaneal bursitis' above.)
●Gruberi bursitis – The Gruberi bursa (also known as the sinus tarsi bursa) is located between the extensor digitorum longus (EDL) tendons and the talus [61]. This bursa lines the inferior extensor retinaculum (frondiform ligament) as it passes over the EDL tendons at the anterior ankle joint. Because it can be mistaken for tenosynovitis, it has also been called a pseudotenosynovitis of the EDL tendons. Bursitis in this area can cause pain over the dorsolateral portion of the ankle. It may be difficult to distinguish Gruberi bursitis from sinus tarsi syndrome, which can also cause pain and swelling in the lateral ankle; however, the latter condition is typically caused by trauma or excessive movements of the subtalar joints that leads to subsequent bleeding and/or inflammation of the synovial recesses of the sinus tarsi [62]. (See "Hindfoot pain in adults: Evaluation and diagnosis of common causes", section on 'Sinus tarsi syndrome'.)
●Other rarely reported areas of ankle bursitis involve the subcutaneous bursa of the medial malleolus and lateral malleolus, and lateral premalleolar bursa in the dorsolateral aspect of the foot.
INFORMATION FOR PATIENTS —
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics". The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basic patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Bursitis (The Basics)")
●Beyond the basics topic (see "Patient education: Bursitis (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Overview of bursitis – A bursa (bursae in plural) is a lubricated, fluid-filled sac or pouch adjacent to or in between hard or soft tissues that reduces friction and tension between bones, joints, tendons, and/or skin. Bursitis happens when a bursa becomes irritated or inflamed. (See 'Overview of bursitis' above.)
●Etiology – Bursitis can develop in response to trauma, chronic overuse, infection (also known as septic bursitis), or certain systemic rheumatic diseases (eg, gout, rheumatoid arthritis [RA]). (See 'Etiology' above.)
●Diagnostic evaluation
•Physical examination – The most common signs of bursitis are pain, swelling, and tenderness near a joint.
-Acute bursitis – Pain and functional limitations from acute bursitis usually develop over the course of days. Acute bursitis of superficial bursae often causes swelling, warmth, and erythema of the overlying skin, while acute bursitis of deep bursae rarely causes visible changes on examination. Active motion of muscles adjacent to the involved bursa and joint flexion that compresses the bursa typically make the pain worse. By contrast, passive motion and joint extension usually do not worsen pain. (See 'Physical examination' above.)
-Chronic bursitis – Patients with chronic bursitis often present with symptoms that have been present for weeks to months and may present with functional limitations. Patients with chronic bursitis of superficial bursae may have bursal swelling and bursal wall thickening that can be felt on examination. Local warmth and overlying redness are usually less marked than in an acute process, and pain is less than expected given the degree of swelling. (See 'Physical examination' above.)
•When to drain a bursa – Fluid should be removed from an inflamed bursa whenever there is a question of an infectious cause or question of bursitis due to another inflammatory cause. In cases where the affected bursa is deep, relatively inaccessible, and/or near other important structures (eg, a major artery or nerve), imaging (eg, ultrasound or CT) can be used for guidance rather than palpation alone. If the aspirated fluid appears grossly inflammatory (eg, cloudy or purulent), we send testing including a Gram stain, bacterial culture (aerobic and anaerobic), white blood cell count (WBC) with differential, and assessment for crystals by polarizing light microscopy. (See 'When to aspirate' above.)
•When to image – Most patients do not require imaging; however, it may be indicated in the setting of trauma, when guidance is needed for bursal drainage or intrabursal glucocorticoid injection, and/or to exclude alternative diagnoses where timely intervention is imperative. (See 'When to image' above and 'Specific bursitis syndromes' above.)
●Diagnosis – The diagnosis of bursitis is made clinically based on a suggestive history and consistent physical examination. Key clinical features of bursitis depend on the cause, location, and chronicity but often include tenderness, pain with movements that increase bursal pressure (often joint flexion), swelling of superficial bursae, and or bursal wall thickening in chronic bursitis. Bursal fluid should be non-bloody and bland (WBC <500/mm3) in cases of bursitis that are not caused by infection, gout, or other autoimmune disease. (See 'Diagnosis' above.)
●Treatment – The primary treatment goal for patients with bursitis is reducing pain and therefore improving mobility. It is also important to address any contributing factors, such as joint overuse, mechanical imbalance, or underlying systemic rheumatic diseases. (See 'Treatment' above.)
•Initial therapy for all patients – Patients with all types of bursitis can benefit from conservative management, including relative rest, joint protection with compression bandages and padding, cold compresses, and pain relievers. In patients who do not have a contraindication to nonsteroidal antiinflammatory drugs (NSAIDs), we typically provide a one- to two-week course of NSAIDs to help reduce inflammation and pain (eg, ibuprofen 600 to 800 mg three times daily). (See 'Initial therapy for all patients' above.)
Additional therapeutic measures may be helpful for patients with certain bursitis syndromes (eg, physical therapy, specific cushions). (See 'Specific bursitis syndromes' above.)
•Intrabursal glucocorticoid injections– For most patients with bursitis in a deep location, we suggest an intrabursal glucocorticoid injection as an adjunctive therapy with NSAIDs rather than giving NSAIDs alone (Grade 2C). Intrabursal glucocorticoid injections are not given when there is a concern for potential septic bursitis. Intrabursal injections for superficial bursitis may increase the risk of complications. (See 'Intrabursal glucocorticoid injections' above.)
ACKNOWLEDGMENT —
The UpToDate editorial staff acknowledges Karina Torralba, MD, MACM, RhMSUS, who contributed to earlier versions of this topic review.
