INTRODUCTION AND DEFINITION — A bursa is a fluid-filled, saclike structure lined by synovial membrane that forms in clefts between mobile structures in the musculoskeletal system. Bursae deep in the tissues, such as the trochanteric or subacromial bursae, reduce the friction of muscles as they glide over each other or over prominences of bone. The more superficial bursae, such as the olecranon, ischial, or prepatellar bursae, serve to cushion the rubbing between skin and bone.
The term "bursitis" implies inflammation. In many clinical scenarios this is a misnomer, as many specific bursitis syndromes are associated only with tenderness over the bursal structure and not necessarily with overt inflammation that can be documented upon physical exam or imaging.
This topic will review the overall approach to the diagnosis and management of bursitis. A more detailed discussion on specific bursae and septic bursitis can be found elsewhere. (See "Greater trochanteric pain syndrome (formerly trochanteric bursitis)" and "Knee bursitis" and "Septic bursitis".)
ETIOLOGY — Bursitis may result from any one or combination of the following causes:
●Direct injury or trauma. This often results in a hemorrhagic bursitis.
●Prolonged pressure. This can occur after prolonged kneeling or leaning on a structure, such as the elbow.
●Overuse or strenuous activity.
●Crystal-induced processes. This can be seen with acute gouty bursitis or longstanding tophaceous gout.
●Inflammatory arthritis. This can occur in conditions such as rheumatoid arthritis (RA) or spondyloarthritis (eg, psoriatic arthritis).
●Infection (septic bursitis). This can occur due to transcutaneous transit of bacteria from penetrating injury or microtrauma (most commonly) or hematogenous seeding (less commonly). Note that the presence of another cause of bursitis does not exclude the possibility of concurrent infection (eg, superinfection of a tophaceous olecranon bursa).
CLINICAL PRESENTATION AND PHYSICAL EXAMINATION — Among patients with bursitis, obvious signs of swelling and inflammation may be evident upon physical examination, but this is typical only in superficial processes, such as olecranon, prepatellar, infrapatellar, or retrocalcaneal bursitis. Deeper examples of bursitis, such as anserine, subacromial, or trochanteric bursitis, are seldom associated with visible swelling or erythema. Rather, these processes are more typically characterized by pain, tenderness, and functional limitations. There are also differences in presentation based on the acuity or chronicity of the underlying disease process.
Clinical findings
Acute bursitis — In patients with acute inflammatory bursitis, typically due to trauma, microcrystalline disease, or infection, there is tenderness directly over the bursa, with pain elicited by any active motion that employs muscles adjacent to the involved bursa. Passive motion, in which the muscles are not engaged, is normal unless the motion stretches or compresses the adjacent bursa to the point where there is a rise in intrabursal pressure. Thus, patients with acute olecranon bursitis can fully extend their elbow without difficulty, but full active or passive flexion of the elbow is often uncomfortable. Similarly, patients with acute prepatellar bursitis are typically most comfortable with their knee in full extension, whereas active or passive knee flexion is uncomfortable.
Chronic bursitis — Chronic bursitis is more often due to repetitive overuse, microtrauma, or inflammatory conditions such as rheumatoid arthritis (RA) or chronic tophaceous gout. In these situations, the bursa has had time to expand and accommodate the increased intrabursal fluid and associated pressure. Thus, patients with chronic bursitis tend to have more swelling and thickening of superficial bursae out of proportion to pain, which is often minimal. In other situations, secondary changes of contracture and muscle atrophy related to immobility may take place. This can develop in as little as one week, and is the pathophysiology behind the development of frozen shoulder [1]. (See "Frozen shoulder (adhesive capsulitis)".)
Some features of the history may be misleading, as most patients ascribe musculoskeletal symptoms of any nature to either overactivity or a perceived injury, whether they are factors or not. The search for an overt abrasion, puncture wound, or area of cellulitis is particularly important in the evaluation of superficial bursitis. The coexistence of an underlying systemic inflammatory polyarthritis should always be considered as part of the differential diagnosis. A common site for the formation of both rheumatoid nodules and gouty tophi is in the olecranon bursa, although these typically occur with longstanding disease.
It is important to realize that deep forms of bursitis often occur in conjunction with or secondary to abnormalities of adjacent tendons or joints or even abnormalities in remote locations. As an example, greater trochanteric pain syndrome (formerly trochanteric bursitis) often involves trochanteric bursitis concurrent with gluteus medius tendinosis or partial tears, and can be the result of chronic back pain, core muscle deconditioning, or contralateral knee disease (see "Greater trochanteric pain syndrome (formerly trochanteric bursitis)", section on 'Risk factors'). Similarly, pes anserinus pain syndrome can result from pes planus. Obesity is often an exacerbating factor in these weightbearing forms of bursitis.
DIAGNOSTIC TESTING — Diagnostic testing may be necessary if infection or crystal disease is suspected based on the initial medical history and examination. Appropriate studies vary depending on the suspected etiology of the bursitis and the anatomic location (superficial versus deep).
Bursal fluid aspiration and analysis — The two main indications to aspirate a bursa are to rule out infection, and to aid in the diagnosis of a microcrystalline disorder like gout. Non-bloody bland fluid (white blood cell count [WBC] <500/mm3) is a feature of noninfectious and noncrystalline bursitis.
In the case of superficial bursae, aspiration of the bursal fluid is almost always warranted when there is an effusion and signs of local inflammation, such as erythema or tenderness. There is a high incidence of septic bursitis in the superficial olecranon and prepatellar bursae related to skin infections [2,3]. (See "Septic bursitis", section on 'Obtaining bursal samples'.)
There is seldom an indication for a diagnostic aspiration of deep bursae, unless there is evidence of systemic toxicity in which septic bursitis is part of the differential, or if there is suspicion of adjacent septic arthritis. As an example, because the iliopsoas bursa often communicates with the hip joint, imaging evidence of iliopsoas septic bursitis should prompt diagnostic aspiration. This typically requires image assisted needle placement using ultrasonography or computed tomography (CT) guidance.
The bursal fluid obtained can be visually classified as clear, hemorrhagic, cloudy, or purulent. In gouty olecranon bursitis, tophaceous chalk-like material may occasionally be visible to the naked eye. Laboratory analysis of bursal fluid is discussed in more detail elsewhere. (See "Septic bursitis", section on 'Obtaining bursal samples'.)
The need for imaging — Imaging studies are typically not necessary, particularly in the case of superficial bursa where the signs of inflammation are demonstrated on the physical examination. The need for imaging in the evaluation of deep bursal syndromes is dependent on other factors, and a precise anatomical diagnosis is often not necessary, particularly in the initial evaluation. There is little evidence that a strong correlation exists between the clinical presentation of local tenderness and the anatomical evidence of inflammation of the deeper bursae as might be suggested by ultrasound or magnetic resonance imaging (MRI) [4,5].
However, there are some instances in which imaging of suspected bursitis is appropriate. We use imaging in the following scenarios:
●Any situation in which the establishment of a more accurate diagnosis seems imperative. As an example, the classical presentation of iliopsoas bursitis is the presence of groin pain, accentuated by flexing the hip against resistance (see 'Iliopsoas bursitis' below). This finding would also be characteristic of labral tears, early avascular necrosis of the femoral head, or any inflammatory process involving the hip joint. All of these syndromes could be associated with a normal plain radiograph of the hip, and making a definitive early diagnosis may be warranted, depending on the clinical scenario. By contrast, the need to establish a definite diagnosis of subacromial bursitis in the shoulder is generally not critical at the time of presentation.
●Conditions in which the entrance of a needle into the area occupied by the bursa is associated with a significant risk of injury to an adjacent neurovascular structure. This is a factor in attempting an aspiration of the iliopsoas bursa related to its proximity to the femoral artery and nerve.
Choice of imaging typically includes plain radiographs, ultrasonography, and MRI.
As bursae are not radio-opaque, they are not evident on plain radiographs of the joints. A plain film may be taken in the initial evaluation to exclude fracture or the presence of a foreign body. Plain films may also detect calcifications in the region of a bursa, but there is no firm evidence that the presence or absence of a calcification in the region of the bursa correlates with the clinical course of bursitis. One should assume that the calcification was present prior to the onset of symptoms of clinically acute bursitis. Radiographic evidence of gas within a bursa suggests either recent instrumentation (ie, injection of air) or the presence of gas-producing bacteria.
Both ultrasonography and MRI are equally useful in the diagnosis of deep bursal syndromes. When available, we prefer ultrasonography since this imaging technique permits dynamic assessment of the bursa and adjacent structures in motion. Further, ultrasonography can be used simultaneously to guide needle aspiration of the bursa, if necessary.
PRINCIPLES OF MANAGEMENT — With the exception of septic bursitis, the underlying management principle is that isolated bursitis is a self-limited condition that is reversible. In addition, unlike cartilage, the bursa has the ability to heal. In short, bursitis will get better. Therefore, the goal of treatment is to relieve the immediate symptoms, to prevent the secondary complications related to immobilization (muscle atrophy and joint contracture), and to maintain range of motion. Bursitis that is associated with adjacent pathology may improve partially with treatment, but optimal treatment may require techniques specifically directed at the adjacent pathology as well.
Patients should be taught the principles of joint protection and, unless contraindicated, affected individuals should also receive analgesia, which usually consists of a nonsteroidal antiinflammatory drug (NSAID). In addition, our initial approach to the management of presumed irritation of the deeper bursae is typically an intralesional injection of a combination of local anesthetic and glucocorticoid. However, we do not recommend the use of intralesional glucocorticoids in the treatment of the superficial forms of bursitis (olecranon, prepatellar, and retrocalcaneal bursitis) due to the risk of infectious complications, local tendon injury, draining sinus tract, or overlying skin atrophy. Application of an ice pack (for no more than 20 minutes at a time) can offer therapeutic relief of a superficially inflamed bursa. For deep forms of bursitis such as that due to greater trochanteric pain syndrome, a heating pad is often more helpful than ice. Caution must be taken so that a patient does not use the heating pad for more than 20 minutes at a time or fall asleep on an electric heating pad, as to avoid thermal burn.
Joint protection — Patients should be educated in the recognition of aggravating factors, and joint protection advice should be given to the patient. (See "Patient education: Bursitis (Beyond the Basics)" and "Joint protection program for the upper limb" and "Joint protection program for the lower limb".)
The use of kneeling pads is of value for carpet-layers and others whose daily activities predispose them to mechanical injury to the prepatellar bursa. Patients with Achilles-region bursitis may benefit from cutting a "V" groove into the back of their footwear to reduce pressure on the area. The use of soft cushions worn over the olecranon bursa seems to be less effective, but a hard, removable, concave orthosis can be firmly affixed to the elbow with a Velcro strap to provide both shielding and external pressure to prevent fluid from recurring in the bursa after an aspirate. This orthosis should not impede range of motion, and can be custom-fit by an occupational therapist, with soft padding on the inner surface to cushion the elbow.
Nonsteroidal antiinflammatory drugs (NSAIDs) — Nonsteroidal antiinflammatory drugs (NSAIDs) can be used either in conjunction with a local injection, or alone when a local injection is contraindicated or declined by the patient. A randomized trial showed the superiority of either celecoxib (400 mg once followed by 200 mg twice daily) or naproxen (500 mg twice daily) versus placebo for 14 days for treating bursitis [6]. However, the results of this study were not dramatic.
In general, we advocate the initial use of NSAIDs in those patients without a relative contraindication (see "Nonselective NSAIDs: Overview of adverse effects" and "NSAIDs: Adverse cardiovascular effects"). We recommend regular use of a nonselective NSAID, such as ibuprofen (600 to 800 mg three times daily) or naproxen (375 mg or 500 mg twice daily), for several days as initial treatment for acute, nonseptic bursitis. For patients at increased risk of gastroduodenal damage from an NSAID (eg, those with prior ulcer disease, with gastrointestinal bleeding, or currently receiving glucocorticoids or on anticoagulants), a selective cyclooxygenase inhibitor or concurrent prophylactic use of a proton pump inhibitor may be used instead. In addition, for superficial forms of bursitis in which systemic NSAIDs are contraindicated, topical NSAIDs (eg, topical diclofenac) may be an option. Although there is no published clinical trial studying the efficacy of topical NSAIDs in the setting of bursitis specifically, several studies have demonstrated the benefit and safety of topical NSAIDs in various forms of soft tissue musculoskeletal syndromes [7-9]. In our opinion, therefore, it is reasonable to offer a topical NSAID to most patients when systemic NSAIDs are not an option. (See "NSAIDs (including aspirin): Primary prevention of gastroduodenal toxicity".)
For individuals with acute microcrystalline bursitis and a contraindication to the use NSAIDs, a short course of prednisone in the range of 20 mg, tapering down to zero over 10 to 14 days, may be helpful.
Intrabursal injections of glucocorticoids — Our initial approach to the management of presumed inflammation of the deeper bursae is typically an intralesional injection of a combination of local anesthetic and glucocorticoid because of possible therapeutic benefit and additional diagnostic value. This approach is particularly useful for presumed inflammation of subacromial, anserine, medial collateral ligament (in the knee), and trochanteric bursae. (See 'Subacromial bursitis' below and 'Pes anserinus pain syndrome (formerly anserine bursitis)' below and 'Greater trochanteric pain syndrome (formerly trochanteric bursitis)' below and 'Medial collateral ligament bursitis' below.)
The ability to alleviate pain during the anesthetic phase of the procedure provides strong diagnostic evidence that the pain is arising from the area of the bursa. While this does not necessarily confirm that it is an inflammatory process, it can address the condition and avoid, at least in the early stage of evaluation, the perceived need for unnecessary imaging of the adjacent articular structure.
Among patients with superficial forms of bursitis (olecranon, prepatellar, and retrocalcaneal), we generally do not use intralesional glucocorticoids. Available data do not support their benefit, and there is an increased risk of infectious complications, skin atrophy, and development of a draining sinus tract. As an example, a retrospective review of 47 patients with sterile olecranon bursitis described the subsequent clinical course in 25 patients injected with 20 mg of triamcinolone hexacetonide and the 22 patients who received only a diagnostic aspiration [10]. The steroid group responded more rapidly, although both groups were symptom-free after six months. However, complications of infection (three cases), skin atrophy (five cases), and chronic local pain when leaning on the elbow (seven cases) were seen only in the group who received steroids. These complications were felt to be related to skin atrophy associated with the injection, which seemed to have predisposed to the development of the infection.
The injection technique employed is to instill into the presumed site of the bursa with a mixture of 1 to 2 mL of 1 percent Xylocaine and a depository glucocorticoid using a 22 gauge, 1.5 inch needle. Our recommendations concerning choice of glucocorticoid agent and dose are discussed separately (see "Intraarticular and soft tissue injections: What agent(s) to inject and how frequently?", section on 'Use of glucocorticoid injections'). The rationale behind using a larger bore needle is to avoid injecting steroids into a tendon. If one feels resistance when using a larger bore needle, one can assume that the needle is not in a space but is instead in a structure, such as a tendon, which should be avoided. However, if the needle is injected into such a location, its position may then be manipulated until flow is easy. (See "Intraarticular and soft tissue injections: What agent(s) to inject and how frequently?".)
An occasional complication of local steroid injection is the postinjection flare, which is an inflammatory response presumably related to the vehicle of the glucocorticoid preparation. The symptoms arise about 6 to 18 hours after the injection and subside when the steroids become active, less than a day later.
SPECIFIC SYNDROMES
Subacromial bursitis — The subacromial bursa (also known as the subdeltoid bursa) separates the bony acromion process of the scapula from the supraspinatus muscle and tendon (figure 1). Pain arising from subacromial bursitis is typically present at rest, accentuated by use, and referred to the insertion of the deltoid muscle about four inches (or 10 cm) down the outer upper arm. Pain may be severe and can often interrupt sleep; this is related either to applying local pressure to the structure or to the motion that the shoulder makes when one turns and alters the position of the arms during sleep. Frozen shoulder, or adhesive capsulitis, may develop as a consequence of persistently restricted mobility of the shoulder (see "Frozen shoulder (adhesive capsulitis)"). The subacromial bursitis pattern of symptoms usually occurs in conjunction with other pathology such as rotator cuff disease, an impingement syndrome, frozen shoulder, or a systemic inflammatory disorder such as polymyalgia rheumatica (PMR) or rheumatoid arthritis (RA).
The differentiation between a rotator cuff tear, rotator cuff tendinitis, and subacromial bursitis usually cannot be made on the basis of history and physical exam (see "Evaluation of the adult with shoulder complaints"). Theoretically, the presence of a rotator cuff tear is suggested by demonstrated weakness in the involved muscle. However, guarding or atrophy related to the pain tends to cause similar findings. Nevertheless, this differentiation may not be necessary at the time of the initial evaluation unless a significant rotator cuff tear is suspected. As noted in the next section, the diagnosis of bursitis is supported by a positive response to an intralesional injection of glucocorticoids.
Management — Our approach is to offer an injection to the majority of patients with suspected subacromial bursitis. An initial injection into the subacromial bursa may be curative in bursitis, but provide only partial or incomplete benefit in partial rotator cuff tear or a frozen shoulder. In neither of the two latter conditions would an initial injection be detrimental to the patient's long-term welfare. However, it is important to exclude the possibility of a complete rotator cuff tear prior to the injection, since injecting such patients may temporarily relieve pain but delay the diagnosis such that the optimal window of time for surgical correction of the tear is missed. If clinical history or shoulder examination suggests the possibility of a complete tear of the rotator cuff, additional imaging should be considered (eg, ultrasound or MRI). (See "Presentation and diagnosis of rotator cuff tears".)
Patients who do not respond to the initial injection may require more definitive diagnostic imaging at follow-up. These include patients with a complete rotator cuff tear that was initially not recognized. In addition, patients with PMR or RA that is undetected at the time of the initial evaluation may often describe not only rapid local benefit, but also a systemic improvement in symptoms for the few days in which a systemic level of steroids was operative. Statements such as "I did not realize that I was stiff all over, rather than just in the shoulder" are clues to such a diagnosis. For these and other reasons, it is reasonable to consider re-examining the patient within two to three weeks after an injection.
Data are limited about the number or frequency of injections that may be reasonably done for the treatment of bursitis. A systematic review of steroid injections for subacromial shoulder impingement syndrome concluded that patients could potentially benefit from up to three injections administered over a period up to 12 weeks [11]. In our opinion, if the original injection provides several weeks of significant relief, the diagnosis of a soft tissue process seems secure, and a repeat injection may be tried if symptoms warrant. Some data suggest that the frequency of steroid injections for subacromial bursitis is not a risk factor for the development of rotator cuff tears [12]. A Cochrane review of various common interventions for rotator cuff disease, which included many patients with disease not resulting from bursitis, concluded that there were insufficient data to either provide support for or to refute the use of intralesional injections [13]. This uncertainty may therefore be related to the lack of uniformity within the underlying diagnosis.
Limited data suggest that ultrasound-guided injections of the subacromial bursa may be more effective than a "blind" unguided injection [14,15]; however, this was not validated in a large systematic review [16]. As ultrasound guidance is not available in real time in many practices, we do not advocate that the use of ultrasound-guidance is essential when injecting the subacromial bursa.
In addition to the local injection of a depository glucocorticoid into the painful area, nonsteroidal antiinflammatory drugs (NSAIDs) can be advised, unless contraindicated. A physical therapy program aimed at maintenance and/or restoration of motion is paramount and should also be included. Injection prior to physical therapy can control pain and lead to more effective and less painful rehabilitative exercise.
Scapulothoracic bursitis — Scapulothoracic bursitis results from the mechanical pressure and friction between the superior-medial angle of the scapula and the adjacent ribs. Pain and a "popping" sensation are typical complaints. Aggravating activities include repetitive movements such as working overhead, reaching up and forward, or doing pushups. Local tenderness and palpable crepitus are characteristic. An effusion or hemorrhage into the area may be seen on MRI (image 1).
Management — Scapulothoracic bursitis has a relatively benign course and spontaneously regresses in most patients [17]. We therefore suggest an initial conservative approach with referral to physical therapy for postural and scapular strengthening exercises [18]. The addition of NSAIDs may also be helpful. If physical therapy does not relieve symptoms after several weeks, then a glucocorticoid injection may be an option. However, any injection of the upper chest wall structures may cause a pneumothorax and/or nerve injury, and an image assisted approach may be useful [19,20].
Most patients improve with nonoperative measures, but surgical resection of the bursa and a portion of the scapula may provide relief in refractory cases [21,22].
Olecranon bursitis — The olecranon bursa, located posteriorly over the olecranon process of the ulna, may become swollen in relation to trauma, hemorrhage, sepsis, or any inflammatory arthritis. It is also a common site for the development of rheumatoid nodules or gouty tophi.
Due to its superficial location, swelling of the olecranon bursa is easy to detect by both the patient and the examiner (picture 1). It may be distinguished readily from an effusion of the elbow joint if the patient is able to fully extend the elbow joint without accentuating the pain. Full extension of the elbow reduces the volume available within the joint and thus increases the pressure and results in pain when an effusion of the elbow joint exists.
Management — All patients with presumed olecranon bursitis are managed with joint protection (with an orthosis). In addition, a search is made for any abrasion or cellulitis in the area that might possibly result in septic bursitis. As noted above, the two main indications to aspirate the olecranon bursa are to rule out infection and to diagnose a microcrystalline disorder like gout. If not contraindicated, antiinflammatory agents can also be used. (See 'Bursal fluid aspiration and analysis' above and "Septic bursitis".)
Fluid aspiration can also be used to decompress the bursal sac and give the protective elbow orthosis a better chance of preventing the fluid from reaccumulating. However, repeated aspiration of a sterile process for therapeutic purposes is seldom advocated as the fluid will reaccumulate and the added trauma and small risk of introducing an infection is not warranted.
It is common for fluid to return rapidly into the bursa after drainage unless measures are taken to correct the causative factors, such as abrasive microtrauma. To accomplish this, a hard, removable, concave orthosis can be firmly affixed to the elbow with a Velcro strap to provide both shielding of the bursa and external pressure. This orthosis should not impede range of motion, and can be custom-fit by an occupational therapist, with soft padding on the inner surface to cushion the elbow. Drainage and shielding is very effective for the majority of noninfectious bursitis syndromes. Holding the elbow in full extension can also help alleviate pain.
As previously mentioned, we do not inject glucocorticoids in patients with olecranon bursitis. (See 'Intrabursal injections of glucocorticoids' above.)
Chronic, persistent olecranon bursitis often results in a rubbery thick capsule to the bursa, which can be treated with surgical removal. This may be performed arthroscopically [23]. A review of the surgical experience at the Mayo Clinic found good to excellent results in 15 of 16 patients with intractable, nonseptic olecranon bursitis that was not associated with RA [24]. By comparison, only two of five patients with RA experienced benefit. The specific indications for surgical removal are unclear. We advise against surgical excision in patients with RA who have evidence of active disease based on the apparent high rate of recurrence. In other conditions, decision for surgery can be made on a case-by-case basis.
Ischial bursitis — "Weaver's bottom," or "tailor's bottom," refers to pain in the bursa that lies between the ischial prominence and the gluteus maximus. When the patient with this condition stands erect, the muscle covers the bursa and the patient is generally asymptomatic. When seated, the muscle slides away and the bursa is in direct contact with the subcutaneous tissue. Hence, the pain is significantly accentuated when seated. As the bursa is also adjacent to the sciatic nerve, lancinating pain, suggestive of sciatica, may occur [25]. This aspect of the syndrome's relationship to posture and local pressure when seated tends to distinguish it from sciatica arising from conditions of the spine.
Variants of ankylosing spondylitis, as well as other conditions causing sacroiliitis, are often associated with an enthesopathy of the iliac spine, which has common features with the symptoms of an isolated ischial bursitis. A history and physical aimed at the possible diagnosis of a spondyloarthritis, as well as a careful neurologic evaluation, should be part of the diagnostic workup.
Management — A therapeutic trial of NSAIDs, stretching exercises (knee to chest stretch while lying down), and the use of foam pad "doughnut" cushion are helpful. We do not use local anesthetic-glucocorticoid injection into the site of maximum tenderness. This is related both to the proximity of the sciatica nerve to the bursa and a concern about creating soft-tissue atrophy in this bursa whose major function is to serve as a cushion.
Greater trochanteric pain syndrome (formerly trochanteric bursitis) — The trochanteric bursa lies between the tendon of the gluteus medius and the posterolateral prominence of the greater trochanter. However, pain in this area is usually due to a tendinopathy of the gluteus medius or minimus tendons, with trochanteric "bursitis" occurring as a secondary or associated finding. Patients with this syndrome often volunteer that pain is exacerbated while lying on the affected side at night. Extension of the hip in walking often produces pain, while weightbearing without extension usually does not cause symptoms. Arthritis of the hip joint, sciatica, or any condition causing an abnormal gait may provoke stress on the region of the bursa and bring on symptoms. Physical exam shows local tenderness over the lateral trochanter and relatively free motion of the hip. Tenderness overlying the greater trochanter can also be indicative of iliotibial band (ITB) syndrome, although the tenderness of ITB syndrome typically is greatest at the lateral femoral condyle of the knee and diminishes as one palpates proximally toward the trochanteric bursa.
The clinical manifestations, diagnosis, and management of greater trochanteric pain syndrome are discussed in detail elsewhere. (See "Greater trochanteric pain syndrome (formerly trochanteric bursitis)" and "Approach to the adult with unspecified hip pain".)
Iliopsoas bursitis — The iliopsoas bursa lies between the iliopsoas muscle and the anterior aspect of the hip joint. It frequently may connect with the cavity and synovium of the hip joint. Pain is felt in the groin and may be accentuated by flexion of the hip against resistance. Iliopsoas bursitis can be associated with hip pathology due to arthritis, such as RA or osteoarthritis; overuse injuring, for example from running; septic arthritis; or acute trauma [26].
The clinical presentation of iliopsoas bursitis is similar to intrinsic disorders of the hip, such as hip joint synovitis, labral tears, and avascular necrosis of the femoral head, all of which are usually associated with a normal plain film of the hip. For this reason, further imaging by MRI or ultrasound may be indicated to exclude these entities. In addition, because of the proximity of the bursa to the neurovascular bundle in the femoral canal, ultrasound guidance may be required in order to avoid an injury to this structure if needle aspiration or injection is attempted.
There are no systematic studies of treatment approaches, but management generally consists of rest, NSAIDs, and physical therapy. Some patients benefit from glucocorticoid injection [26,27]. Surgical excision is generally not required.
Prepatellar and infrapatellar bursitis — Prepatellar bursitis ("housemaid's knee") and infrapatellar bursitis are common conditions usually related to recurrent trauma and is seen in individuals who frequently kneel. It may also be related to an infection, gout, or, on occasion, another systemic form of arthritis. In acute bursitis of these areas, a diagnostic aspiration of fluid for cell count, culture, and crystal identification is typically indicated. The clue to distinguish this condition from an articular effusion of the knee is that patients with prepatellar and infrapatellar bursitis prefer to lie with the knee fully extended. Patients with an articular effusion prefer to flex the knee, and thus reduce the intraarticular pressure.
The majority of patients will resolve with avoidance of trauma and the use of NSAIDs. We recommend that injection of glucocorticoids be avoided for the same reason as mentioned in olecranon bursitis: concern about producing skin atrophy and its complications. However, other clinicians inject glucocorticoids in certain subsets of patients. The clinical manifestations, diagnosis, and management of prepatellar bursitis are discussed in detail elsewhere. (See "Knee bursitis", section on 'Prepatellar and superficial infrapatellar bursitis'.)
Medial collateral ligament bursitis — The medial collateral ligament (MCL) bursa is located between the MCL and the joint capsule. This bursitis presents with tenderness over the medial aspect of the knee joint and is seldom associated with a demonstrable effusion. It may also be a component of any inflammatory joint disease. Included in the differential diagnosis are:
●Injury to the MCL – This can usually be excluded on physical exam by the failure to accentuate the pain when the valgus stress is applied to the knee, a maneuver which would increase symptoms if the MCL was injured.
●Avascular necrosis of the tibia or a medial tibia plateau fracture – These conditions may be evident on plain radiographs, would certainly show up on MRI, and would be associated with pain over the bone and not the joint line.
●Medial meniscal tear – This condition is not usually associated with marked tenderness and its symptoms would be accentuated by the McMurray maneuver, in which the tibia is rotated upon the femur. A history of instability of the knee is also characteristic of meniscal lesions.
As is the case with pes anserinus pain syndrome, the patient may respond dramatically to a local injection of an anesthetic with a steroid, a result which tends to confirm the diagnosis of bursitis [28,29].
Pes anserinus pain syndrome (formerly anserine bursitis) — The anserine bursa lies about 5 cm below the medial joint line of the knee between the tibia and the insertions of the sartorius, gracilis, and semi-tendinosis muscles (termed the "pes anserine" because it resembles a goose's foot). The usual presentation is of relatively abrupt accentuation of medial knee pain, particularly at night, in an individual with an underlying condition, usually osteoarthritis, of the knee. A palpable effusion is seldom seen, and the diagnosis of this common condition is based on history and local tenderness. The clinical manifestations, diagnosis, and treatment of pes anserinus pain syndrome are presented in detail elsewhere. (See "Knee bursitis", section on 'Pes anserinus pain syndrome (formerly anserine bursitis)'.)
Retrocalcaneal bursitis — The retrocalcaneal bursa occupies the space between the calcaneal bone and the Achilles tendon, and it serves as a cushion to absorb impact when walking. Retrocalcaneal bursitis may coexist with or be confused with tendinitis and the enthesopathies seen with ankylosing spondylitis and its variants. The clinical manifestations, diagnosis, and treatment of retrocalcaneal bursitis are presented in detail elsewhere. (See "Plantar fasciitis".)
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 topics (see "Patient education: Bursitis (The Basics)")
●Beyond the basics topics (see "Patient education: Bursitis (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Definitions – A bursa is a fluid-filled, saclike structure lined by synovial membrane which forms in clefts between mobile structures in the musculoskeletal system. Specific bursitis syndromes may occur with or without inflammation, since many such syndromes are not associated with an inflammatory process but only with tenderness over the affected structure. (See 'Introduction and definition' above.)
●Etiology – Bursitis may result from any one or combination of the following causes: direct injury or trauma; prolonged pressure; overuse or strenuous activity; crystal-induced arthropathy; and inflammatory arthritis. (See 'Etiology' above.)
●Clinical presentation – Obvious signs of swelling and inflammation may be evident upon physical exam only in superficial processes. Common but deeper processes are seldom associated with visible swelling or erythema. There are also differences in presentation based on the acuity or chronicity of the process. In patients with acute inflammatory bursitis, the inflamed bursa is tender directly over the bursa, with pain elicited by any active motion that employs muscles adjacent to the involved bursa. Patients with chronic bursitis tend to have more swelling and thickening of superficial bursae out of proportion to pain, which is often minimal. (See 'Clinical presentation and physical examination' above.)
●Diagnostic testing – Diagnostic testing may be necessary if infection or crystal disease is suspected based on the initial medical history and examination. Appropriate studies vary depending on the suspected etiology of the bursitis and the anatomic location of the bursa (superficial versus deep). (See 'Diagnostic testing' above.)
•The two main indications to aspirate a bursa are to rule out infection, and to aid in the diagnosis of a microcrystalline disorder like gout.
•Imaging studies are typically not necessary for diagnostic purposes. However, imaging is appropriate when the establishment of a more accurate diagnosis seems imperative, or to guide a needle for aspiration or injection when trying to avoid a vital structure.
●Management principles – With the exception of septic bursitis, the underlying management principle is that bursitis is a self-limited, presumably inflammatory, condition that is reversible. Therefore, the goal of treatment is to relieve the immediate symptoms, to prevent the secondary complications related to immobilization (muscle atrophy and joint contracture), and to maintain range of motion. (See 'Principles of management' above.)
•Patients should be taught the principles of joint protection and, unless contraindicated, affected individuals should also receive analgesia, which usually consists of a nonsteroidal antiinflammatory drug (NSAID). (See 'Principles of management' above.)
•Among patients with presumed inflammation of deep bursae, we suggest that initial therapy include an intralesional injection of a combination of local anesthetic and glucocorticoid (Grade 2C). If the original injection provides several weeks of significant relief, the diagnosis of a soft tissue process seems secure, a repeat injection may be tried if symptoms warrant. (See 'Intrabursal injections of glucocorticoids' above.)
•Among patients with superficial forms of bursitis, we generally do not use intralesional glucocorticoids. Available data do not support their benefit, and there is an increased risk of infectious complications, skin atrophy, and development of a draining sinus tract. (See 'Intrabursal injections of glucocorticoids' above.)
●Specific syndromes – Unique clinical and management issues emerge based upon the specific affected bursae. It is important to realize that each bursitis syndrome may have to be approached and managed somewhat differently. (See 'Specific syndromes' above.)
ACKNOWLEDGMENT — The editorial staff at UpToDate acknowledge Ronald J Anderson, MD, who contributed to an earlier version of this topic review.
