ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Septic bursitis

Septic bursitis
Literature review current through: Sep 2023.
This topic last updated: Sep 15, 2022.

INTRODUCTION — Bursitis is an inflammation of the sac-like structures that protect the soft tissues from underlying bony prominences [1]. Septic bursitis refers to inflammation of the bursa that is due to infection. Aseptic (ie, non-infectious) bursitis is more common than septic (infectious) bursitis; septic bursitis accounts for about a third of bursitis cases [2].

Issues related to septic bursitis are discussed here. Types of aseptic bursitis in the knee and hip are discussed elsewhere. (See "Knee bursitis" and "Greater trochanteric pain syndrome (formerly trochanteric bursitis)".)

PATHOGENESIS AND EPIDEMIOLOGY — There are more than 150 bursae in the human body; these structures act as friction buffers to facilitate movement of adjacent connective tissue structures against each other. Bursae are lined by synovial cells that produce a small amount of lubricating fluid under normal circumstances.

Superficial bursae are located immediately deep to the subcutaneous tissue layer; they separate skin from deeper tissues such as periosteum or ligaments. Deep bursae reduce friction between fibrous structures (such as tendons) and adjacent bone [1].

Septic bursitis usually involves the superficial bursae, given the predisposition to trauma associated with these areas. The most common mechanisms of infection are by percutaneous inoculation of organisms into the bursae or via contiguous spread from adjacent cellulitis [1,3,4]. Rarely, septic bursitis (superficial or deep) arises in the setting of hematogenous dissemination. Additionally, deep septic bursitis may occur in the setting of contiguous septic arthritis [1].

The most common sites of septic bursitis are the olecranon, prepatellar, and superficial infrapatellar bursae, given their subcutaneous locations. Bursitis may be associated with occupations or activities that predispose to specific local tissue trauma:

Olecranon bursitis may occur in athletes, plumbers, carpenters, miners, combat soldiers, patients with chronic obstructive pulmonary disease (possibly the result of leaning on the elbows), and patients receiving hemodialysis via upper extremity vascular access [1,3,5,6].

Prepatellar and superficial infrapatellar bursitis may occur in athletes, domestic workers, carpet layers, gardeners, and clergy who kneel [1].

Other specific epidemiologic associations include ischial bursitis in individuals with spinal cord injuries (from contiguous infection), and subacromial-subdeltoid or iliopsoas bursitis after local glucocorticoid injection [7-10].

Risk factors for septic bursitis include the following [3,4,11-14]:

Physical trauma or trauma related to overuse or repeated pressure

Antecedent noninfectious bursa inflammation (such as gout or rheumatoid arthritis)

Impaired immune response to infection (such as diabetes mellitus, alcohol abuse, chronic steroid therapy)

Loss of skin integrity (for example, due to chronic skin conditions such as atopic dermatitis, psoriasis)

Recent joint aspiration or injection

Male sex

MICROBIOLOGY — Staphylococcus aureus is the causative organism in approximately 80 percent of cases of culture-proven septic bursitis [1,3,11,13,15-19]. Streptococci of various species are the next most commonly reported cause [3,4,13]. In one series including 44 cases of septic bursitis, 64 percent were due to methicillin-susceptible S. aureus and 16 percent were due to methicillin-resistant S. aureus [11].

Less commonly reported organisms causing acute septic bursitis include coagulase-negative staphylococci, Cutibacterium (formerly Propionibacterium) spp, Enterococcus spp, Escherichia coli, Pseudomonas aeruginosa, and anaerobes [3,20,21]. Polymicrobial infections constitute a significant proportion of non-S. aureus septic bursitis, especially when trauma was the inciting event (10 to 36 percent of cases) [3,13,19,20].

Subacute or chronic bursitis may be due to Brucella abortus, mycobacteria (Mycobacterium tuberculosis or atypical mycobacteria such as Mycobacterium marinum or Mycobacterium kansasii [22]), fungi (such as Candida, sporotrichosis, dematiaceous fungi [23], molds), and algae including Prototheca [1,24-38]. In cases of septic bursitis due to Brucella or M. tuberculosis, the patient should be evaluated for systemic infection [1]. (See "Brucellosis: Epidemiology, microbiology, clinical manifestations, and diagnosis" and "Clinical manifestations and complications of pulmonary tuberculosis" and "Diagnosis of pulmonary tuberculosis in adults".)

CLINICAL MANIFESTATIONS

Signs and symptoms — Patients with acute septic bursitis typically present with acute onset of erythema, warmth, pain, swelling, and fullness at the site of a bursa [39-41]. Fever may be present (40 to 44 percent of cases in two series) [39,40]. A puncture wound or abrasion of the skin overlying the bursa may be observed (suggesting antecedent trauma), with or without a foreign body. Loss of skin integrity from dermatologic disease (such as psoriasis) may be observed. Subacute presentations may occur in the setting of infection due to indolent pathogens.

Patients with superficial septic bursitis commonly present with erythema, pain, swelling, and warmth, typically involving the olecranon, prepatellar, or infrapatellar bursae. In the setting of isolated septic bursitis, adjacent joint motion is generally preserved.

Patients with deep septic bursitis may present with bursal pain and systemic symptoms of infection; the diagnosis of deep septic bursitis can be challenging and is often delayed.

Patients with complicated bursitis may present with abscess, a draining sinus, and/or adjacent infection requiring debridement (eg, involving the skin and soft tissues, joint, or bone).

If septic bursitis is accompanied by septic arthritis, limitation of joint motion is observed [3]. Occasionally an aseptic sympathetic knee effusion may develop concomitantly in the setting of prepatellar or infrapatellar septic bursitis, in response to the overlying bursal infection; in such cases, synovial fluid analysis demonstrates a relatively low white blood cell count (typically <1,000 cells/microL) [42,43]. (See "Septic arthritis in adults".)

Rarely, septic bursitis may cause complications due to mass effect, although these findings are more commonly seen with aseptic bursitis. Mass effect may be associated with diminished perfusion of the overlying soft tissue or pressure necrosis; manifestations may include overlying soft tissue compromise with skin ulceration requiring local or regional soft tissue reconstruction. Additionally, mass effect due to bursitis may cause a compression neuropathy. As an example, in the pelvis, iliopsoas bursitis may be associated with compression neuropathy of the femoral nerve. In the upper limb, radial bursitis may be associated with compression neuropathy of the median/anterior interosseous nerve or the posterior interosseous nerve in the proximal forearm. In such cases, manifestations include muscle weakness and/or sensory loss in the distribution of the affected nerve(s). (See "Overview of lower extremity peripheral nerve syndromes", section on 'Femoral nerve' and "Overview of upper extremity peripheral nerve syndromes", section on 'Anterior interosseous neuropathy'.)

Distinguishing between septic and inflammatory (noninfectious bursitis) may be difficult [16]. In one review of patients with olecranon bursitis, features distinguishing septic from aseptic bursitis included tenderness (88 versus 36 percent), erythema/cellulitis (83 versus 27 percent), warmth (84 versus 56 percent), trauma or skin lesion (50 versus 25 percent), and fever (38 versus 0 percent) [18].

Septic bursitis may occur independently or in association with other conditions including cellulitis, septic arthritis, and crystal-induced bursitis (gout or pseudogout) [11]. (See 'Differential diagnosis' below.)

If not treated adequately, septic bursitis may progress to chronic bursal infection; potential complications include osteomyelitis, cutaneous fistula formation, or full-thickness breakdown of the overlying skin.

Physical examination — Findings on physical examination may include fever, bursal warmth, erythema, tenderness to palpation, and edema (fluctuant and well-demarcated). Local skin abrasion or contusion may be observed. Palpation may help to define the extent of bursal expansion.

In patients with prepatellar or infrapatellar bursitis, diminished active range of motion may be observed, with preservation of passive range of motion. In patients with olecranon bursitis, elbow range of motion is usually normal, although the end range of elbow flexion may be limited.

In some cases, crepitus may be appreciated during motion of an adjacent joint or soft tissues; as an example, in the setting of radial bursitis, forearm pronation and supination may be associated with crepitus at the distal biceps insertion.

Although rare with septic bursitis, findings consistent with mass effect of the expanded bursa include signs of overlying soft tissue compromise (such as skin ulceration or breakdown) or compression neuropathy (such as muscle weakness and/or sensory loss in the distribution of the affected nerve[s]). (See "Overview of lower extremity peripheral nerve syndromes" and "Overview of upper extremity peripheral nerve syndromes".)

Laboratory findings — Leukocytosis with neutrophilia and an increased proportion of immature neutrophils (ie, bandemia) may be observed [44]. Acute phase reactants (eg, erythrocyte sedimentation rate and C-reactive protein) are usually elevated.

Bacteremia is seen in up to a third of cases; if observed, it should prompt consideration of deep bursitis and/or septic arthritis [1,18]. In one series including more than 70 patients with septic bursitis, blood cultures were positive in 4 percent of cases [13]. In another series including more than 60 patients with septic bursitis, blood cultures were positive in 19 percent of cases [44].

DIAGNOSIS

Clinical suspicion — Septic bursitis should be suspected in patients with acute onset of erythema, warmth, pain, swelling, and fullness at the site of a bursa, with or without relevant risk factors (eg, trauma, underlying bursa inflammation, immunosuppression) [39-41]. The diagnosis is confirmed by positive Gram stain or culture of a bursal fluid sample. (See 'Clinical manifestations' above and 'Bursal fluid and tissue samples' below.)

Although common bacteria (eg, S. aureus) cause most septic bursitis, atypical infection should be suspected in certain situations (eg, gardeners at risk for sporotrichosis, fishermen at risk for M. marinum, immunosuppressed patients, or culture-negative bursitis). (See 'Microbiology' above.)

Initial evaluation

The following tests should be obtained for all patients in whom septic bursitis is suspected:

Bursal aspiration – This test is required to make a definitive diagnosis of septic bursitis. The process for bursal sampling and interpretation of results are discussed in detail below. (See 'Obtaining bursal samples' below and 'Bursal tests' below and 'Interpreting bursal fluid test results' below.)

Blood cultures (two sets).

Plain radiographs (three views) – Imaging can neither confirm nor rule out the diagnosis of septic bursitis. However, plain radiographs should be performed to evaluate for complications such as fracture, foreign body, osteomyelitis, or other pathologic conditions (eg, adjacent joint effusion, calcific tendinosis). In some cases of septic bursitis, foci of air or synovial thickening can be seen.

In certain situations, additional testing may be helpful:

Arthrocentesis is generally unnecessary. However, in patients with joint effusion or limitation of joint motion, it should be performed to rule out concomitant septic arthritis. When aspirating an adjacent joint, care should be taken to enter the joint other than through the infected bursa. (See "Septic arthritis in adults".)

If there is uncertainty about presence of bursal fluid based upon physical examination, musculoskeletal ultrasound can be helpful. Sonographic findings of bursitis (aseptic or septic) may include soft tissue alterations such as bursal distension with fluid of mixed echogenicity, synovial thickening, and peribursal edema. If infection is present, bursal fluid may contain echogenic foci consistent with air, although this finding is not universal and can also be seen after joint or bursal aspiration. If no fluid is evident by ultrasound, the diagnosis of septic bursitis is unlikely.

If musculoskeletal ultrasound is not available or does not reveal suspected abnormalities or if deep bursal involvement is suspected, computed tomography (CT) or magnetic resonance imaging (MRI) of the involved region may be performed, but these tests are rarely necessary. Such tests can reveal bursal effusion, synovial thickening, abscesses, and involvement of adjacent structures including soft tissue, tendons, joint, and bone [1,45-48].

Bursal fluid and tissue samples — The only way to confirm a diagnosis of septic bursitis is by microbiologic testing of bursal fluid or tissue. In most cases, obtaining bursal fluid is adequate and tissue biopsy is unnecessary.

Obtaining bursal samples — Diagnostic bursal fluid aspiration should be performed prior to administration of antibiotics. During bursal sampling, as much fluid as is easily accessible should be removed to optimize culture results. Presence of erythema over an infected bursa is not a contraindication to bursal aspiration.

In cases of suspected superficial olecranon, prepatellar, and superficial infrapatellar bursitis, bursal fluid may be obtained by bedside needle aspiration; the techniques are discussed separately. (See "Evaluation of elbow pain in adults", section on 'Olecranon bursa aspiration' and "Knee bursitis", section on 'Prepatellar and superficial infrapatellar bursitis'.)

In cases of suspected deep bursitis, bursal fluid aspiration typically requires ultrasonography or CT guidance [45].

Bursal tests — Bursal fluid should be sent for Gram stain, bacterial culture (aerobic and anaerobic), white blood cell count with differential, and assessment for crystals by polarizing light microscopy.

Fungal and mycobacterial stains and cultures should be obtained if there is suspicion for atypical infection. Situations that should raise suspicion of atypical infection are discussed above. (See 'Clinical suspicion' above and 'Microbiology' above.)

If surgical bursectomy is performed, tissue stains and culture (for aerobic and anaerobic bacteria, mycobacteria, and fungi) and histologic examination of excised tissue should be performed.

Interpreting bursal fluid test results — Analysis of bursal fluid requires interpretation of microbiologic and non-microbiologic results:

Microbiologic results – A definitive diagnosis of septic bursitis is made by a positive Gram stain or culture of bursal fluid or tissue.

The sensitivity of bursal fluid Gram stain for detection of organisms ranges from 15 to 100 percent in studies [1,39,49]. For olecranon bursitis, a positive Gram stain has been observed in one-half to two-thirds of cases [3,18].

Bursal fluid culture is the gold standard for diagnosis of septic bursitis. However, cultures may be negative despite infection, especially in the setting of recent antimicrobial therapy or infection with an atypical or fastidious organism [18].

Bursal fluid analysis – Bursal fluid analysis typically demonstrates the following in cases of septic bursitis:

Leukocyte counts generally >2000 cells/microL [1,14,16,18,50]. However, the diagnosis of septic bursitis cannot be made definitively based on the bursal leukocyte count alone since bursal leukocyte counts may also be elevated above 2000 cells/microL in aseptic inflammatory bursitis.

In one study including 36 patients with olecranon or prepatellar bursitis, bursal white blood cell count >2000 cells/microL had a sensitivity, specificity, and positive predictive value of 94 percent, 79 percent, and 80 percent, respectively [16]. The median cell count was 5200 cells/microL (range 1200 to 34,600 cells/microL). In another review of olecranon bursitis, the average bursal cell count for septic bursitis was 62,923 cells/microL (range 900 to 392,500 cells/microL) compared with 2215 cells/microL for aseptic bursitis (range 50 to 11,700 cells/microL) [18].

Neutrophils may be more common in bursal fluid with septic bursitis, while monocytes may be more common with aseptic bursitis [18]. Neutrophil counts in septic bursitis are often >85 percent [11].

Crystals in bursal fluid are diagnostic of crystal-induced bursitis (eg, gout, pseudogout). However, concomitant septic bursitis and crystal-induced bursitis can occur, in which case there will be both a positive culture (or Gram stain) and crystals in the bursal fluid [51].

There can be substantial overlap in the laboratory findings between septic and aseptic bursitis; in patients with purulent bursal fluid but negative bursal fluid Gram stain and culture, a presumptive diagnosis of septic bursitis may be made, especially when systemic symptoms suggesting infection are present and no crystals are identified.

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of septic bursitis includes the following:

Aseptic bursitis – Causes of aseptic (noninfectious) bursitis are numerous, including direct trauma, prolonged pressure or overuse, crystals (eg, gout, pseudogout), or inflammatory arthritis (eg, rheumatoid arthritis). These conditions may occur independently or in association with septic bursitis. In general, the presentation of aseptic bursitis is subacute and less pronounced than cases in which infection is present [18]. Further detail regarding aseptic bursitis of the hip and knee is found elsewhere. (See "Knee bursitis" and "Greater trochanteric pain syndrome (formerly trochanteric bursitis)".)

Cellulitis – Cellulitis may precede or accompany septic bursitis or occur independently. The diagnosis of cellulitis is usually based upon clinical manifestations of skin erythema, edema, and warmth. In some cases, imaging may be useful to distinguish between cellulitis and bursitis. (See 'Initial evaluation' above and "Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis".)

Septic arthritis – Septic arthritis refers to infection in a joint. The mechanisms for development of septic arthritis are the same as those for septic bursitis; these conditions may occur independently or coexist. Septic arthritis should be suspected in the setting of limited range of joint motion; the diagnosis is established based on joint aspiration with synovial fluid analysis and culture. (See 'Initial evaluation' above and "Septic arthritis in adults".)

Acute monoarthritis – Manifestations of acute monoarthritis include joint pain and limited joint mobility; these manifestations may be accompanied by joint effusion. Causes include inflammatory conditions (such as crystal-induced arthritis [gout or pseudogout], reactive arthritis, inflammatory arthritis (such as psoriatic arthritis or rheumatoid arthritis) and noninflammatory conditions (such as osteoarthritis, trauma, avascular necrosis, and hemarthrosis). (See "Monoarthritis in adults: Etiology and evaluation" and "Synovial fluid analysis".)

Hemobursa – Hemobursa refers to bleeding into a bursa associated with trauma or anticoagulation; manifestations include pain and swelling. The diagnosis may be established when grossly bloody bursal fluid is present. However, in some cases, bursal aspiration may not yield significant blood or fluid if clotted blood cannot be withdrawn through the needle.

Patellar osteomyelitis – Patellar osteomyelitis refers to infection of the patella bone. This rare condition should be considered when prepatellar or infrapatellar bursitis appears to relapse [52]. The diagnosis may be established with imaging (plain radiography, computed tomography, or magnetic resonance imaging).

TREATMENT

Clinical approach — In general, initial management of septic bursitis consists of antibiotic therapy and serial assessment with surgical consultation. (See 'Antibiotic therapy' below and 'Recurrent infection' below.)

For patients in whom the bursal fluid collection persists despite 36 to 48 hours of antibiotic therapy, bursal drainage is warranted. Indications for surgical intervention include presence of abscess, presence of adjacent infection requiring debridement (eg, involving the skin and soft tissues, joint, or bone), and presence of a foreign body. (See 'Bursal drainage' below.)

For symptomatic management (eg, to reduce inflammation and ameliorate discomfort), nonsteroidal anti-inflammatory drugs may be used.

Patients with a loss of skin integrity (such as from puncture wounds) should be assessed for the need for tetanus prophylaxis. (See "Infectious complications of puncture wounds", section on 'Tetanus immunization'.)

Antibiotic therapy

Spectrum of therapy — For immunocompetent patients, empiric antibiotic therapy for septic bursitis should include activity against staphylococci and streptococci. Inclusion of empiric therapy against methicillin-resistant S. aureus (MRSA) is warranted in the following circumstances:

Systemic signs of toxicity (fever >100.5°F/38°C, sustained tachycardia)

Bursitis overlying an indwelling device (prosthetic joint or vascular graft)

Prior episode of MRSA, known MRSA colonization, or risk factor(s) for MRSA infection (such as hospitalization or surgery in last 60 days, residence in a long-term care facility, hemodialysis, HIV infection)

Lack of clinical response to an antibiotic regimen that does not include activity against MRSA

Common intravenous regimens include vancomycin (for activity against MRSA and streptococci) and cefazolin (for activity against methicillin-susceptible S. aureus [MSSA] and streptococci). Common oral regimens include trimethoprim-sulfamethoxazole (for activity against MRSA and streptococci) or cephalexin (for activity against MSSA and streptococci). An approach to antibiotic selection and dosing for immunocompetent patients is summarized in the algorithm (algorithm 1).

The rationale and approach to the choice of antibiotic agent for treatment of soft tissue infection due to staphylococci and streptococci is discussed separately. (See "Acute cellulitis and erysipelas in adults: Treatment".)

In the setting of a potentially contaminated wound (such as associated with trauma), broader empiric antibiotic therapy including gram negative coverage (with a fluoroquinolone or cephalosporin) is reasonable (algorithm 1).

For immunosuppressed patients, empiric therapy should include activity against staphylococci and streptococci (as for immunocompetent patients). In addition, for immunosuppressed patients with septic bursitis associated with trauma, we favor inclusion of an agent with activity against Pseudomonas spp (such as ciprofloxacin, ceftazidime, or cefepime, or piperacillin-tazobactam). Antimicrobial therapy should be guided further by individual patient factors and bursa fluid Gram stain results [44,53].

The initial antibiotic regimen should be tailored to culture and susceptibility results when available. For patients with negative Gram stain and culture but high clinical concern for septic bursitis, continuation of a full course of empiric therapy may be warranted; consultation with a provider with expertise in these situations is advised.

Oral versus parenteral therapy — For immunocompetent patients with mild to moderate infection, oral antibiotic therapy may be administered.

Parenteral antibiotic therapy is warranted in the following circumstances:

Systemic signs of toxicity (eg, fever >100.5°F/38°C, hypotension, or sustained tachycardia)

Rapid progression of erythema

Progression of clinical findings after 48 hours of oral antibiotic therapy

Inability to tolerate oral therapy

Proximity of infection to an indwelling medical device (eg, prosthetic joint or vascular graft)

The decision to initiate parenteral therapy should be based on individual clinical circumstances including severity of clinical presentation and patient comorbidities.

Presence of an immunocompromising condition (such as neutropenia, recent organ transplant, advanced HIV infection, B cell or T cell deficiency, or use of immunosuppressive agents) should lower the threshold for parenteral therapy.

For patients initially treated with parenteral therapy with signs of clinical improvement and no evidence of systemic toxicity, antibiotics may be transitioned from parenteral to oral therapy.

Duration — The optimal duration of antibiotic therapy for treatment of septic bursitis is uncertain; duration should be guided by clinical response and individual patient circumstances. In general, 10 days of therapy is appropriate for patients with improvement in clinical manifestations within this time-period. Extension of antibiotic therapy (up to 14 to 21 days) may be warranted in the setting of severe infection, slow response to therapy, or immunosuppression.

The duration of therapy has not been evaluated in randomized trials, and observational studies reveal conflicting results. A multicenter, retrospective observational study of 272 individuals with olecranon and prepatellar bursitis noted a higher recurrence rate in those treated for less than 14 days rather than longer [19]. In contrast, a systematic review of ten prepatellar bursitis studies showed no difference in recurrence among those treated for less than 8 days versus those who received longer courses (OR, 0.66; 95% CI, 0.13-3.29) [54]. Longer duration of symptoms prior to clinical presentation has been associated with longer time to resolution after initiation of treatment [55].

Among patients who undergo surgical bursectomy, a shorter duration of antibiotic therapy (≤7 days) may be sufficient [13,56]. In one study including more than 300 patients with severe septic bursitis managed with bursectomy, the likelihood of cure was comparable among patients treated with ≤7 days, 8 to 14 days, or >14 days [13].

Bursal drainage — Infected bursae should be drained when symptoms persist despite 36 to 48 hours of antibiotic therapy or if there are signs of mass effect of the expanded bursa (eg, diminished perfusion of the overlying soft tissue, compression neuropathy). Bursal drainage may be performed either by needle aspiration or surgical drainage, as described below:

Needle aspiration – In general, the initial approach to bursal drainage consists of serial needle aspiration (every one to three days); in some cases, a catheter is placed following aspiration to aid with drainage. Needle aspiration (with or without catheter drainage) is at least as effective and safe as surgical drainage. In one systematic review including 29 studies (mostly retrospective) and more than 1200 patients with olecranon septic bursitis, nonsurgical management was associated with higher likelihood of clinical resolution (93 versus 87 percent) and lower likelihood of complications (13 versus 25 percent) than surgical management [17,19].

Surgical drainage – Surgical intervention, with bursectomy (ie, debridement) in some cases, is indicated for patients whose septic bursitis is refractory to antibiotic therapy and needle or catheter drainage. Other indications for surgical intervention include the presence of abscess, adjacent infection requiring debridement (eg, skin and soft tissue, joint, or bone), or foreign body [1,3,14]. Patients with a draining sinus typically warrant resection of the sinus with concomitant drainage and/or resection of the bursa.

Surgical methods for superficial septic bursitis include endoscopic or open incision with drainage and lavage, with or without bursectomy. Endoscopy may be associated with a lower likelihood of soft tissue trauma compared with open bursectomy: in two case series of patients with prepatellar and olecranon septic bursitis managed with endoscopic bursectomy, endoscopy was associated with better wound healing and shorter hospital stay compared with historic controls of patients treated with open bursectomy [57,58]. Furthermore, recurrence rates of bursitis appear to be similar among patients treated with endoscopic versus open bursectomy [54].

For patients with superficial septic bursitis who undergo open bursectomy and lavage, a one-stage procedure (open debridement with primary closure) is preferred over a two-stage procedure (open debridement with the wound left open and subsequent closure several days later). In a randomized trial including more than 160 patients with olecranon or prepatellar septic bursitis, patients who underwent single-stage procedures had lower rates of wound dehiscence compared with two-stage procedures (1 of 66 versus 9 of 64 [1.5 versus 14 percent]) [56].

In the setting of deep septic bursitis, the threshold for surgical intervention is lower compared with superficial septic bursitis, given difficulties associated with access for aspiration and clinical monitoring. In addition, the complexity of the local anatomy and risks of joint sepsis, osteomyelitis, or local tissue compromise in the setting of deep septic bursitis may raise the acuity for intervention. The surgical approach consists of open debridement; in some cases, staged debridement may be required to ensure adequate resection of nonviable and/or infected tissue, followed by wound reconstruction if needed.

For all patients who undergo bursectomy, careful soft tissue handling is critical to optimize wound healing. For areas with tenuous soft tissue coverage (the posterior elbow is a common site of soft tissue compromise), preemptive flap coverage may improve wound healing and enhance local vascular perfusion for antibiotic delivery [59]. (See "Overview of flaps for soft tissue reconstruction".)

Recurrent infection — Management of recurrent septic bursitis consists of repeating bursal aspiration and antibiotic therapy as well as consideration for surgical drainage (including exploration for a retained foreign body) or bursectomy (with soft tissue reconstruction in some cases) [3]. In addition, individuals with recurrent septic olecranon or patellar bursitis may benefit from the use of knee or elbow pads during activities that predispose to developing bursitis.

Bursal fluid obtained upon re-aspiration should be sent for bacterial culture as well as fungal and mycobacterial stains and cultures (see 'Bursal tests' above). Antibiotic therapy should be guided by repeat culture results, if positive. In cases in which the cultures were positive during the initial episode but were negative at the time of recurrence, a repeat course of antibiotics targeting the original pathogen is appropriate. (See 'Antibiotic therapy' above.)

If cultures were negative at the time of initial treatment and repeat cultures (off antibiotics) remain negative at the time of recurrence, noninfectious causes of bursitis should be considered (see 'Differential diagnosis' above)

The duration of antibiotic therapy should be guided by clinical improvement. A longer course of antibiotics (up to twice the initial duration of therapy) may be warranted for recurrences.

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 Basics 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 email 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)")

SUMMARY AND RECOMMENDATIONS

Definition – Bursitis is an inflammation of the sac-like structures that protect the soft tissues from underlying bony prominences. Septic bursitis refers to inflammation of the bursa that is due to infection. (See 'Introduction' above.)

Anatomic sites – Septic bursitis usually involves the superficial bursae, given the predisposition to trauma associated with these areas. The most common sites are the olecranon, prepatellar, and superficial infrapatellar bursae. Rarely, septic bursitis arises from hematogenous dissemination or contiguous septic arthritis. (See 'Pathogenesis and epidemiology' above.)

Clinical manifestations – Patients have acute onset of erythema, warmth, pain, swelling, and fullness at the site of a bursa. They may or may not have relevant risk factors, such as trauma, underlying bursa inflammation, or immunosuppression. (See 'Signs and symptoms' above.)

Physical examination findings may include fever, warmth, erythema, tenderness to palpation, and edema (fluctuant and well-demarcated). (See 'Physical examination' above.)

Diagnostic tests – The primary test for septic bursitis is bursal aspiration. The bursal fluid should be sent for Gram stain, bacterial culture (aerobic and anaerobic), white blood cell count with differential, and assessment for crystals by compensated polarizing light microscopy. Bursal fluid fungal and/or mycobacterial cultures may be useful in some circumstances. Blood cultures should be obtained as well. (See 'Initial evaluation' above and 'Bursal fluid and tissue samples' above.)

Plain radiography should be performed in all patients to evaluate for possible complications, such as fracture, foreign body, and osteomyelitis. (See 'Initial evaluation' above.)

Diagnosis – A definitive diagnosis of septic bursitis is established if there is a positive Gram stain or culture of bursal fluid. In patients with a bursal fluid (leukocyte count >2000 cells/microL) but negative Gram stain and culture, a presumptive diagnosis of septic bursitis may be made. (See 'Interpreting bursal fluid test results' above.)

Antimicrobial therapy – Antibiotics are indicated for all patients with septic bursitis. The choice of empiric antibiotic therapy depends on the severity of infection and likelihood of methicillin-resistant Staphylococcus aureus (MRSA) involvement (see 'Antibiotic therapy' above):

For immunocompetent patients, empiric antibiotic therapy for septic bursitis should include activity against staphylococci and streptococci:

-For immunocompetent patients with mild to moderate infection in the absence of concern for MRSA, we suggest oral therapy with dicloxacillin (Grade 2C); in the setting of concern for MRSA, we suggest oral therapy with trimethoprim-sulfamethoxazole (Grade 2C). Additional regimens are summarized in the algorithm (algorithm 1).

-For immunocompetent patients who warrant parenteral therapy (eg, rapid progression of erythema, progression of clinical findings on oral therapy, inability to tolerate oral therapy) in the absence of concern for MRSA, we suggest parenteral therapy with cefazolin (Grade 2C); in the setting of concern for MRSA, we suggest parenteral therapy with vancomycin (Grade 2C). Additional regimens are summarized in the algorithm (algorithm 1).

For immunosuppressed patients, empiric therapy should include activity against staphylococci and streptococci (as for immunocompetent patients). In addition, for immunosuppressed patients whose septic bursitis is associated with trauma, we suggest inclusion of an agent with activity against Pseudomonas spp (Grade 2C), such as ciprofloxacin, ceftazidime, cefepime, or piperacillin-tazobactam.

The typical duration of antibiotic therapy is 10 days for patients with clinical improvement. Extension of antibiotic therapy (up to 14 to 21 days) may be warranted in the setting of severe infection, slow response to therapy, or immunosuppression.

Indications for bursal drainage – Many patients do not require bursal drainage. For patients who have persistent symptoms after 36 to 48 hours of antibiotic therapy or rare signs of mass effect (eg, diminished perfusion of the overlying soft tissue, compression neuropathy), we suggest bursal drainage in addition to antibiotic therapy rather than antibiotic therapy alone (Grade 2C). (See 'Bursal drainage' above.)

For most patients who require bursal drainage, we suggest serial needle aspiration or catheter drainage rather than surgical drainage (Grade 2C). Surgical drainage is associated with a higher risk of complications. (See 'Bursal drainage' above.)

Surgical drainage (with bursectomy in some cases) is reserved for patients with septic bursitis that is refractory to antibiotic therapy and needle or catheter drainage. Surgical intervention is also required in the presence of abscess, presence of adjacent infection requiring debridement (eg, involving the skin and soft tissues, joint, or bone), and presence of a foreign body. For patients who require surgical drainage, we suggest endoscopic over open debridement for the majority of cases (Grade 2C). (See 'Bursal drainage' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Dr. Robert Sheon, who contributed to earlier versions of this topic review.

  1. Small LN, Ross JJ. Suppurative tenosynovitis and septic bursitis. Infect Dis Clin North Am 2005; 19:991.
  2. Lormeau C, Cormier G, Sigaux J, et al. Management of septic bursitis. Joint Bone Spine 2019; 86:583.
  3. Zimmermann B 3rd, Mikolich DJ, Ho G Jr. Septic bursitis. Semin Arthritis Rheum 1995; 24:391.
  4. Valeriano-Marcet J, Carter JD, Vasey FB. Soft tissue disease. Rheum Dis Clin North Am 2003; 29:77.
  5. Enzenauer RJ, Pluss JL. Septic olecranon bursitis in patients with chronic obstructive pulmonary disease. Am J Med 1996; 100:479.
  6. Schermann H, Karakis I, Dolkart O, et al. Olecranon Bursitis in a Military Population: Epidemiology and Evidence for Prolonged Morbidity in Combat Recruits. Mil Med 2017; 182:e1976.
  7. Drezner JA, Sennett BJ. Subacromial/subdeltoid septic bursitis associated with isotretinoin therapy and corticosteroid injection. J Am Board Fam Pract 2004; 17:299.
  8. Rubayi S, Montgomerie JZ. Septic ischial bursitis in patients with spinal cord injury. Paraplegia 1992; 30:200.
  9. Canoso JJ, Sheckman PR. Septic subcutaneous bursitis. Report of sixteen cases. J Rheumatol 1979; 6:96.
  10. Crawford AM, Grisdela PT, Maguire JH, von Keudell AG. Septic Iliopsoas Bursitis After Intra-articular Methylprednisolone Injection to the Hip: A Case Report. JBJS Case Connect 2021; 11.
  11. Lieber SB, Fowler ML, Zhu C, et al. Clinical characteristics and outcomes of septic bursitis. Infection 2017; 45:781.
  12. Söderquist B, Hedström SA. Predisposing factors, bacteriology and antibiotic therapy in 35 cases of septic bursitis. Scand J Infect Dis 1986; 18:305.
  13. Perez C, Huttner A, Assal M, et al. Infectious olecranon and patellar bursitis: short-course adjuvant antibiotic therapy is not a risk factor for recurrence in adult hospitalized patients. J Antimicrob Chemother 2010; 65:1008.
  14. Baumbach SF, Lobo CM, Badyine I, et al. Prepatellar and olecranon bursitis: literature review and development of a treatment algorithm. Arch Orthop Trauma Surg 2014; 134:359.
  15. Laupland KB, Davies HD, Calgary Home Parenteral Therapy Program Study Group. Olecranon septic bursitis managed in an ambulatory setting. The Calgary Home Parenteral Therapy Program Study Group. Clin Invest Med 2001; 24:171.
  16. Stell IM, Gransden WR. Simple tests for septic bursitis: comparative study. BMJ 1998; 316:1877.
  17. Sayegh ET, Strauch RJ. Treatment of olecranon bursitis: a systematic review. Arch Orthop Trauma Surg 2014; 134:1517.
  18. Reilly D, Kamineni S. Olecranon bursitis. J Shoulder Elbow Surg 2016; 25:158.
  19. Charret L, Bart G, Hoppe E, et al. Clinical characteristics and management of olecranon and prepatellar septic bursitis in a multicentre study. J Antimicrob Chemother 2021; 76:3029.
  20. Cea-Pereiro JC, Garcia-Meijide J, Mera-Varela A, Gomez-Reino JJ. A comparison between septic bursitis caused by Staphylococcus aureus and those caused by other organisms. Clin Rheumatol 2001; 20:10.
  21. Fischer PA, Kopp A, Massarotti EM. Anaerobic septic bursitis: case report and review. Clin Infect Dis 1996; 22:879.
  22. Mathew SD, Tully CC, Borra H, et al. Septic subacromial bursitis caused by Mycobacterium kansasii in an immunocompromised host. Mil Med 2012; 177:617.
  23. Gertner E. Chronic septic bursitis caused by dematiaceous fungi. Am J Orthop (Belle Mead NJ) 2007; 36:E10.
  24. Ramírez I, Nieto-Ríos JF, Ocampo-Kohn C, et al. Protothecal bursitis after simultaneous kidney/liver transplantation: a case report and review. Transpl Infect Dis 2016; 18:266.
  25. Ramos-Pascua LR, Carro-Fernández JA, Santos-Sánchez JA, et al. Bursectomy, Curettage, and Chemotherapy in Tuberculous Trochanteric Bursitis. Clin Orthop Surg 2016; 8:106.
  26. Davis JM, Broughton SJ. Prepatellar bursitis caused by Brucella abortus. Med J Aust 1996; 165:460.
  27. Guiral J, Reverte D, Carrero P. Iliopsoas bursitis due to Brucella melitensis infection--a case report. Acta Orthop Scand 1999; 70:523.
  28. McDermott M, O'Connell B, Mulvihill TE, Sweeney EC. Chronic Brucella infection of the supra-patellar bursa with sinus formation. J Clin Pathol 1994; 47:764.
  29. Friedman ND, Sexton DJ. Bursitis due to Mycobacterium goodii, a recently described, rapidly growing mycobacterium. J Clin Microbiol 2001; 39:404.
  30. Crespo M, Pigrau C, Flores X, et al. Tuberculous trochanteric bursitis: report of 5 cases and literature review. Scand J Infect Dis 2004; 36:552.
  31. Ornvold K, Paepke J. Aspergillus terreus as a cause of septic olecranon bursitis. Am J Clin Pathol 1992; 97:114.
  32. Wall BA, Weinblatt ME, Darnall JT, Muss H. Candida tropicalis arthritis and bursitis. JAMA 1982; 248:1098.
  33. Torres HA, Bodey GP, Tarrand JJ, Kontoyiannis DP. Protothecosis in patients with cancer: case series and literature review. Clin Microbiol Infect 2003; 9:786.
  34. Samuel S, Boopalan PR, Alexander M, et al. Tuberculosis of and around the ankle. J Foot Ankle Surg 2011; 50:466.
  35. Al-Qattan MM, Al-Namla A, Al-Thunayan A, Al-Omawi M. Tuberculosis of the hand. J Hand Surg Am 2011; 36:1413.
  36. Garrigues GE, Aldridge JM 3rd, Toth AP, Stout JE. Nontuberculous mycobacterial olecranon bursitis: case reports and literature review. J Shoulder Elbow Surg 2009; 18:e1.
  37. Leth S, Jensen-Fangel S. Infrapatellar bursitis with Mycobacterium malmoense related to immune reconstitution inflammatory syndrome in an HIV-positive patient. BMJ Case Rep 2012; 2012.
  38. Ahbel DE, Alexander AH, Kleine ML, Lichtman DM. Protothecal olecranon bursitis. A case report and review of the literature. J Bone Joint Surg Am 1980; 62:835.
  39. Ho G Jr, Tice AD, Kaplan SR. Septic bursitis in the prepatellar and olecranon bursae: an analysis of 25 cases. Ann Intern Med 1978; 89:21.
  40. Ho G Jr, Tice AD. Comparison of nonseptic and septic bursitis. Further observations on the treatment of septic bursitis. Arch Intern Med 1979; 139:1269.
  41. Smith DL, McAfee JH, Lucas LM, et al. Septic and nonseptic olecranon bursitis. Utility of the surface temperature probe in the early differentiation of septic and nonseptic cases. Arch Intern Med 1989; 149:1581.
  42. Strickland RW, Raskin RJ, Welton RC. Sympathetic synovial effusions associated with septic arthritis and bursitis. Arthritis Rheum 1985; 28:941.
  43. Tan IJ, Barlow JL. Sympathetic Joint Effusion in an Urban Hospital. ACR Open Rheumatol 2019; 1:37.
  44. García-Porrúa C, González-Gay MA, Ibañez D, García-País MJ. The clinical spectrum of severe septic bursitis in northwestern Spain: a 10 year study. J Rheumatol 1999; 26:663.
  45. Ginesty E, Dromer C, Galy-Fourcade D, et al. Iliopsoas bursopathies. A review of twelve cases. Rev Rhum Engl Ed 1998; 65:181.
  46. Beltran J. MR imaging of soft-tissue infection. Magn Reson Imaging Clin N Am 1995; 3:743.
  47. Manueddu CA, Hoogewoud HM, Balague F, Waldeburger M. Infective iliopsoas bursitis. A case report. Int Orthop 1991; 15:135.
  48. Turecki MB, Taljanovic MS, Stubbs AY, et al. Imaging of musculoskeletal soft tissue infections. Skeletal Radiol 2010; 39:957.
  49. Canoso JJ, Yood RA. Reaction of superficial bursae in response to specific disease stimuli. Arthritis Rheum 1979; 22:1361.
  50. Khodaee M. Common Superficial Bursitis. Am Fam Physician 2017; 95:224.
  51. Abrazhda D, Andras L, Van Linthoudt D. [Concomitant septic and gouty olecranon bursitis]. Praxis (Bern 1994) 2007; 96:1479.
  52. Choi HR. Patellar osteomyelitis presenting as prepatellar bursitis. Knee 2007; 14:333.
  53. Roschmann RA, Bell CL. Septic bursitis in immunocompromised patients. Am J Med 1987; 83:661.
  54. Brown OS, Smith TO, Parsons T, et al. Management of septic and aseptic prepatellar bursitis: a systematic review. Arch Orthop Trauma Surg 2022; 142:2445.
  55. Ho G Jr, Su EY. Antibiotic therapy of septic bursitis. Its implication in the treatment of septic arthritis. Arthritis Rheum 1981; 24:905.
  56. Uçkay I, von Dach E, Perez C, et al. One- vs 2-Stage Bursectomy for Septic Olecranon and Prepatellar Bursitis: A Prospective Randomized Trial. Mayo Clin Proc 2017; 92:1061.
  57. Dillon JP, Freedman I, Tan JS, et al. Endoscopic bursectomy for the treatment of septic pre-patellar bursitis: a case series. Arch Orthop Trauma Surg 2012; 132:921.
  58. Meade TC, Briones MS, Fosnaugh AW, Daily JM. Surgical Outcomes in Endoscopic Versus Open Bursectomy of the Septic Prepatellar or Olecranon Bursa. Orthopedics 2019; 42:e381.
  59. Bayne CO, Slikker W 3rd, Ma J, et al. Clinical Outcomes of the Flexor Carpi Ulnaris Turnover Flap for Posterior Elbow Soft Tissue Defects. J Hand Surg Am 2015; 40:2358.
Topic 7650 Version 27.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟