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Bursae are the satellite structures that form to protect tissues from bony prominences. The superficial bursae, including the olecranon, prepatellar, infrapatellar, and bursae over the first metatarsophalangeal bunions, are more likely to become infected than are the deep bursae, such as the subacromial, trochanteric, and iliopsoas bursae.
Olecranon bursitis may occur in as many as 10 in 100,000 persons per year. The majority of cases occur in men, and antecedent trauma to the skin is frequent.
Septic bursitis of superficial bursae is most commonly due to direct inoculation through the overlying skin; less commonly, it is secondary to overlying cellulitis. Most cases of deep septic bursitis are due to contiguous spread from adjacent infected joints or hematogenous seeding.
Predisposing risk factors for septic bursitis include trauma to the skin. For example, olecranon septic bursitis may occur in plumbers, athletes, and patients with chronic obstructive pulmonary disease (COPD) who frequently lean on their elbows; prepatellar or infrapatellar septic bursitis can occur in housecleaners, gardeners, and carpet layers. At least one third of patients with septic bursitis have an underlying comorbid illness such as diabetes mellitus, rheumatoid arthritis, gout, COPD, or alcohol use disorder.
In immunocompetent patients, septic bursitis often but not always presents with fever as well as erythema and warmth of the overlying skin; there may be swelling of the bursae. In contrast to patients with septic arthritis, patients with septic bursitis of superficial bursae have intact range of motion of the joints, which may be limited only at the extremes of flexion. Pain on motion of the joint and restriction of joint range of motion are highly suggestive of septic arthritis. Acute phase reactants such as C-reactive protein, the sedimentation rate, and the white blood cell (WBC) count may be elevated.
Radiography should be performed to look for a foreign body and to evaluate the surrounding bones. Aspiration of bursal fluid is helpful in the diagnosis of patients who have pain, erythema, and/or swelling of an affected area. However, given the risk for contaminating the bursa if the aspiration occurs through cellulitic skin, many clinicians choose to aspirate a bursa only if empirical antimicrobial therapy has failed. Ultrasound or computed tomography (CT) guidance greatly enhances the successful aspiration of superficial bursae. Care must be taken not to violate the joint space when aspirating a bursa to avoid inoculating it.
The leukocyte count of the bursal fluid is generally lower than what is seen in septic arthritis. A leukocyte count greater than 2000/μL has a sensitivity of 94% and a specificity of 79% for superficial (olecranon or prepatellar) bursitis. Bacterial culture and in vitro susceptibilities must be obtained; if additional fluid is available, a Gram stain may be obtained, although its sensitivity may be as low as 15%. The presence of crystals does not exclude the possibility of septic bursitis ( Chapter 252 ). Concomitant bacteremia can occur, and blood cultures should be obtained before the initiation of therapy if possible.
Staphylococcus aureus ( Chapter 267 ), which is the most common cause of septic bursitis, accounts for more than 70% of culture-proven cases, followed by β-hemolytic streptococci. Aerobic gram-negative bacilli, including Escherichia coli, and pseudomonas, are less common causes of septic bursitis. Polymicrobial infection can also occur. Chronic bursitis may be associated with infections due to Brucella spp, atypical mycobacteria, or Mycobacterium tuberculosis, as well as fungi; the presence of these infections should raise the possibility of systemic infection.
In the immunocompetent host, nonseptic bursitis ( Chapter 242 ) may have a somewhat more indolent presentation than septic bursitis. The differential diagnosis includes gout and pseudogout ( Chapter 252 ), arthritis, and trauma with hemobursa. An overlying cellulitis may be confused with bursitis. Fever is usually not present in nonseptic bursitis because of mechanical or friction trauma.
Treatment of septic bursitis is guided by knowledge of the putative underlying organisms, in most cases, S. aureus ( Chapter 267 ). Because the Gram stain result is frequently negative and culture results are delayed, empirical therapy is guided by the clinical presentation, the host’s risk factors, and knowledge of common pathogens causing infection. Most patients can be treated as outpatients, but patients who are immunocompromised may require hospitalization for intravenous antibiotic therapy ( Table 251-2 ).
Initial ambulatory treatment in patients without comorbid conditions may consist of an oral antistaphylococcal penicillin (e.g., dicloxacillin 500 mg orally four times daily) or a first-generation cephalosporin (e.g., cephalexin 500 mg orally four times daily). If community-acquired methicillin-resistant S. aureus (MRSA) is suspected, cotrimoxazole (e.g., one double-strength tablet orally twice daily), doxycycline (e.g., 100 mg orally twice daily), or minocycline may be added to one of these agents. In patients who are allergic to penicillin, oral clindamycin (e.g., 300 mg orally four times daily) or linezolid (e.g., 600 mg orally twice daily) may be used. In all cases, the choice among antibiotics and their doses should be guided by the patient’s renal and hepatic function as well as any drug allergies or intolerances.
Patients who have severe inflammation, are septic, or are immunocompromised may require hospitalization for initiation of treatment with intravenous nafcillin, oxacillin, or cefazolin (see Table 251-2 ). If MRSA is suspected, intravenous vancomycin, daptomycin, or linezolid (see Table 251-2 ) should be used ( Chapter 267 ). Vancomycin also can be used in patients who are allergic to penicillin.
The duration of antimicrobial therapy is guided by the clinical response and comorbid conditions. Antibiotics should be continued until bursal inflammation resolves. Resolution may require several weeks of intravenous or oral therapy and multiple aspirations. Failure of the septic bursitis to respond to initial antibiotic therapy mandates a second course of therapy. Recurrence thereafter or inability to drain the bursa adequately with needle aspiration is an indication for surgical intervention.
Because superficial septic bursitis is often associated with occasional or avocational activities involving kneeling or resting on the elbows, using protective padding may be helpful.
The optimal duration of therapy is unknown, but prognosis of superficial bursitis is generally excellent. The presence of comorbid conditions, especially conditions associated with deep bursal infections (e.g., including septic arthritis, bacteremia, and osteomyelitis), is associated with more intractable and difficult disease.
Septic arthritis, which refers to infection of a joint by a microorganism, is associated with increased morbidity and mortality as well as loss of articular integrity and function. Septic arthritis is usually caused by a bacterial infection, but other microorganisms also can cause infections with clinical characteristics that differ from those of bacterial infections.
The incidence of septic arthritis affecting native joints is approximately 10 per 100,000 patient years. Among patients presenting with an acutely swollen and painful joint, bacterial pathogens are the most common etiology. Nongonococcal septic arthritis is the most common form of septic arthritis and is somewhat more common in men than in women.
Staphylococci or streptococci are the most common pathogen to cause septic arthritis, but the microbiology depends on the mechanism of the infection ( Table 251-1 ). Septic arthritis can result from direct inoculation (e.g., accidents, bites, surgery) or by extension from infected bone into an adjacent joint space. Approximately 75% of cases are due to hematogenous spread, particularly in patients who use injection drugs, have indwelling catheters, or are immunocompromised. Iatrogenic septic arthritis due to needle arthrocentesis (is estimated to be between <1/10,000 to 1/3000 procedures) or arthroscopy (estimated to be between 0.0009 to 1.1%) is very rare.
SEPTIC ARTHRITIS | OSTEOMYELITIS: ACUTE AND CHRONIC | ||
---|---|---|---|
MICROORGANISM | FREQUENCY (%) | MICROORGANISM | FREQUENCY (%) |
Gram-Positive | 60-90 | Gram-Positive | 80-90 |
Staphylococcus aureus Group A, B, C streptococci Coagulase-negative staphylococci Streptococcus pneumoniae Enterococcus sp Corynebacterium sp |
50-70 15-30 6-20 1-3 <1 <1 |
Staphylococcus aureus Group A, B, C streptococci Staphylococcus epidermidis Streptococcus pneumoniae Enterococcus sp Corynebacterium sp |
60-80 10-20 10-15 <1 1-2 1-2 |
Gram-Negative | 5-25 | Gram-Negative | 5-20 |
Salmonella sp Pseudomonas aeruginosa Escherichia coli Klebsiella pneumoniae Enterobacter sp Kingella kingae ∗ Haemophilus influenzae |
<1-3 ∗ |
Salmonella sp Enterobacter sp Pseudomonas aeruginosa Brucella sp Pasteurella multocida Bartonella henselae Propionibacterium sp |
|
Anaerobes | 1-2 | Anaerobes | |
Fusobacterium sp Bacteroides fragilis |
Bacteroides sp | ||
Miscellaneous | <5 | Miscellaneous | 5-7 |
Borrelia burgdorferi Mycoplasma Ureaplasma Mycobacterium sp Fungi Viruses Algae |
Mycobacterium sp Fungi (candidiasis, coccidioidomycosis, blastomycosis, histoplasmosis) |
Bacteria causing septic arthritis produce an acute inflammatory reaction in the synovial membrane. Synovial hyperplasia and inflammatory cell immigration, with the release of pro-inflammatory and cartilage-destroying cytokines and proteases, result in damage to cartilage and bone. Bacterial toxins and DNA as well as superantigens, such as those seen in staphylococcal toxic shock syndrome, also damage cartilage and bone.
Risk factors for the development of septic arthritis include penetrating trauma, diabetes, alcohol use disorder, cutaneous ulcers, injection drug use, prosthetic joints, rheumatoid arthritis, osteoarthritis, and low socioeconomic status, as well as advanced age, skin infection, indwelling intravenous catheters, cancer, and immunosuppressive therapies, including biologic response modifiers used in the management of autoimmune diseases such as rheumatoid arthritis and inflammatory bowel disease.
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