Bursae are fluid-filled sac-like structures located between mobile structures of the musculoskeletal system, between skin and bone, or between the joints. There are upward of 150 superficial and deep bursae located in between bone, muscle, tendons, and skin. Small amounts of synovial fluid are produced within the bursa and reduce friction by lubrication. Inflammation of the bursa causes excess fluid production and leads to swelling and irritation, known as bursitis. This inflammation can be caused by prolonged pressure, overuse, inflammatory and crystalloid arthritis, and direct injury or trauma. Common locations of bursitis include prepatellar, olecranon, and trochanteric.
Septic (or infectious) bursitis occurs when infection from either direct inoculation (usually superficial bursa) or hematogenous or direct spread from other sites (deep bursa involvement) causes inflammatory bursitis. Septic bursitis can be acute, subacute, or recurrent/chronic. The clinical features of septic bursitis are sometimes indistinguishable from non-infectious bursitis; therefore, bursa aspiration and fluid analysis must be completed to make an accurate diagnosis.
Inoculating the bursa with infections bacteria causes septic bursitis. This happens most often from micro-trauma or direct puncture of the overlying skin causing subsequent infection. Contiguous spread of overlying cellulitis of the skin is also a common cause of superficial septic bursitis. In 80% to 90% of cases, Staphylococcus aureus is the most common organism in acute septic bursitis and Streptococcus species being the next. Other organisms include Escherichia coli, Enterococcus, Pseudomonas aeruginosa, and coagulase-negative staphylococci. Chronic, infectious bursitis is likely due to atypical mycobacteria and fungi and should warrant prompt evaluation for systemic infection.
Septic bursitis happens more commonly in males with the mean age at onset approximately 50 years. Some studies suggest increases in the incidence of septic bursitis in relation to people with comorbid disease conditions, but most cases are due to repetitive trauma related to occupational behaviors. Plumbers, carpenters, roofers, clergy, and athletes are commonly affected. Septic bursitis can also be caused by joint steroid injections meant to relieve the symptoms of non-infectious bursitis. Patients with underlying crystal-induced arthropathy like Gout have an increased amount of bursal fluid and can have higher incidences of septic bursitis. People with inflammatory arthritis, for example, rheumatoid arthritis, are also at an increased risk.
Bursitis is the result of inflammation that leads to increased fluid production from the synovial cells that line the bursa. Increased fluid production leads to increasing pressure of the bursa and in the result, increased pain. Trauma or puncture of skin at the site of a bursa can lead to the direct introduction of bacteria and subsequent inflammation and infection. Overlying skin and soft tissue infections such as cellulitis can also lead to secondary infectious bursitis. In deep bursa, an infectious spread is more likely related to spread from blood or joint infections such as septic arthritis.
History may allude to the recent trauma of the affected area or an occupation suspicious for a high likelihood of septic bursitis. Therefore, it is important to ask relevant questions. Clinical findings may be indistinguishable from non-infectious bursitis and sometimes even a septic joint. Patients with septic bursitis are more likely to present with pain or tenderness overlying the bursa, edema, erythema, and warmth. Patients may also have signs of trauma or wounds and lesions with or without symptoms of cellulitis. Fever may or may not be present but is more likely to be present when bursitis is infectious versus when it is non-infectious. Joint motion is usually unaffected in septic bursitis and likely limited with septic arthritis. The findings discussed above are not completely reliable in distinguishing between infectious and non-infectious bursitis, and therefore, additional diagnostic testing must be done.
Routine blood work is somewhat unhelpful in the diagnosis and distinguishing septic bursitis versus non-infectious bursitis. The peripheral white blood count (WBC) may not differ between infectious and non-infectious bursitis and may not even be elevated above the normal range. However, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) usually are elevated in septic bursitis. A uric blood acid level should also be checked if suspicion of underlying crystal arthropathy exists. Antinuclear antibody and rheumatoid factor can be ordered in chronic cases or when the underlying autoimmune disease is suspected. Plain film radiography is usually performed, but it is unnecessary and unhelpful in most cases of septic bursitis. Spurs may be seen in chronic cases of bursitis, but joint effusions are not normally present. Computed tomography (CT) and magnetic resonance imagining (MRI) are not needed unless suspicion for osteomyelitis or septic arthritis exists, or if the physician is evaluating a severe case of septic bursitis in which surgical management may be necessary.
Aspiration and analysis of bursal fluid is the gold standard of diagnostic criteria. A bursal fluid analysis should always be performed in any case of bursitis to rule out septic or crystal-induced bursitis. Fluid should be evaluated for cell count with differential, gram stain, culture, and crystals. In recent literature summaries, the average bursal WBC was found to be around 63,000/mm; although, other studies show leukocytosis of more than 2000/mm was 94% sensitive and 79% specific for septic bursitis. Septic bursitis usually has a predominance of polymorphonuclear leukocytes while non-infectious has a predominance of mononuclear cells. Gram staining can vary between 15% and 100% sensitive and may only be positive in half of septic bursitis cases. However, a negative gram stain with WBC more than 50,000/hpf and clinical signs and suspicion for septic bursitis should be treated accordingly. The culture of bursal fluid should always be done in order to evaluate for any bacterial growth in order to help guide treatment.
Although non-infectious bursitis can be managed with conservative measures aimed at reducing inflammation, treatment for septic bursitis is always antibiotic therapy. Treatment can be done on an outpatient basis; although, inpatient treatment with intravenous antibiotic therapy may be needed in patients who are immunocompromised, show systemic signs and symptoms, or have joint involvement. In chronic or severe cases, incision and drainage or bursectomy may be warranted. An orthopedic surgeon should be consulted for all cases of septic bursitis.
Antibiotic therapy should initially be aimed at the most likely organisms and tailored as needed to gram-stain and culture results. Methicillin-resistant Staphylococcus aureus coverage with oral clindamycin, doxycycline, and trimethoprim-sulfamethoxazole is recommended for empiric therapy until culture results are finalized. If there is a severe local infection or in an immunocompromised patient, admission for intravenous vancomycin is most appropriate. For those patients with a penicillin allergy, the recommended treatment is ciprofloxacin and rifampin.
Duration and type of therapy are debated. Recommendations include a minimum of 10 days of treatment in mild cases, and repeat aspirations and continuation of antibiotics until bursal fluid is clear of infectious signs in severe cases. Treatment can usually be guided by clinical response and culture results.
Although debate over the duration of treatment exists, the fact of the matter is septic bursitis requires antibiotic treatment. Chronic septic bursitis can develop if initially not treated appropriately. Complications such as osteomyelitis and continual pain can occur. Overlying ligaments and tendons can become weak and may rupture due to chronic infection. Therefore, tendinitis must be a consideration when diagnosing septic bursitis.