Septic Bursitis

Etiology

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.[5][6][7]

Epidemiology

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.

Pathophysiology

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 and Physical

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. In a nutshell, the following should be the focus of the examination; swelling size, consistency (soft, firm, hard), fluctuance, associated cellulitis, and any lymphadenopathy. Also, the range of movement and pain of the adjacent joint should be carefully assessed and documented.

Evaluation

Ideally, investigations checking inflammatory markers and blood culture should be performed prior to starting antibiotic therapy. 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.[8][9][10].Magnetic resonance imaging has been reported in the literature as a reliable negative predictor of septic bursitis when there is no bursal and soft tissue enhancement [11].

 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.

Treatment / Management

Although non-infectious bursitis can be managed with conservative measures aimed at reducing inflammation, treatment for septic bursitis is always antibiotic therapy. Injection of non-steroidal anti-inflammatory drugs (NSAIDs) can be offered to control pain and injection of corticosteroids can be offered to cases where pain can not be controlled by NSAIDs. Treatment can be done on an outpatient basis with or without needle aspiration [12][13]; although, inpatient treatment with intravenous antibiotic therapy may be needed in patients who are immunocompromised, show systemic signs and symptoms, or have joint involvement [14]. 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, or 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. (B2)

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

Indications for Operative Intervention

• Significant pointing swellings [15].
• Severe cases that are unresponsive to medical treatment with antibiotics alone.
• Chronic cases.
• Recurrent cases.
(B2)

Operative Intervention

• Needle aspiration together with systemic antibiotics.
• Incision and drainage if aspiration fails due to loculation [15].
• Suction irrigation [16].
• Open or arthroscopic bursectomy: it was reported that single-stage acute bursectomy has higher recurrence rates in comparison to two-stage bursectomy with delayed primary closure [14]. The arthroscopic approach has a lower risk of wound complications in comparison with open approach.
(B2)

Differential Diagnosis

• Cellulitis

• Gout and Pseudogout

• Rheumatoid Arthritis

• Soft Tissue Knee Injury

• Tendonitis

Staging

Ho and Su classification system based on clinical signs [12]:

• Mild Bursitis: local inflammation with no associated systemic signs.
• Moderate Bursitis: significant local inflammation with or without mild systemic signs.
• Severe Bursitis: intense peri-bursal cellulitis with or without infected wound with systemic signs e.g. pyrexia or rigors, or a serum leukocytosis >10,000/mm.

Severity within the classification increases one level if there is a comorbidity that is likely to affect healing or immune response.

Complications

• Bursa rupture.
• Osteomyelitis.
• Wound healing problems (e.g. Dehiscence, excessive exudate, chronic sinus and skin necrosis).
• Recurrence: The most significant independent risk factor for recurrence is failure to intervene operatively when it is indicated (14.6% versus 80%) [14]. Whilst, in post operative cases, immunosuppression is the single independent risk factor for recurrence.