Given the challenges of diagnosing septic bursitis, these authors discuss key clinical signs, pertinent diagnostic tests and insights on effective treatment.

Bursitis is an inflammatory process involving any bursae that can be caused by infection, trauma, rheumatologic disorders, crystal deposition or idiopathic etiology.¹ Bursitis most commonly affects the subacromial, olecranon, trochanteric, prepatellar and infrapatellar bursae.

Septic bursitis refers to inflammation of the bursa due to infection, which typically is a result of bacterial inoculation that is direct (e.g., puncture wound), spread from nearby soft tissues (e.g., cellulitis), hematogenous (e.g., bacterial endocarditis) or indirect (e.g., direct blow). The two most common sites of infection are the olecranon and prepatellar bursae.² Mycobacterium, fungi or algae are less common causative agents.

Patients with a medical history of diabetes, alcoholism, uremia and/or chronic skin conditions are at an increased risk for infection.³

What You Should Know About Superficial Bursae And Deep Bursae
A bursa is a small, fluid-filled sac at the point where muscle or tendon slides across bone. Bursae reduce friction between the two moving surfaces. There are more than 150 bursae in the human body. Bursae are lined by synovial cells. Under ordinary circumstances, these cells produce a small amount of lubricating fluid.⁴

Superficial bursae are subcutaneous and separate skin from deeper tissues such as periosteum or ligaments. The superficial or subcutaneous bursae can become infected as a result of skin trauma, either from an occupational incident or a recreational activity, or due to a concomitant disease.1 Direct inoculation due to puncture of the overlying skin or contiguous spread from cellulitis are presumed to be the most common mechanisms involved in superficial septic bursitis.⁵

There are certain patient populations who may be more susceptible to septic bursitis. For example, clinicians may see olecranon septic bursitis in plumbers, carpenters, miners and athletes due to repetitive trauma. You may also diagnose this condition among patients with chronic obstructive pulmonary disease and those who receive chronic hemodialysis via vascular access in the arm.

Prepatellar or infrapatellar septic bursitis commonly affects carpet layers and gardeners who continually kneel for long periods of time. One may detect ischiogluteal septic bursitis among weavers and patients with spinal cord injuries.

When it comes to patients with hallux valgus, a bursa may form over the medial aspect of the first metatarsophalangeal joint. Pressure due to poorly fitting shoes can cause skin breakdown and bursal infection.

Deep bursae serve to reduce friction between fibrous structures such as tendons from adjacent bone. In regard to deep bursae, direct inoculation is uncommon but in rare cases, iatrogenic infection resulting from bursal injections of glucocorticoids (subacromial or trochanteric bursae) may occur. In the absence of a known inoculation, deep bursae infection is usually caused by hematogenous seeding or spread from an adjacent septic condition such as contiguous septic arthritis.⁵

Pertinent Insights On Initial Signs And Symptoms
The differential diagnosis of septic bursitis includes: rheumatoid arthritis, cellulitis, gout/pseudogout, soft tissue knee injury, Osgood Schlatter disease, tendonitis, septic arthritis, ligamentous injury, fracture, osteoarthritis and nonseptic bursitis.

Some of the symptoms of septic bursitis include swelling, tenderness to palpation and increased tactile warmth in the area of the infected bursa, fever and redness. Some people also have swollen glands near the infected bursa.⁵ Patients with superficial septic bursitis will typically present with pain, erythema, warmth and an effusion. Pain, fever, tenderness and decreased range of motion may indicate septic bursitis of the deep bursae. Clinicians may note peripheral blood leukocytosis, neutrophilia and a shift to immature forms in these cases.

Prepatellar or infrapatellar septic bursitis commonly affects gardeners and carpet layers, who continually kneel for long periods of time.

The absence of fever does not exclude infection. Also keep in mind that one-third of those with septic bursitis are afebrile.⁶

Some patients with septic bursitis may experience radiation of paininto the involved limb. Swelling is common in olecranon bursitis. While erythema may be present, it does not necessarily indicate sepsis. Patients with septic bursitis will usually have pain when clinicians ask them to execute a maneuver that stresses the involved motor unit. For example, asking a patient to abduct the hip against gravity will cause pain if the patient has trochanteric bursitis.⁷

While there may be clues in the patient history and physical exam, clinicians cannot rely solely upon these findings to differentiate between septic and aseptic bursitis. Further diagnostic studies are warranted. One should perform aspiration of the affected bursa for a cell count and differential. Clinicians should also obtain a Gram’s stain and culture to make an accurate diagnosis.²

Key Tips On Aspiration Procedures
When it comes to prepatellar bursal aspirations, ensure the patient is in a supine position. After spraying ethyl chloride on the skin, the clinician inserts a 1 1/2 inch, 18-gauge needle at the base of the bursa. Pass the needle into the center of the sac to a depth of 1 1/2 to 3/8 of an inch and proceed to aspirate fluid.

In regard to aspiration of the olecranon bursa, one would ensure supine positioning with the patient’s elbow flexed to 90 degrees and his or her forearm lying over the chest. Apply ethyl chloride to the skin for anesthesia. Insert a 1 1/2 inch, 18-gauge needle distally at the base of the bursa, nearly parallel to the ulna. Inject 1/2 mL of lidocaine subcutaneously prior to aspirating the bursal fluid.

A Guide To Bursal Fluid Analysis
Laboratory analysis of bursal fluid consists of determining the white blood cell (WBC) count, Gram’s stain and culture for bacteria. Fungal and/or mycobacterial stains and cultures may be appropriate in selected patients. Gardners, fishermen and immunosuppressed patients may be at risk for sporotrichosis, Mycobacterium marinum and atypical infections respectively. While anaerobic infection is rare, consider this when cultures are initially negative but infectious signs and symptoms persist.

Septic bursal fluid is characteristically cloudy or purulent in appearance, with greater than 15,000 white blood cells/mm3 and a positive culture.¹ The range of bursal fluid nucleated cell counts in septic bursitis is wide and the best threshold value is uncertain. Counts greater than 1,000 cells/mm3 indicate inflammation from infection, rheumatoid arthritis or gout.

In regard to cell count, one will note lower bursal fluid nucleated cell counts with bacterial infection of the bursa whereas synovial fluid nucleated cell counts are typically greater than 50,000/mm3 (5.0 x 10(9)/L) with septic bursitis.⁴ This was illustrated in a study, in which eight of 13 patients with culture-proven septic bursitis had bursal fluid leukocyte counts of less than 20,000/mm3. In contrast, only one of the 18 patients with septic arthritis had synovial fluid nucleated cell counts less than that threshold. The lowest bursal fluid WBC count in a culture-proven case of septic bursitis was 1200/mm3 (1.2 x 10(9)/L).⁴ Immunocompromised hosts may have a more limited inflammatory response.

The reported sensitivity of Gram's stain in detecting organisms ranges from 15 to 100 percent. When one does detect an organism, it can be helpful in guiding antibiotic therapy.4 Staphylococcus aureus is the causative organism in more than 80 percent of cases. Streptococci of various species are the next most commonly reported cause. Less commonly reported organisms causing acute septic bursitis include: coagulase-negative staphylococci, Enterococcus, Escherichia coli, Pseudomonas aeruginosa and anaerobes.

In regard to crystal identification, compensated polarized microscopy by an experienced clinician or technician is recommended. If crystals are present, the experienced technician can classify them on the basis of their shape and birefringence. The technique is the same as that one would employ to identify crystals in joint fluid. ⁸ The erythrocyte sedimentation rate is commonly mildly to moderately elevated in patients with septic bursitis.⁶

Here one can see a lateral view of hallux valgus showing instability in the dorsal and plantar planes. When it comes to patients with hallux valgus, a bursa may form over the medial aspect of the first metatarsophalangeal joint. Pressure due to poorly fitting shoes can cause skin breakdown and bursal infection. (Photo courtesy of Babak Baravarian, DPM)

Imaging Studies: Are They Worthwhile For Septic Bursitis?
Imaging studies are expensive and are not typically helpful with acute, superficial (e.g., olecranon or prepatellar) bursitis. However, when bursitis has a traumatic origin, clinicians may consider radiologic soft tissue techniques (e.g., xerography or plain films) or magnetic resonance imaging (MRI) to detect possible foreign body penetration.

If you suspect septic bursitis of a deep bursa, imaging with ultrasonography, CT or MRI may be required to confirm the presence of bursal fluid, associated abscesses or affected adjacent structures. One may incorporate ultrasonography or CT to guide needle aspiration of the bursa.⁸

Essential Treatment Considerations
Clinicians should suspect an infection when a patient has a red, warm bursa that yields cloudy or purulent fluid and is associated with overlying cellulitis and/or fever. One should accordingly aspirate the bursa, smear the fluid for a direct Gram’s stain and send for a microbiologic culture.

Pending the results of the fluid aspiration, clinicians can treat patients with mild symptoms as outpatients, prescribing 500 mg of dicloxacillin or cefalexin orally four times daily. In regard to patients who have penicillin allergies, it is best to use vancomycin. Always consider the severity of inflammation and microbiology of soft tissue infections in the community setting when considering initial empiric antibiotic therapy in patients whom you suspect of having superficial septic bursitis.

When treating a patient with an infected bursa, daily aspirations, typically made every one to three days, may be needed.^4,9 Clinicians should emphasize immobilization of the affected area and instruct the patient to avoid activities that may aggravate symptoms for one or two weeks. Patients may use nonsteroidal antiinflammatory drugs (NSAIDs) such as ibuprofen for mild to moderate inflammation.¹⁰

In regard to patients who demonstrate no improvement or appear to be getting worse despite oral antibiotics and bursal aspirations, those with more severe infections and those who are markedly symptomatic, clinicians should consider hospitalization. The need for hospitalization depends on both the severity of the infection and the degree of compromise. Patients with high fevers and chills, intense surrounding cellulitis, deep bursal involvement, extrabursal infection or suspicion of an uncommon organism should be hospitalized for parenteral antibiotics such as nafcillin or cefalexin IV.

In chronic cases refractory to antibiotics, a bursectomy may be indicated.¹¹
Surgical intervention may be warranted for acute septic bursitis in the following scenarios:
• when clinicians are unable to adequately drain the bursa using needle aspiration or catheter placement;
• when a foreign body is present; or
• when an adjacent skin or soft tissue infection requires debridement.

If the patient does not respond to initial treatment within 48 hours, inject a local anesthetic and then incise, drain and pack the area of infection.10 Up to 75 percent of patients with septic bursitis require surgical incision and drainage (I&D).¹² If there is no response to an I&D, the clinician should perform a surgical bursectomy and primary closure of the wound over a drain.²

How To Address Septic Bursitis In Pediatric Patients
Prepatellar pyogenic bursitis is common in children and is frequently misdiagnosed as septic arthritis, especially when the bursa is very large and the purulent accumulation produces significant swelling. Patients with this condition respond well to one or two daily aspirations, appropriate immobilization and/or antibiotic coverage. If there is no improvement after 48 hours, incision and drainage are required.¹³

Acute post-traumatic knee pain is frequently associated with erythema and edema of the anterior soft tissues of the knee. In contrast, patients with septic bursitis present with significant motion loss and tenderness. In these situations, synovial fluid aspiration for culture and sensitivity is mandatory. One may consider arthroscopic lavage.¹⁴

One of the pediatric risk factors for septic bursitis is atopic dermatitis, especially when it comes to olecranon bursitis. While Staphylococcus aureus reportedly colonizes an average of five percent of healthy patients’ skin, S. aureus is present most of the time in people with atopic dermatitis and exhibits superantigenic features that will also make the dermatitis worse.

Multiple studies focus on the fact that the association between atopic dermatitis and soft tissue infections is common and quite underreported. It is useful to remember that atopic skin provides a good environment for colonization, proliferation and invasion of S. aureus. When a patient with atopic dermatitis has acute illness with no apparent source, clinicians should consider the diagnosis of a S. aureus infection.¹⁵