Authors: Roberta J. Pritchard, MD (EM Resident Physician, Virginia Tech-Carilion), Haleigh Bodeau, MD (EM Resident Physician, Virginia Tech-Carilion), Patrick Bonson (MS3, Virginia Tech-Carilion) and Matthew Borloz, MD (Associate Professor of Emergency Medicine, Virginia Tech Carilion School of Medicine) // Reviewed by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit)

Case

A 44-year-old male presents after several days of redness, pain, and swelling to his right elbow that he noticed while roofing.  He is otherwise healthy and has no medical or surgical history.  Vital signs are notable for a temperature of 100.6°F.  Exam reveals fluctuance, warmth, and mild erythema over the olecranon process without any obvious signs of trauma or skin breakdown.  Active range of motion is limited, but passive range of motion is preserved.

What is your differential diagnosis?

Background

Bursae (singular bursa) are mobile, sac-like structures filled with synovial fluid that serve to reduce friction and protect soft tissues from bony projections.  There are more than 150 bursae in the body, classified as either superficial or deep. While most bursae are present at birth, some (called adventitious bursae) develop due to an underlying pathology.  Most bursae are closed; however, some bursae communicate openly with the joint (e.g., the suprapatellar bursa).  Bursitis refers to inflammation of these fluid-filled structures that results in increased fluid production, swelling, and pain.  Septic (or infectious) bursitis occurs when organisms inoculate the bursa from superficial trauma, hematogenous spread, or direct spread from surrounding structures.  The most common bursae affected are the olecranon, prepatellar, and superficial infrapatellar bursae.  Septic bursitis is uncommon and is often difficult to distinguish clinically from aseptic bursitis, cellulitis, and septic arthritis.  The diagnosis is confirmed by needle aspiration and fluid analysis [1, 2, 3, 4].

Pearls

• Septic bursitis – inflammation of a bursa from an infectious organism
• Should be considered in the evaluation of a hot and swollen joint

Anatomy

Only a few of the 150 bursae in the body are clinically relevant.  Most septic and aseptic bursitis occurs in the olecranon or prepatellar bursae, likely secondary to their frequent exposure to minor trauma [1, 5, 6].  Approximately 70% of septic bursitis cases are secondary to trauma, which may be acute or from chronic, repetitive trauma [5].  Numerous other bursae in the body can become inflamed, resulting in aseptic bursitis, but septic bursitis is rare.  These include the subacromialbursa (on the lateral shoulder, inferior to the distal acromion and deep to the proximal deltoid muscle), the iliopsoas bursa (between the anterior aspect of the joint capsule of the hip and the iliopsoas muscle), the popliteal or gastrocnemius-semimembranous bursa (known as a “Baker’s cyst”), the ischiogluteal bursa (located over the ischium), the trochanteric bursa (overlying the femoral greater trochanter), and several small bursae of the ankle and foot [7].

Septic bursitis of the elbow

The olecranon bursa, which is located over the olecranon process of the elbow, is prone to bursitis, or “student’s elbow,” from trauma, infection, and inflammatory processes.  Athletes, plumbers, carpenters, mechanics, miners, soldiers, and those with chronic disease states such as COPD (leaning on elbows to catch their breath) or requiring hemodialysis are predisposed to olecranon bursitis.  Untreated olecranon bursitis can progress to osteomyelitis [4, 7, 8].

The superficial location of the olecranon bursa allows for visualization with ultrasound.  In a normal bursa this is represented by a thin, hypoechoic layer, with potential septations in the subcutaneous tissues that may be difficult to see in the absence of pathology.  This is best visualized with the elbow in 90° of flexion with a thick layer of gel and minimal pressure.  Imaging may reveal complex fluid, synovial hypertrophy, hyperemia on color Doppler flow, and possibly gas; however, none of these are diagnostic [9].  These findings, particularly gas, should trigger the strong consideration for alternative diagnoses including necrotizing fasciitis.

Image A – Long axis view of olecranon bursitis. Case courtesy of Dr Maulik S Patel, Radiopaedia.org. From the case rID: 19682

Image B – Short axis view of olecranon bursitis. Case courtesy of Dr Maulik S Patel, Radiopaedia.org. From the case rID: 19682

The recommended approach to aspiration of the olecranon bursa involves a 20-gauge needle and 10-mL syringe held parallel to the forearm and advanced into the bursal fluid collection.  To minimize the risk of persistent drainage and infection, the needle insertion site should be 2-3 cm away from the bursa using aseptic technique.  This procedure may be augmented by ultrasound, but it is typically unnecessary.  In suspected septic bursitis, injection of steroids is contraindicated [10].

Septic bursitis of the knee

The next most common location of septic bursitis are the patellar bursae, which were more frequently associated with underlying diabetes mellitus than olecranon bursitis in one study [6].  Professions predisposed to patellar bursitis include maids, nuns, roofers, gardeners, and tugboat operators. There are three significant anterior bursae.

Prepatellar bursa -The prepatellar bursa is located between the patella and the superficial tissues. When inflamed, it is referred to as “housemaid’s” or “carpet-layer’s” knee.  This is the most common bursa in the knee to become infected. On ultrasound, it is visualized as a fluid collection directly superficial to the patella [9].

Suprapatellar bursa – The suprapatellar bursa is located between the femur and the quadriceps tendon and communicates with the knee joint.  It is often referred to as the suprapatellar recess.  This is best visualized in the sagittal plane with the knee flexed to 30° [9].

Infrapatellar bursa – The infrapatellar bursa is actually two bursae located at the distal portion of the patellar tendon, near the tibial tuberosity.  These are described as superficial and deep, denoting their relative location about the patellar tendon.  Inflammation of this bursa is called “clergyman’s knee.”  Ultrasound over the tibial tuberosity will show a focal fluid collection. These views are best obtained with minimal pressure and generous ultrasound gel [9].

Aspiration of the patellar bursae should be performed with a 2.5-cm, 20-gauge needle and 10-mL syringe held parallel to the extremity and introduced using aseptic technique.  Milking the affected bursa during aspiration may help to facilitate removal of fluid in what is often a multi-loculated space.  Again, ultrasound may help to guide the needle and evaluate for adequacy of drainage [10].

Pearls

• The olecranon and prepatellar bursae are the most common sites of septic bursitis
• Ultrasound may be helpful but is not diagnostic
• Bursal aspiration is within the scope of practice of emergency physicians and is the most helpful diagnostic tool
• Bursal steroid injection is contraindicated in septic bursitis

Presentation, Evaluation, and Diagnostic Workup

Septic bursitis predominantly affects males aged 40-60 [2].  The presentation overlaps with several other conditions, rendering the diagnosis challenging.  As highlighted below in Table 1, there are several discriminatory findings that are suggestive of septic bursitis, such as fever, increased warmth, and pain.  Overlying cellulitis and evidence of trauma can also be helpful [1, 11].  Classic findings on exam are fever, increased warmth of the skin overlying the bursa, pain over the skin, fluctuance over an anatomical location of a bursa, and preserved passive movement of the joint (a clinical distinction from septic arthritis) [12].  Aseptic bursitis, defined as inflammatory changes of the bursa without infection, may present with similar symptoms. This can include tenderness, erythema, and warmth; however these occur with less severity and frequency.  The key to separating the diagnosis of septic and aseptic bursitis is the presence of fevers and the findings of the bursal aspirate. Differentials for septic bursitis should include cellulitis, arthropathies, aseptic bursitis (including gout & pseudogout), hemorrhagic bursitis, septic arthritis, trauma, abscess, and others.

Table 1. Table adapted from [11,14]

Needle aspiration is the standard for diagnosis and is ideally performed prior to administering antibiotics.  Accessing the superficial bursae is typically straightforward, whereas the deep bursae can be more challenging.  Refer to the aspiration procedures described above.  The aspirate should be sent for cell count with differential, Gram stain, culture (anaerobic, aerobic, and possibly mycobacterial/fungal), and crystal analysis. Of note, the diagnostic WBC threshold in the aspirate is lower than that used for septic arthritis, typically above 5,000 cells/mm³. Levels less than 2,000 cells/mm³ with mononuclear cell predominance suggest nonseptic bursitis. A bursal blood glucose at bedside can be helpful in expediting the diagnosis.  If the glucose-to-serum ratio is less than 50%, it is almost certainly septic bursitis [13].  In the setting of recent antibiotics or infection with a fastidious organism septic bursitis cultures may be negative, and septic bursitis should still be considered [4].   Bursae have limited vascular supply, which minimizes the occurrence of hematogenous spread, but blood cultures should be considered.

Most septic bursitis is caused by Staphylococcus aureus (80-90%), followed by Streptococcus and coagulase-negative Staph.  Other etiologies may be seen in immunocompromised hosts, such as Escherichia coli, Meningococcus, Cutibacterium, Enterococcus, Pseudomonas, anaerobes, and Brucella.  If the septic bursitis is persistent or the host is immunocompromised, consider possible fungal or mycobacterial infection, including TB [3, 15,16].

Pearls

• The diagnostic gold standard for septic bursitis is bursal fluid culture
• Negative bursal fluid culture does not exclude the diagnosis of septic bursitis, especially if due to a fastidious organism or when antibiotics precede culture
• A number of other signs are associated with septic bursitis (Table 1) and can be used to support the dx
• Bursal fluid aspiration should be performed prior to antibiotic use

Treatment

All patients suspected of having septic bursitis should be treated with appropriate antibiotic therapy, whether diagnosed clinically or by laboratory findings.  Therapy should empirically cover S. aureus and Streptococcus as these are the most common species.  In reliable, otherwise healthy patients without concern for septic arthritis, immunocompromise, or clinical instability, a trial of outpatient oral antibiotic therapy (up to 14 days) is reasonable for uncomplicated septic bursitis.  Treat with dicloxacillin (500 mg orally four times daily), sulfamethoxazole and trimethoprim 800/160 mg (1-2 tabs twice daily), or clindamycin (300 mg four times daily) and arrange for follow up within 48 hours.  Rates of failure to outpatient therapy defined as persistent infection requiring inpatient or surgical management) vary, therefore clear return precautions and a reliable patient are essential.  For those with complicated septic bursitis, particularly with significant symptoms coverage should include vancomycin (15-20 mg/kg IV x 1 with subsequent doses based on levels and renal function).  Some studies support outpatient treatment with IV antibiotics if close follow up is available [13].  Once cultures result, antibiotics should be tailored.

Repeat needle aspiration may improve both symptoms and clinical outcome. Follow-up is recommended to assess for improvement. In persistent septic bursitis that fails conservative management, surgical intervention with incision and drainage or bursectomy may be required [1, 6, 7].  There are no data to support early surgical intervention; however, for those who develop signs of sepsis, worsening cellulitis, or other signs of clinical worsening surgical consultation is recommended [17].  Below is a proposed treatment algorithm for management in the Emergency Department modified from Orthopedic management guidelines published by Baumbach et al., which specifically addresses prepatellar and olecranon bursitis [14].  This algorithm has not been prospectively validated in an ED population.

Adapted from figure in [14].

Pearls

• Antibiotics should include empiric coverage for S. aureus and Streptococcus
• Close follow up within 48 hours

References / Further reading:

1. Hanrahan JA. Recent developments in septic bursitis. Curr Infect Dis Rep. 2013 Oct;15(5):421-425.
2. Reed MJ, Carachi A. Management of the nontraumatic hot swollen joint. Eur J Emerg Med. 2012 Apr;19(2):103-107.
3. Truong J, Ashurst JV. Septic Bursitis. [Updated 2019 Feb 14]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan.
4. Kotton DN, Kay J, Leversedge FJ. Septic Bursitis. In: UpToDate, Isaac, Z(Ed). (Accessed on January 20, 2020.)
5. Small LN, Ross JJ. Suppurative tenosynovitis and septic bursitis. Infect Dis Clin North Am. 2005; 19:991-1005.
6. Lieber SB, Fowler ML, Zhu C, Moore A, Shmerling RH, Paz Z. Clinical characteristics and outcomes of septic bursitis. Infection. 2017 Dec;45(6):781-786.
7. Zimmermann B 3^rd, Mikolich DK, Ho G Jr. Septic bursitis. Semin Arthritis Rheum. 1995; 24:391-410.
8. Sayegh ET, Stauch RJ. Treatment of olecranon bursitis: a systematic review. Arch Orthop Trauma Surg. 2014 Nov;134(11):1517-1536.
9. Ruangchaijatuporn T, Gaetke-Udager K, Jacobson JA, Yablon CM, Morag Y. Ultrasound evaluation of bursae: anatomy and pathological appearances. Skeletal Radiol. 2017;46(4):445-462.
10. Gupta N. Treatment of bursitis, tendinitis, and trigger points. In: Roberts JR, Custalow CB, Thomsen TW, eds. Roberts and Hedges’ Clinical Procedures in Emergency Medicine and Acute Care. 7^th Philadelphia, PA: Elsevier; 2019.
11. Wasserman AR, Melville LD, Birkhahn RH. Septic bursitis: a case report and primer for the emergency clinician. J Emerg Med. 2009 Oct;37(3):269-272.
12. Blumberg G, Long B, Koyfman A. Clinical mimics: an emergency medicine-focused review of cellulitis mimics. J Emerg Med. 2017 Oct;53(4):475-484.
13. Hogrefe C, Jones E. Tendinopathy and bursitis. In: Walls RM, Hockberger RS, Gausche-Hill M, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 9^th Philadelphia, PA: Elsevier; 2018.
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; 134:359-370.
15. Oda R, Sekikawa Y, Hongo I. Meningococcal bursitis. Intern Med. 2017 Dec 15;56(24):3403-3404.
16. Herring K, Mathern S, Khodaee M. Septic infrapatellar bursitis in an immunocompromised female. Case Rep Orthop. 2018; 2028:9086201.
17. Abzug JM, Chen NC, Jacoby SM. Septic olecranon bursitis. J Hand Surg. Aug 11;37(6):1252-1253.