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The Case:
This 55 year old corporate executive with well controlled hypertension presents with swelling of the right elbow for about 3 weeks. Over this time he has “bumped” his elbow more than once and is having increased pain in the area. He denies any obvious cuts to the elbow, fevers or rashes. Upon arrival to the ED his vital signs are unremarkable. His examination is significant only for a boggy prominence over his right elbow apex which is slightly erythematous and tender to palpation. He grimaces when passive motion is attempted. The right elbow is slightly warmer than the left. There is no axillary lymphadenopathy and the rest of his joints appear normal as does the remainder of his physical examination.

Any time a patient presents to the emergency department with a swollen joint the good emergency physician has to think “worst first.” Septic arthritis is probably the most serious thing on the differential that needs to be excluded, and must be entertained whenever a patient presents with any type of joint swelling. A missed diagnosis can result in destruction of the joint, fulminant sepsis and even death. The prevalence of septic arthritis has been estimated to be as high as 28% in one prospective ED study, and other studies have found the prevalence to be 10%.

From the history and physical exam it is quite obvious that this patient has an olecranon bursitis. He has the classic prominence over the olecranon with no joint involvement, and being a corporate executive puts him at risk for repetitively rubbing his elbow up against his desk while writing or typing. Other entities on the differential for a swollen joint include fracture, dislocation, tendonitis, crystal arthropathy, systemic disorders such as systemic lupus erythematosus and rheumatoid arthritis, and osteochondritis desiccans. The appropriate history and physical exam findings, in addition to radiographs if needed, can help in making these diagnoses.

Once we’ve decided this is likely an olecranon bursitis the next important question is whether it is infectious or sterile–differentiating between the two can be a clinical dilemma for even the most astute EP. So how can we differentiate between infectious and non-infectious bursitis? Are there any clinical findings or laboratory values that have been proven to be more indicative of a septic picture? Do we really need a bursa aspiration with classic elevation in WBC and low glucose to rule in the diagnosis while awaiting culture results?

Little research has been done looking at this dilemma. There have been a few studies that have looked specifically at septic arthritis, and it reasonably follows that the data can be extrapolated to be applied to olecranon bursitis. Margaretan et al did a PUBMED and EMBASE search and found 14 studies that examined risk factors as well as laboratory findings in assessing a patient’s likelihood of having septic arthritis. They specifically looked at the likelihood ratios that made the patient more or less likely to have septic arthritis. One study by Kaandorp et al found 8 clinical risk factors that increase the likelihood of septic arthritis in a patient (see table). Another study out of Rwanda (where the prevalence of HIV is as high as 30%) found that infection increases the likelihood of septic arthritis with a LR of 1.7 (95% CI 1-2.8). While no studies looked at the specificity of clinical symptoms for septic arthritis, 6 looked at the sensitivity. Interestingly, the presence of sweats and rigors, classically associated with septic pathology, were not found to be very predictive with sensitivities near 30%. What does this mean for the emergency room physician? If a patient has the relevant historical and clinical symptoms, the joint (or bursa in this case) should be aspirated and synovial fluid examined for signs of infection.This leads us to the next question. Are the classic synovial WBC, gram stain and culture all that is needed to rule in/out the diagnosis of olecranon bursitis? Is there any test that can affect our management while we are waiting for the gram stain and culture? Synovial WBC elevation progressively increases the likelihood of septic arthritis at progressively higher levels. According to four studies, elevation in polymorphonuclear cells apparently increases the likelihood as well, with a 90% predominance increasing the likelihood significantly (LR 3.4, 95% CI 2.8-4.2). What’s even more interesting is that a PMN predominance less than 90% actually decreased the likelihood ratio significantly (LR .34, 95% CI .25-.47).

What about serum laboratory values? Can we effectively rule in or out septic arthritis with an erythrocyte sedimentation rate and complete blood count? Apparently the answer is no, which may be against classic teaching and what some of our orthopedic colleagues may encourage us to do.  One prospective study from Jeng et al looked at 75 patients presenting with acute monoarticular arthritis to the emergency department and found that a WBC greater than 10,000/µl had a likelihood ratio of 1.4 ( 95 % CI 1.1-1.8) and ESR greater than 30 mm/h had a likelihood ratio of 1.3 ( 95% CI 1.1-1.8). With both of these confidence ratios approaching 1, it is fair to say that the presence of these elevated values does not significantly change our pretest probability of septic arthritis. 

What’s the bottom line?
Most patients with classic olecranon bursitis probably do NOT need their joint aspirated, unless they have the risk factors mentioned. If the bursa is aspirated the level of WBC elevation and especially polymorphonuclear cells significantly increases the likelihood of a septic bursa. Synovial glucose also is not very sensitive for predicting a septic joint. A change from common practice, a lactate dehydrogenase level should be sent with the synovial fluid analysis, with the understanding that it has a low specificity but high sensitivity. As for WBC and ESR, one could argue that it is pointless to even send them.

Risk Factors for Septic Arthritis
> Local Trauma
> Joint Surgery
> Prosthetic Joint
> Penile Sores/History of Gonorrhea
> Immunodeficiency
> Diabetes
> Previous Joint Disease (i.e. Gout)
> IV Drug Use
> Age Over 80


# question for the authorReader 2008-12-15 16:46
I have always aspirated it, if the patient had risk factors for a septic bursea or joint, and it the fluid was grossley normal, then, assumed that it was not septic. Is this wrong? Are you saying that you need a white count and a grm stain on the aspirated fluid to really rule out a spetic process?
# lab testsMark Silverberg 2008-12-16 19:28
I agree that you can tell by looking at a sample if the fluid is grossly purulent. You just know it is infected. However, some infections can be "new" or mild and not look terrible but the stain will reveal organisms. Sometimes the fluid may also look terrible but only be crystals and not an infection. You need to send the fluid to the lab and get the number of WBC's and stain of it to be sure. Even if you make the diagnosis by eye, you still need to get a sample of the fluid to the lab to get sensitivities just in case your treatment fails. In my opinion, it is unsafe to just look at a sample by eye and decide if it is infected or not.
# Editorial Advisory Board, EPMonthlyDavid Hoyer, MD FAAEM 2008-12-27 20:25
This article may cause confusion in that it uses the terms "arthritis" and "bursitis" interchangeably despite the fact that they are usually separate clinical entities. The authors' assumption that data for septic arthritis can be applied to olecranon bursitis in spite of anatomic and prognostic disease differences seems unwarranted.

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