The biggest challenge in diagnosing septic arthritis is to think of it. Once you think of it, there is a diagnostic process that you activate. The second biggest challenge is that that diagnostic process we learn in training is flawed. We have no alternatives right now, so I will share with you my thoughts on how we should use our judgment as clinicians.
Triggers to consider septic arthritis essentially are the same triggers as infection anywhere. Celsus’ cardinal signs of inflammation are dolor (pain), calor (warmth), rubor (redness), tumor (swelling). Some authors have written that fluor (flow) should be the 5th cardinal sign and in this case the effusion is one of the most important clinical signs.
The detection of effusion at the bedside has been covered elsewhere but includes inspection, palpation, and milking. Smaller volumes of fluid are harder to detect. Ultrasound can be utilized to improve our accuracy.
The clinician generates hypotheses at the bedside and then circles back to revisit risk factors. This is an underappreciated process that deserves more attention. The following risk factors have high specificity:
-joint surgery (mainly recent)
-joint prosthesis (at any time)
There are others but those are the main ones. You might think of it as “compromised immune system” and “compromised joint.” If it helps you in remembering this, recall that the synovium is a vascular tissue. It lacks a basement membrane (which tends to filter out bacteria in other tissues, like the cornea). The joint relies on the immune system to protect us from bacterial translocation. Recall also that bacteria love to find crevices to hide in. A disrupted joint, or a compromised immune system creates the setting for septic arthritis.
They don’t all have to have those high risk features though. Often the clinician is left with enough suspicion to pursue a risk stratification process before considering a tap. In low risk patients that process can involve inflammatory markers (traditionally WBC, CRP, ESR, with emerging roles for procalcitonin and perhaps other markers) to lower your suspicion back below the threshold of further testing. I recommend you use as many of these as you need to reassure you in a low risk patient that there is no infection. All of them have limitations but if the results are normal, you are greatly reassured.
For patients where doubt continues to exist, the diagnostic pathway for septic arthritis ends in arthrocentesis, though its results may be less clear than we realize. Common practice is to use synovial blood counts (often 50K) as disease-defining, which does not actually work very well. Synovial WBC cutoffs at all levels will both miss and overcall septic arthritis. Even if you use the cutoff as 25K, it still misses as many as 1/4 of all cases, one prospective study said it would miss more than 1/3 of all cases (Margaretten JAMA2007). Meanwhile there will continue to be patients with WBC above 50K who have other causes (gout for example).
The gram stain sensitivity is as low as 40% (Ross Infect Dis Clin North Am2017). If you have strong suspicion based on risk factors, drain the joint and have them follow up in 24 hours, giving antibiotics while awaiting culture results.
-Septic arthritis is considered when the patient has an inflamed joint (effusion, warmth, pain).
-Inflammatory markers, if all normal, can lower your concern enough in a low risk patient to rule out disease.
-Risk factors (compromise of joint, compromise of immune system) may be more important than the other tests.
-Synovial WBC has significant limitations in sensitivity and specificity, and is not a disease-defining reference standard.
Infect Dis Clin North Am. 2017 Jun;31(2):203-218. doi: 10.1016/j.idc.2017.01.001. Epub 2017 Mar 30.
Margaretten ME, Kohlwes J, Moore D, Bent S.
JAMA. 2007 Apr 4;297(13):1478-88. Review.