Either as an acute presentation or as a possible postop complication, the physician may aspirate an acute joint effusion and send fluid for exam and culture. If there are numerous polys (neutrophiles) on the fluid exam, they could be due to infectious organisms vs crystallosis (such as gouty pyoarthrosis) vs STERILE ASEPTIC PYARTHROSIS reasons: such as PAPA syndrome... pyogenic arthritis, pyoderma gangrenosum, & acne⁶ vs "streaking leukocyte syndrome" (recurrent episodes of sterile pyarthrosis unresponsive or poorly responsive to antibiotic therapy but rapidly and completely responsive to prednisone therapy) or even vs FMF (Melungeon [mixed American Indian, black & white...tri-racial] USA people...and others of Mediterranean ancestry...tend to run an elevated total WBC & a proportion may reflect "familial Mediterranean fever" [FMF...a cause of night sweats, fever, pains, chronic fatigue]).

Postop joint appliance loosening due to sepsis & leading to joint revision (one stage if aseptic & 2 stage if septic) often lacks clinical clues as to sepsis. But, preop quantitative CRP levels being normal confers a strong likelihood that the loosening is non-septic⁴. Frozen section has excellent specificity and negative predictive value⁴. Pre-operative joint aspirations of these loosening cases are notoriously false negative by culture when the joint is actually septic (and, intra-operative cultures are also 50% false negative²). Until shown to be septic, a non-crystalosis pyarthrosis can still include rare instances of "idiopathic sterile pyarthrosis" [CN08-43]...see first paragraph, above. And, of course, the loosening can be due to aseptic reasons. Joint fluids also may be sent looking for morpological evidence of prosthesis failure: polys and/or organisms or joint-prosthesis debris.

Unless a frozen section is performed, special processing is advisable [HERE] so that the urate crystals in the specimen avoid aqueous processing and can be visualizable in wet preps or permanent tissue sections as refractile under polarized light exam.

CAUTION: Microbiologic culture of joint samples at surgery has been shown to yield both false positive & false negative results⁴. And innoculating a joint sample into a blood culture flask/bottle gains a better rate of true "positive cultures"³...& case positivity can also be enhanced if the prosthesis (in addition to that media innoculation) is sent sterile to microbiology for special handling. Feldman² modified Mirra's criteria: the surgeon (decisions 70% specific for sepsis²) selects the clinically "most suspcious" area...pink-tan tissue and NOT white fibrous scar tissue (of a pseudocapsule or the joint-cement interface) and sends at least two samples (or more) for frozen sections. The pathologist finds the 5 most cellular areas in a specimen for evaluation of concentration of tissue polys (do not count any surface exudate). Not counting any degenerating cells (cell margins and nuclei must be intact), 40x exam of at least the 5 areas makes a diagnosis of "septic" IF there are MORE than 5 polys per high power field in at least 5 separate high power fields. But, even this has only a 50% sensitivity. And, are all such positive cultures actually reflective of septic pathogenicity or just a reaction to "biofilms" of bacteria on the prosthesis surface which somehow impede the osteointegration of the prosthesis³? The most common organism is coag. neg. Staph³. And, aseptic calcinosis may be documented [L07-9036].

References:

1. Kaplan DL, et. al., "Pyogenic Arthritis...", J. Clinical Rheumatology 8(5): 273-275, October 2002.
2. Feldman DS, et. al., "The Role of Intraoperative Frozen Sections in Revision Total Joint Arthroplasty", J. Bone & Joint Surgery 77:1807-1813, 1995.
3. Bori G, et. al., "Low Sensitivity of Histology to Predict the Presence of Microorganisms in Suspected Aseptic Loosening of a Joint Prosthesis" , Modern Pathology 19(6):874-877, June 2006.
4. Kanner WA, et. al., "Reassessment of the Usefulness of Frozen Section Analysis for Hip and Knee Joint Revisions", AJCP 130(3):363 - 368, September 2008.
5. Mirra JM, et. al. 1976 & 1982.
6. Edrees AF, et. al., Pyogenic Arthritis...", J. Clin. Rheum. 8(5):273-275, October 2002.

(posted 21October 2007; latest addition 15 November 2009)