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Abstract

Objective—Inconclusive findings about infection risks, importantly the use of immunosuppressive medications, in patients who have undergone large-joint total joint arthroplasty challenge efforts to provide evidenced-based perioperative total joint arthroplasty recommendations to improve surgical outcomes. Thus, the aim of this study was to describe risk factors for developing a postoperative infection in patients undergoing TJA of a large joint [total hip arthroplasty, total knee arthroplasty, or total shoulder arthroplasty] by identifying clinical and demographic factors, including the use of high risk medications (i.e., prednisone and immunosuppressive medications) and diagnoses (i.e., rheumatoid arthritis [RA], osteoarthritis [OA], gout, obesity, diabetes mellitus), that are linked to infection status, controlling for length of follow-up.

Methods—A retrospective, case-control study (N = 2,212) using de-identified patient health claims information from a commercially-insured, U.S. dataset representing 15 million patients annually (January 1, 2007 - December 31, 2009) was conducted. Descriptive statistics, t-test, chi-square test, Fisher's exact test, and multivariate logistic regression were used.

Results—Male gender (OR = 1.42; p < .001), diagnosis of RA (OR = 1.47; p = .031), diabetes mellitus (OR = 1.38, p = .001), obesity (OR = 1.66, p < .001) or gout (OR = 1.95; p = .001), and a prescription for prednisone (OR = 1.59; p < .001) predicted a post-operative infection following total joint arthroplasty. Persons with post-operative joint infections were significantly more likely to be prescribed allopurinol (p = .002) and colchicine (p = .006; no significant difference was found for the use of specific disease modifying anti-rheumatic drugs and TNF-α inhibitors.

Conclusion—High-risk, post-operative joint infection groups were identified allowing for precautionary clinical measures to be taken.

Document Type

Article

Publication Date

2-2017

Notes/Citation Information

Published in Seminars in Arthritis and Rheumatism, v. 46, issue 4, p. 423-429.

© 2016 Elsevier Inc. All rights reserved.

This manuscript version is made available under the CC‐BY‐NC‐ND 4.0 license https://creativecommons.org/licenses/by-nc-nd/4.0/.

The document available for download is the author's post-peer-review final draft of the article.

Digital Object Identifier (DOI)

https://doi.org/10.1016/j.semarthrit.2016.08.011

Funding Information

This work was supported in part by the National Center for Research Resources and the National Center for Advancing Translational Sciences, National Institutes of Health [UL1TR000117]. Access to the large commercially insured dataset was made available with funding from CTSA UL1TR000117.

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