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      Therapeutics and Clinical Risk Management (submit here)

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      Is Open Access

      Validity of subjective smoking status in orthopedic patients

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          Abstract

          Purpose

          In this level 1 diagnostic study, we analyzed the validity of subjective smoking status and, as secondary research question, the smoking cessation adherence in orthopedic patients during a routine hospital stay of nonunion patients by measuring serum cotinine.

          Methods

          We included patients undergoing revision surgery due to nonunion of long bones. Patients were interviewed about their smoking status. Blood samples were taken from all the patients prior to surgery and for an additional 6 weeks following surgery. Serum levels of cotinine were measured, and coherence between subjective smoking status and objective cotinine analysis was evaluated.

          Results

          Between March 2012 and August 2014, we enrolled 136 patients. Six of the 26 “previous smokers” (23%) and four of the 65 “nonsmokers” (6%) had serum cotinine above cutoff levels. In self-labeled smokers, serum cotinine levels averaged at 2,367.4±14,885.9 ng/mL (with a median of 100 ng/mL), whereas in previous smokers the levels averaged at 4,270±19,619.4 ng/mL (with a median of 0 ng/mL) and in the nonsmokers group the levels averaged at 12±53.9 ng/mL (with a median of 0.03 ng/mL). Overall, the subjective smoking status matched serum cotinine testing in 88% of the cases. Sensitivity was 79.6% and specificity was 93.1%. Ninety-one percent of the patients with preoperative positive serum values were still positive at follow-up.

          Conclusion

          In this study, we could show that subjective smoking status in orthopedic patients is predominantly reliable as validated by objective cotinine measurements; however, patients who declare themselves as “previous smokers” are at elevated risk for underreporting continued smoking and patients who smoked preoperatively are at high risk for continuing their habit. In the future, caregivers should consider introducing effective treatments for smoking cessation to smokers and furthermore offer effective treatments to maintain smoking cessation in previous smokers during their routine consultation prior to orthopedic and trauma surgery.

          Most cited references18

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          Cotinine as a biomarker of environmental tobacco smoke exposure.

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            Wound healing and infection in surgery: the pathophysiological impact of smoking, smoking cessation, and nicotine replacement therapy: a systematic review.

            The aim was to clarify how smoking and nicotine affects wound healing processes and to establish if smoking cessation and nicotine replacement therapy reverse the mechanisms involved. Smoking is a recognized risk factor for healing complications after surgery, but the pathophysiological mechanisms remain largely unknown. Pathophysiological studies addressing smoking and wound healing were identified through electronic databases (PubMed, EMBASE) and by hand-search of articles' bibliography. Of the 1460 citations identified, 325 articles were retained following title and abstract reviews. In total, 177 articles were included and systematically reviewed. Smoking decreases tissue oxygenation and aerobe metabolism temporarily. The inflammatory healing response is attenuated by a reduced inflammatory cell chemotactic responsiveness, migratory function, and oxidative bactericidal mechanisms. In addition, the release of proteolytic enzymes and inhibitors is imbalanced. The proliferative response is impaired by a reduced fibroblast migration and proliferation in addition to a downregulated collagen synthesis and deposition. Smoking cessation restores tissue oxygenation and metabolism rapidly. Inflammatory cell response is reversed in part within 4 weeks, whereas the proliferative response remains impaired. Nicotine does not affect tissue microenvironment, but appears to impair inflammation and stimulate proliferation. Smoking has a transient effect on the tissue microenvironment and a prolonged effect on inflammatory and reparative cell functions leading to delayed healing and complications. Smoking cessation restores the tissue microenvironment rapidly and the inflammatory cellular functions within 4 weeks, but the proliferative response remain impaired. Nicotine and nicotine replacement drugs seem to attenuate inflammation and enhance proliferation but the effect appears to be marginal.
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              Inhibition of fracture healing.

              This paper reviews the current literature concerning the main clinical factors which can impair the healing of fractures and makes recommendations on avoiding or minimising these in order to optimise the outcome for patients. The clinical implications are described.
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                Author and article information

                Journal
                Ther Clin Risk Manag
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                1176-6336
                1178-203X
                2015
                27 August 2015
                : 11
                : 1297-1303
                Affiliations
                Trauma and Reconstructive Surgery, Center for Orthopedics, Trauma Surgery and Spinal Cord Injury, Heidelberg University Hospital, Heidelberg, Germany
                Author notes
                Correspondence: Patrick Haubruck, Trauma and Reconstructive Surgery, Center for Orthopedics, Trauma Surgery and Spinal Cord Injury, Heidelberg University Hospital, Schlierbacher Landstrasse 200a, D-69118 Heidelberg, Germany Tel +49 6221 563 5987, Email patrick.haubruck@ 123456med.uni-heidelberg.de
                [*]

                These authors contributed equally to this work

                Article
                tcrm-11-1297
                10.2147/TCRM.S86212
                4556244
                26345646
                df7ab0b9-ff9e-475f-ba3c-9c56d6cf597a
                © 2015 Bender et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Original Research

                Medicine
                smoking,cotinine,nonunion,smoking behavior,smoking cessation,risk evaluation
                Medicine
                smoking, cotinine, nonunion, smoking behavior, smoking cessation, risk evaluation

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