34
views
0
recommends
+1 Recommend
1 collections
    1
    shares

      To submit to Bentham Journals, please click here

      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The Effect of Air Tourniquet on Interleukin-6 Levels in Total Knee Arthroplasty

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background:

          Air tourniquet-induced skeletal muscle injury increases the concentrations of some cytokines such as interleukin-6 (IL-6) in plasma. However, the effect of an air tourniquet on the IL-6 concentrations after total knee arthroplasty (TKA) is unclear. We therefore investigated the impact of tourniquet-induced ischemia and reperfusion injury in TKA using the IL-6 level as an index.

          Methods:

          Ten patients with primary knee osteoarthrosis who underwent unilateral TKA without an air tourniquet were recruited (Non-tourniquet group). We also selected 10 age- and sex-matched control patients who underwent unilateral TKA with an air tourniquet (Tourniquet group). Venous blood samples were obtained at 3 points; before surgery, 24 h after surgery, and 7 days after surgery.

          The following factors were compared between the two groups; IL-6, C-reactive protein (CRP), creatine phosphokinase (CPK), the mean white blood cell (WBC) counts, and the maximum daily body temperatures.

          Results:

          The IL-6 level at 24 h after surgery was significantly higher than that at any other point (p<0.01). No significant differences were observed in the WBC count, the body temperature, or the CRP, CPK, or IL-6 levels of the two groups at any of the time points.

          Conclusion:

          The effect of ischemia and reperfusion due to the use of an air tourniquet on increasing the IL-6 level was much smaller than that induced by surgical stress in TKA.

          Related collections

          Most cited references40

          • Record: found
          • Abstract: not found
          • Article: not found

          Interleukin-6 and the acute phase response.

            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The pathophysiology of skeletal muscle ischemia and the reperfusion syndrome: a review.

            There are two components to the reperfusion syndrome, which follows extremity ischemia. The local response, which follows reperfusion, consists of limb swelling with its potential for aggravating tissue injury and the systemic response, which results in multiple organ failure and death. It is apparent that skeletal muscle is the predominant tissue in the limb but also the tissue that is most vulnerable to ischemia. Physiological and anatomical studies show that irreversible muscle cell damage starts after 3 h of ischemia and is nearly complete at 6 h. These muscle changes are paralleled by progressive microvascular damage. Microvascular changes appear to follow rather than precede skeletal muscle damage as the tolerance of capillaries to ischemia vary with the tissue being reperfused. The more severe the cellular damage the greater the microvascular changes and with death of tissue microvascular flow ceases within a few hours-the no reflow phenomenon. At this point tissue swelling ceases. The inflammatory responses following reperfusion varies greatly. When muscle tissue death is uniform, as would follow tourniquet ischemia or limb replantation, little inflammatory response results. In most instances of reperfusion, which follows thrombotic or embolic occlusion, there will be a variable degree of ischemic damage in the zone where collateral blood flow is possible. The extent of this region will determine the magnitude of the inflammatory response, whether local or systemic. Only in this region will therapy be of any benefit, whether fasciotomy to prevent pressure occlusion of the microcirculation, or anticoagulation to prevent further microvascular thrombosis. Since many of the inflammatory mediators are generated by the act of clotting, anticoagulation will have additional benefit by decreasing the inflammatory response. In instances in which the process involves the bulk of the lower extremity, amputation rather than attempts at revascularization may be the most prudent course to prevent the toxic product in the ischemic limb from entering the systemic circulation.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Cytokine serum level during severe sepsis in human IL-6 as a marker of severity.

              Forty critically ill surgical patients with documented infections were studied during their stay in an intensive care unit. Among these patients, 19 developed septic shock and 16 died, 9 of them from septic shock. Interleukin 1 beta (IL-1 beta), tumor necrosis factor (TNF alpha), and interleukin 6 (IL-6) were measured each day and every 1 or 2 hours when septic shock occurred. Although IL-1 beta was never found, TNF alpha was most often observed in the serum at a level under 100 pg/mL except during septic shock. During these acute episodes TNF alpha level reached several hundred pg/mL, but only for a few hours. In contrast, IL-6 was always increased in the serum of acutely ill patients (peak to 500,000 pg/mL). There was a direct correlation between IL-6 peak serum level and TNF alpha peak serum level during septic shock and between IL-6 serum level and temperature or C-reactive protein serum level. Moreover, IL-6 correlated well with APACHE II score, and the mortality rate increased significantly in the group of patients who presented with IL-6 serum level above 1000 pg/mL. Thus, IL-6 appears to be a good marker of severity during bacterial infection.
                Bookmark

                Author and article information

                Journal
                Open Orthop J
                Open Orthop J
                TOORTHJ
                The Open Orthopaedics Journal
                Bentham Open
                1874-3250
                30 January 2017
                2017
                : 11
                : 20-28
                Affiliations
                Department of Orthopaedic Surgery, Faculty of Medicine, Saga University, Nabeshima 5-1-1, Saga 849-8501, Japan
                Author notes
                [* ]Address correspondence to this author at the Department of Orthopaedic Surgery, Faculty of Medicine, Saga University, Nabeshima 5-1-1, Saga 849-8501, Japan; Tel: +81-952-34-2343; Fax: +81-952-34-2059; E-mail: epc9719@ 123456yahoo.co.jp
                Article
                TOORTHJ-11-20
                10.2174/1874325001711010020
                5301297
                28217217
                222ddd65-2f79-4f23-89a5-d79451563710
                © Tsunoda et al.; Licensee Bentham Open.

                This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) ( https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

                History
                : 17 September 2016
                : 17 November 2016
                : 02 December 2016
                Categories
                Article

                Orthopedics
                interleukin 6,ischemia,pneumatic tourniquet,reperfusion injury,surgical stress,total knee arthroplasty

                Comments

                Comment on this article