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<article xlink="http://www.w3.org/1999/xlink" dtd-version="1.0" article-type="emergency-medicine-and-critical-care" lang="en">
  <front>
    <journal-meta>
      <journal-id journal-id-type="publisher">JOHS</journal-id>
      <journal-id journal-id-type="nlm-ta">Journ of Health Scien</journal-id>
      <journal-title-group>
        <journal-title>Journal of HealthCare Sciences</journal-title>
        <abbrev-journal-title abbrev-type="pubmed">Journ of Health Scien</abbrev-journal-title>
      </journal-title-group>
      <issn pub-type="ppub">2231-2196</issn>
      <issn pub-type="opub">0975-5241</issn>
      <publisher>
        <publisher-name>Radiance Research Academy</publisher-name>
      </publisher>
    </journal-meta>
    <article-meta>
      <article-id pub-id-type="publisher-id">446</article-id>
      <article-id pub-id-type="doi">http://dx.doi.org/10.52533/JOHS.2025.51106</article-id>
      <article-id pub-id-type="doi-url"/>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Emergency Medicine and Critical Care</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>The Role of Tranexamic Acid (TXA) in Reducing Mortality in Trauma and Bleeding Patients&#13;
</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Alsamdani</surname>
            <given-names>Fawaz</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Alzahrani</surname>
            <given-names>Ahmed</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Alrumaih</surname>
            <given-names>Fahd</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Suliman</surname>
            <given-names>Talal Abu</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Alshahrani</surname>
            <given-names>Muteb</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Oways</surname>
            <given-names>Feras Bin</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Alghamdy</surname>
            <given-names>Basel</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Aljohani</surname>
            <given-names>Abdulsalam</given-names>
          </name>
        </contrib>
      </contrib-group>
      <pub-date pub-type="ppub">
        <day>11</day>
        <month>11</month>
        <year>2025</year>
      </pub-date>
      <volume>5</volume>
      <issue>11</issue>
      <fpage>578</fpage>
      <lpage>586</lpage>
      <permissions>
        <copyright-statement>This article is copyright of Popeye Publishing, 2009</copyright-statement>
        <copyright-year>2009</copyright-year>
        <license license-type="open-access" href="http://creativecommons.org/licenses/by/4.0/">
          <license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY 4.0) Licence. You may share and adapt the material, but must give appropriate credit to the source, provide a link to the licence, and indicate if changes were made.</license-p>
        </license>
      </permissions>
      <abstract>
        <p>Injuries caused by trauma are the leading cause of mortality worldwide. An injury causes imbalance in the homeostatic system which compromises the process of coagulation in which a clot of fibrin is formed to stop bleeding, balanced by the process of fibrinolysis in which plasmin the fibrin clot is degraded by plasmin to maintain normal blood flow. However, the increased release of plasmin leads to uncontrolled bleeding. Tranexamic acid (TXA), a lysine analog that binds to the lysine binding sites on plasminogen and prevents plasmin from degrading fibrin, is a commonly used antifibrinolytic agent to halt bleeding. Given its antifibrinolytic effects, TXA was proven to be effective in various medical applications, including the treatment of hemorrhage associated with trauma, partum, and traumatic brain injury, as proven by various wide-scale clinical trials. The standard dose for treatment of trauma is 1 mg administered intravenously within 3 hours of injury. In contrast, other studies report enhanced efficacy with higher doses and different administration routes. However, higher doses might be associated with adverse outcomes as thrombosis, seizures, and neurological disorders. TXA is a highly effective anti-fibrinolytic agent. However, further research is required to explore the associated adverse effects and assess the administration route and dosage that have maximum efficacy and minimum adverse effects. This review aims to explore the underlying mechanisms of the hemostatic system and how the antifibrinolytic action of TXA contributes to halting hemorrhage associated with various fatal conditions. It also aims to demonstrate recent knowledge on the administration routes and dosage of TXA, in order to provide insights into future research.&#13;
</p>
      </abstract>
      <kwd-group>
        <kwd>Tranexamic acid</kwd>
        <kwd> TXA</kwd>
        <kwd> Fibrinolysis</kwd>
        <kwd> Coagulation</kwd>
        <kwd> Antifibrinolytic Agents</kwd>
        <kwd> Hemorrhage</kwd>
        <kwd> Trauma-Induced Coagulopathy</kwd>
      </kwd-group>
    </article-meta>
  </front>
</article>