The Body 's Clotting Of Clotting Factors

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Until around 2003, the medical community attributed the coagulopathy of trauma to excessive consumption of clotting factors, hemodilution by intravenous crystalloids, all while compounded by hypothermia and acidosis. A group of physicians at the Royal London hospital authored a paper hypothesizing that this was not entirely true and that the syndrome they labeled as Acute Traumatic Coagulopathy(ATC) manifests itself by simultaneously activating protein C, decreasing available fibrinogen, and inhibiting platelet function (Brohi, Singh, Heron, Coats, 2003; Kutcher et al., 2012). Many other factors contribute to the systemic alteration in coagulation; however, these three separate entities highlight pathophysiologically what happens during…show more content…
In the face of hemorrhagic and ischemic shock with endothelial damage, fibrinogen levels fall dramatically. Decreased fibrinogen levels directly alter the body’s ability to form the fine meshwork needed to achieve hemostasis. Normally, thrombin breaks down fibrinogen into fibrin to assist in providing the scaffolding for clotting. When severe tissue injury occurs, the lack of fibrin cannot form the mesh needed to assist in clot formation. The 2010 RCT CRASH-2 study displays the strongest evidence proving that administering tranexamic acid(TXA) to severely shocked trauma patients(MAP <75 mmHg) reduces the amounts of death from bleeding in this population from 18.4% to 14.9% (Napolitano, Cohen, Cotton, Schrieber, & Moore, 2013). Simply put, TXA prevents plasminogen’s conversion to plasmin. The inactivated plasminogen will then allow the clot to become more secure. Because of plasmin’s inherent ability to degrade fibrinogen, the patient’s d-dimer which measures fibrin degradation products, the patient with ATC will have elevated d-dimer levels. Low fibrinogen levels in a patient with ATC warrants cryoprecipitate infusion and has been associated with increased survival outcomes (Rourke, 2012). Impaired platelet function has been described prospectively by Kutcher et al. in response to traumatic tissue injury. This describes the primary hemostatic mechanism in which platelet dysfunction can alter platelet adhesion
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