Update on Antithrombin for the Treatment of Burn Trauma and Smoke Inhalation Injury
A severe imbalance of systemic and alveolar hemeostasis, as evidenced by an increase in pro-coagulant and a decrease in anti-fibrinolytic activities, represents a hallmark of burn trauma and smoke inhalation injury . The resulting hypercoagulable state is established within the initial 24 h after the injury and is characterized by high levels of activated factor VII, thrombin-antithrombin complexes, plasminogen activator inhibitor type-1 (PAI-1), and low levels of protein C as well as antithrombin . Plasma levels of antithrombin decrease by 50% in burn patients within the first five days and represent an independent predictor of length of hospital stay and mortality [1, 3]. However, the host response to burn trauma Cl:s well as to smoke inhalation injury, is not only restricted to coagulation disorders, but also includes a marked activation of the inflammation cascade . Both the systemic inflammatory response syndrome (SIRS) and the pro-coagulatory imbalance in hemostasis ultimately result in multiple organ failure (MOF) and increased mortality rates.
KeywordsAcute Lung Injury Tissue Factor Total Body Surface Area Antithrombin Deficiency Smoke Inhalation Injury
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