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Abstract
rauma is one of the world’s leading causes of death and
disability (Geeraedts et al, 2009).
Hemorrhage with decreased cardiac output is the most common cause of shock in trauma patients (Dutton, 2008).
Blood loss leads to hemodynamic instability, coagulopathy, decreased oxygen delivery, decreased tissue perfusion, and cellular hypoxia (Rossaint et al, 2006).
Coagulation disturbances following trauma appear to follow a trimodal pattern, with an immediate hypercoagulable state, followed quickly by a hypocoagulable state, and ending with a return to a hypercoagulable state (Brohi et al, 2007), Hyperfibrinolysis might also be an important issue in trauma patients (Hess et al, 2008).
Appropriate management of trauma patients with massive bleeding includes the early identification of potential bleeding sources followed by prompt measures to minimize blood loss, restore tissue perfusion and achieve haemodynamic stability (Rossaint et al, 2010).
The plasma expanders most widely used are isotonic crystalloids and synthetic colloids (Fluid Study Investigators for the Scandinavian Critical Care Trials Group, 2008), The essential advantage of a colloid is that its expansion property is always higher and more rapid than that of a crystalloid (Verheij et al, 2006), Albumin is a multifunctional protein with both colloidal and pharmacological activity (Quinlan et al, 2005), Albumin is considered necessary to increase COP to prevent extravasation of fluid from the intravascular space (Jain et al, 2004). HES solutions have a good plasma-expansive property, which lasts several hours. (Zaar et al, 2009).
Hemostatic alterations associated with the use of fluids are related to non-specific dilutional effects and colloid-specific effects (Kozek-Langenecker, 2009).
Albumin is considered to be the colloid with the least negative influence on coagulation, but some procoagulatory or anticoagulatory effects have been described with albumin (Boldt, 2008), Albumin has an antithrombotic, anticoagulant effect, possibly because of its capacity to bind nitric oxide (NO) to form S-nitrosothiols (Evans, 2002).
HES solutions interfere with coagulation and that the effects vary accord¬ing to the dose and type of solution administered (Traylor and Pearl, 1996), HES administration reduces circulating factor VIII and von Willebrand factor levels and leads to impairment of platelet function, prolongation of partial thromboplastin time and activated partial thromboplastin time with the subsequent risk of bleeding complications (Barron et al 2004), HES could favor fibrinolysis by incorporation of HES macromolecules in the clot (Strauss et al 2002), or increased plasminogen activator activity (Ickx et al 2002).