ISSN: 2041-6792

Clinical Investigation

Postoperative Coagulopathy

 During hemostasis, coagulation factors participate during a complex cascade culminating within the generation of thrombin, which catalyzes the conversion of fibrinogen to fibrin. Fibrinogen plays a critical role in achieving and maintaining hemostasis; it is the precursor to fibrin, an important component of blood clots. Subsequent polymerization forms fibrin strands, which become covalently cross-linked by activated clotting factor XIII [2]. Fibrinogen also promotes platelet aggregation by binding glycoprotein IIb/IIIa receptors. These platelets strengthen the clot by becoming enmeshed within the fibrin strands.   Physiological hemostasis may be a balance between coagulation (clot formation) and fibrinolysis (clot breakdown) to guard against extreme situations like hemorrhage and thrombosis. An imbalance in physiological hemostasis results in coagulopathy, a condition characterized by inability of the blood to clot. Coagulopathy could also be caused by a discount or complete absence of blood-clotting proteins or as a results of dysfunction or reduced levels of platelets. This condition can lead on to spontaneous bleeding or can exacerbate bleeding resulting from trauma, surgical procedures or medical therapy. However, in critically ill patients, activation of the coagulation system as a results of trauma, inflammation, or infection may cause thrombosis or thromboembolic complications. within the clinical settings of cardiovascular surgery, trauma and obstetrics, the first causes of bleeding are usually anatomical instead of pathophysiological and therefore the initiative to management often involves surgical measures.

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