Abstract

Hemostasis is the process by which the body maintains the integrity of blood vessels and regulates blood circulation. It involves arresting bleeding, and possibly mending broken or severed blood vessels. It is achieved through a series of steps, including vascular spasm, platelet plug formation, coagulation cascade, and fibrinolysis. Skipping any of these steps causes severe bleeding and death. During pregnancy, the hemostatic system undergoes significant changes to adapt to the physiological demands. These changes aim to prevent excessive bleeding during and after childbirth. Hypercoagulability, characterized by elevated clotting factors and reduced fibrinolytic activity, is common during pregnancy. While these alterations in the coagulation system help prevent postpartum bleeding, they also increase the mother's risk of thrombosis by a factor of five. This hypercoagulable state is caused by pregnancy-related factors like venous stasis, endothelial damage, and hormonal fluctuations. However, studies have shown that an increase in Factor VIII levels poses as a risk factor for both venous and arterial thrombosis. The determination of plasma factor VIII levels is influenced by genetic factors, as well as the levels of von Willebrand factor (VWF) and the individual's blood group. The findings of familial investigations have revealed that the concentration of factor VIII is indeed hereditary, exhibiting a lesser degree of variability among twins when compared with individuals who lack a familial connection. Continuous monitoring should be performed on pregnant patients with thrombosis risk factors. This intervention is implemented with the aim of mitigating the potential aggravation of deep vein thrombosis (DVT) and the subsequent development of post-thrombotic syndrome.

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