STH Review: Hemostasis and Menstrual Bleeding

Menstrual bleeding is one of the most common physiological bleeding events in humans, yet the mechanisms that terminate bleeding remain poorly defined. Current models of menstruation focus primarily on progesterone withdrawal, inflammation, vascular changes, tissue breakdown, local coagulation and fibrinolysis, and endometrial repair. However, considerably less is known about how hemostasis is controlled at individual bleeding vessels exposed during endometrial shedding. Spiral arterioles supply the functional endometrium and terminate in a dense capillary network, whose distal segments are disrupted during menstruation. Control of bleeding may depend on several interacting mechanisms, including uterine contraction, vascular tone, platelet-mediated primary hemostasis, coagulation, fibrin stabilization, fibrinolysis, and rapid tissue repair. Importantly, the relative contribution of these mechanisms depends on local hemodynamics. In arterial and arteriolar vessels, high shear rates trigger primary hemostasis through von Willebrand factor (VWF)-mediated platelet adhesion, also known as shear-induced platelet aggregation. This review examines current evidence on menstrual hemostasis and considers how vascular anatomy and hemodynamics may influence the mechanisms available to stop bleeding at the exposed endometrial surface. The flow conditions at bleeding spiral arterioles during menstruation have not been directly characterized. Defining these conditions may help determine how uterine contraction, platelet-VWF interactions, coagulation, and fibrinolysis interact to limit physiological menstrual blood loss and how disruption of this balance may contribute to heavy menstrual bleeding.