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Although hemorrhage caused by intracranial, aneurysmal, and gastrointestinal pathologies account for a significant proportion of all deaths in the older-than-60-year age group, fatal bleeding caused by primary defects in coagulation and platelets are less common. Nevertheless, the development of a bleeding diathesis in an elderly patient presents clinical challenges that form the focus of this chapter.

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Hemostasis is a highly regulated process involving a dynamic balance between coagulation and fibrinolytic proteins and their inhibitors, platelets, and the vascular endothelium. The overall aim of the coagulation system is to rapidly generate a hemostatic plug at sites of vascular injury to prevent catastrophic blood loss from severed vessels. Congenital or acquired disturbances of the delicate balance between coagulation and fibrinolysis may result in thrombotic or hemorrhagic clinical manifestations.

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Elderly patients more commonly present with acquired bleeding disorders, but occasionally a mild congenital bleeding diathesis may remain hidden until later years when surgical procedures become common, when comorbid disease develops (such as renal or hepatic dysfunction), or when an additional acquired condition creates an additive challenge to the hemostatic system, such as the introduction of antiplatelet agents or anticoagulant therapy. Focusing on bleeding in the elderly, this chapter (a) provides a brief overview of hemostatic mechanisms, (b) discusses the clinical assessment of an elderly patient with a history of bleeding, (c) details the main inherited and acquired hemorrhagic conditions and their presentation in an elderly population, and (d) outlines the treatment of elderly patients with hemorrhagic states.

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Following damage to the endothelium, blood is exposed to subendothelial components, such as von Willebrand factor (vWF) and collagen. Platelets adhere to the subendothelium and are activated, releasing substances that further recruit and activate platelets inducing platelet aggregation. A platelet plug is formed at the site of injury providing initial arrest of bleeding, in a process known as “primary hemostasis”. A process referred to as “secondary hemostasis” follows to ensure stabilization of the platelet plug.

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Vascular injury also exposes tissue factor (TF), a membrane-bound procoagulant factor that triggers the coagulation cascade. The coagulation cascade is a highly regulated series of enzymatic reactions involving the sequential conversion of proenzymes into their active forms. Activated platelets provide a phospholipid surface membrane on which coagulation enzymes localize and assemble into complexes that accelerate the serial enzymatic reactions. Such amplification processes translate a small initiating signal into an explosion of thrombin generation, thereby resulting in rapid fibrin formation. The polymerization of fibrin stabilizes the platelet plug and results in secondary hemostasis.

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Removal of the fibrin clot takes place by activation of the fibrinolytic system. Plasminogen, a zymogen, is converted into plasmin, an enzyme that degrades the fibrin matrix of the clot into soluble fragments. Hemostatic mechanisms rely on dynamic interactions between platelets, the coagulation cascade, the fibrinolytic system, and the endothelium (see Figure 106-1). Disturbances of the equilibrium, caused by acquired or congenital factors, may result in unexpected or excessive bleeding ...

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