Читать книгу Pathy's Principles and Practice of Geriatric Medicine - Группа авторов - Страница 566

Disseminated intravascular coagulation (DIC) is a failure of haemostatic homeostasis (Figure 23.1). The haemostatic system comprises five components: the coagulation cascade, the fibrinolytic cascade, platelets, the natural anticoagulant pathway, and vascular endothelial cells. It is a complex system that normally maintains blood fluidity when blood is confined within the intravascular vessels but can trigger rapid and localized coagulation if vascular integrity is breached. The intravascular space usually contains no exposed tissue factor, but all cells outside the vascular system express tissue factor in their cell membranes that initiates coagulation through the extrinsic pathway, as tissue factor binds to Factor VII and activates Factor X and hence the final common pathway of coagulation. In DIC, there is unregulated and uncontrolled activation of the coagulation cascade and platelets, leading to thrombotic occlusion of the microvascular capillaries and vessels and resulting in dysfunction of critical organs, such as acute kidney injury (AKI) and pulmonary dysfunction (ARDS). The consumption of coagulation factors and platelets by intravascular activation outpaces production, and the levels of coagulation factors and platelets fall. Simultaneously, there is activation of the fibrinolytic cascade, generating plasmin and resulting in fibrinogen degradation (high D‐dimers), together with depletion of components of the natural anticoagulant pathway (Antithrombin, Protein C, and Protein S) that contribute to systemic bleeding diathesis.^1,2 Hence the paradox of DIC is that the clinical manifestations are of bleeding while the patient suffers morbidity and mortality due to organ damage due to microvascular thrombosis. The most common cause of DIC is sepsis, which occurs in 20–80% of severe cases and has a mortality of 20–50%. DIC usually has an acute onset with bleeding manifestations dominating the clinical picture; however, a chronic form can occur, the manifestations of which are very different, usually with presentation as recurrent thrombosis together with bruising, low platelets, and high D‐dimers. The management of this form of condition likewise differs.