DIAGNOSIS AND THERAPY OF DISSEMINATED INTRAVASCULAR COAGULATION

Consumptive coagulation disorders are frequently observed in critically ill patients secondary to other underlying diseases. Initial hypercoagulability leads to subsequent hypocoagulability due to consumption of procoagulant proteins, inhibitors, and platelets. This process evolves in three distinct phases: an initial increase in coagulation activity is characterised by the activation of coagulation factors and platelets without any clinical symptoms of a haemorrhagic diathesis. The ongoing process of activation and accelerated consumption of coagulation factors and inhibitors causes a critical reduction in the haemostatic potential. The time of onset of the clinical symptoms of bleeding depends on the patient's underlying disease and its pharmacological management. Coagulation processes that are restricted locally under normal conditions become disseminated when the inhibitory potential - mainly represented by antithrombin III (AT III) - is exhausted. Therefore, thrombin formation occurs, especially in the microcirculation, where fibrin clot deposition begins to cause inhomogeneities of blood flow and thus to reduce oxygen delivery to the tissues. Hypocoagulability, reactive hyperfibrinolysis, and diffuse bleeding lead to an irreversible systemic breakdown of haemostatic mechanisms (disseminated intravascular coagulation, DIC). The laboratory diagnosis of accelerated consumption is based on the course of global coagulation tests (e.g., prothrombin time, activated partial thromboplastin time, platelet count) and more sensitive (''dynamic'') activation parameters such as prothrombin fragment F1+2, thrombin-AT III complex, fibrin monomers, or d-dimer. Measurements of plasminogen, tissue plasminogen activator, plasminogen activator inhibitor 1, and alpha2-antiplasmin-plasmin complex provide information on fibrinolytic turnover. Therapy is adjusted to the three phases of DIC and is aimed at re-establishing the inhibitor-procoagulator balance within the coagulation cascade. At III is given when its endogenous activity is below 70 %. The deterioration of global clotting parameters indicates the shift from hyper- to hypocoagulability, and the administration of fresh frozen plasma (FFP) and packed red cells together with repeated substitution of AT III to maintain AT III activity above 80 % may be required. Concentrates of procoagulators such as prothrombin complex (PPSB) are indicated whenever normalisation of procoagulants in a bleeding patient cannot be ensured by FFP alone. If the restriction of procoagulant turnover is ineffective, irreversible hypocoagulability and impaired perfusion due to fibrin deposits in the microcirculation will lead to tissue hypoxia and multiorgan failure.