HaematologyintheICU-PhilippeLeFevre.pptVIP

DIC The clinical and laboratory manifestations of DIC result from the combined effects of thrombin and plasmin produced in excess of that required for normal hemostasis. Bleeding from venepuncture sites Spontaneous thrombosis Lab diagnosis Evidence of fragmentary haemolysis, fibrinogen and platelet consumption, combined with enhanced fibrinolytic activity ie ? fibrinogen, ? platelets, ? XDP’s, and characteristic blood film PT is usually prolonged, reflecting coagulation factor consumption APTT is variable, depending on FVIII levels TT is prolonged (interference by FDP with fibrin polymerization +/- hypofibrinogenaemia) DIC - treatment Treat underlying disease process Treat the coagulopathy that results in the thrombotic and haemorrhagic manifestions patients who are bleeding or who have thrombosis require treatment of their coagulopathy Maintain platelets 20 FFP to replace consumed coagulation factors Cryoprecipitate if fibrinogen 1.5 DIC – further treatment Failure of the plt count or fibrinogen level to increase despite vigorous replacement = ongoing consumption (common) Heparin (low doses, 10 units/kg/hr) may be used to block activation of the coagulation system, or if there is thrombosis Fibrinolytic inhibitors - ε-aminocaproic acid or transexamic acid not useful (exaggerate the thrombotic component) DIC – other treatment Use of endogenous inhibitors of coagulation as a specific therapy for severe sepsis Often complicated by DIC Recombinant APC in a 96 hr infusion was shown to improve survival in a recent trial Pts with significant coagulopathies or thrombocytopaenia were excluded Antithrombin has not been shown to be effective in improving survival with sepsis Coagulation – the basics The tissue-factor VIIa complex is the most important in vivo initiator of coagulation Coagulation – the basics TF is a transmembrane protein expressed by fibroblasts in the subendothelium During activation of coagulation in response to vascular injury, TF is expressed on the s