Hemostasis and Thrombosis in Continuous Renal Replacement Treatment

Abstract

During continuous renal replacement therapy, the delicate equilibrium of hemostasis is disturbed. Owing to a complex interaction of critical illness, uremia, use of an extracorporeal circuit and anticoagulation, patients exhibit both hypercoagulability and an increased risk of bleeding. Contact of blood with foreign material initiates coagulation by triggering the contact activation coagulation pathway, the tissue factor–factor VIIa pathway and activation of platelets and monocytes, which adhere to the membrane. The interaction with critical illness induced alterations further enhances coagulation and inflammation. Classical markers of coagulation, prothrombin and activated thromboplastin time, and platelet count do not detect the procoagulant state. Critically ill patients also have in increased risk of bleeding and anticoagulation used for circuit clotting enhances this risk. Heparin is most commonly used. Heparin increases the risk of bleeding. Its efficacy and safety are further compromised by antithrombin deficiency, heparin binding to acute phase proteins and apoptotic and necrotic cells, and by its unpredictable effects on inflammation. Its interference with anticoagulation is therefore unreliable during critical illness. Citrate provides regional anticoagulation and increases biocompatibility. It is better tolerated than heparin and confers less bleeding, less transfusion, and longer circuit life.