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.
Keywords
coagulation - anticoagulation - sepsis - heparin - citrate - acute kidney injury
