Hepatic Dysfunction: Coagulopathy w/liver disease usually multifactorial in etiology since liver synthesizes all procoagulant proteins but factor VIII & vWF. Abnormalities include thrombocytopenia, deficiencies of vitamin K-dependent & non-dependent coag factors, disseminated intravascular coagulation (DIC), & impaired clearance of activated fibrinolytic enzymes. PT most useful test in detecting coagulopathy secondary to liver disease. FFP is replacement of choice for severe hemorrhage because it contains all coag factors synthesized by liver. Vitamin K should always be given to pts w/suspected coagulopathy secondary to liver disease.
Hypothermia: An important cause of perioperative & post-traumatic coagulopathy. Hypothermia prolongs the PT & aPTT by slowing the reaction rates in the involved enzymatic steps of the coag cascades. Hypothermia induces reversible but profound hepatic & splenic sequestration of platelets, and therefore affects platelet count & function. Morphologic changes also occur to platelets making them sticky & prone to clumping. Sequestration & clumping may contribute to thrombocytopenia. Platelet secretion of vasoactive substances also impaired, thus affecting primary hemostasis. Rewarming from deep hypothermia may liberate tissue thromboplastin into circulation, stimulating coagulation including DIC.
Hemodilution: Dilutional coagulopathy can complicate fluid resuscitation from trauma or major perioperative hemorrhage, or it may be from elective normovolemic hemodilution induced during perioperative use of blood/cell saver. Hemodilution to hematocrit no less than 20% maintains normal surgical hemostasis since most hemostatic components are in excess in normal blood, but w/progressive blood loss or elective hemodilution to crit <20% may find deficiency of multiple coag factors. Thus, in OR setting where normothermia can be preserved, perfusion maintained, & packed red cells used, FFP is the replacement product best suited to restoring hemostatic function from normovolemic anemia.