DIC—review.pptVIP

3. Hypercoagulable status Pregnancy: Coagulation factors↑, anti-coagulation factors↓ Acute DIC occurs easily in placental abruption and amniotic fluid embolism 4. Disorder of microcirculation Disorder of microcirculation Platelet adhesion EC injury 5. Acidosis Acidosis Platelet adhesion EC injury Stages of DIC Hypercoagulable stage Consumed hypocoagulable stage Secondary fibrinolytic stage (Self-study and familiar with the pathogenesis of every stages) DIC characters: Blood coagulation increase first and then decease (due to secondary fibrinolysis) Self-study Acute DIC: Develop rapidly over several hours or 1~2 days With shock and muti-site bleeding problems Occurs in septic shock, traumatic shock, and others Subacute DIC: several days Chronic DIC: Clinical classification of DIC Alterations of metabolism and function 1. Bleeding After abdominal aortic aneurysm surgery Clinical characters of bleeding General and multiple position bleeding and it can’t explained by primary disease Companied by other manifestations (for example shock) Can’t stop by conventional hemostatic drugs Rate: 85%~100% Pathogenesis of bleeding Causes coagulating system actived Consumption of coagulation factors Bleeding Plasmin? tPAs ? FDP? Secondary fibrinolysis Vessel injury Anti-coagulating effect of FDP Anti-thrombin effect: fragment Y、E Anti-aggregation of fibrin monomer: X、Y、D + fibrin monomer ≠ Fbn (fibrin polymer) Anti-adhesion and aggregation of platelet 2. Schock Causes Coagulation system activation Bleeding Blood volume? Thrombopoiesis Returned blood volume? Heart function? Schock Fibrinolytic system activation Vascular capacity? Rate: 50%~80% 3. Organ dysfunction Mechanism: Microthrombus forming, ischemia of organ Bleeding and shock Cytokines release Organ dysfunction and homeostasis cannot be maintained: Acute tubular necrosis(ATN), acute renal failure(ARF) acute respiratory distress syndrome (ARDS) 4. Microangiopathic Hemolytic anemia(MAHA) Schistocyte (the cell debris) R