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Infringements of coagulability of system of blood


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Infringements of coagulability of system of blood

  1. 1. Infringements of coagulability of system of blood
  2. 2. Infringements of coagulability of system of blood <ul><li>Infringements of a hemostasis, a coagulopathy - infringement of function of coagulative and anticoagulative systems of a blood. </li></ul>
  3. 3. Coagulation <ul><li>Coagulation is a complex process by which blood forms clots. </li></ul>
  4. 4. Hemostasis <ul><li>Primary (platelets form a plug at the site of injury </li></ul><ul><li>Secondary (proteins in the blood plasma respond in a complex cascade to form fibrin strands, which strengthen the platelet plug) </li></ul>
  5. 7. Regulators of anticoagulation <ul><li>Protein C is a vitamin K-dependent serine protease enzyme that is activated by thrombin into activated protein C (APC). </li></ul><ul><li>Antithrombin is a serine protease inhibitor (serpin) that degrades the serine proteases. </li></ul><ul><li>Tissue factor pathway inhibitor (TFPI) limits the action of tissue factor (TF). </li></ul>
  6. 8. Regulators of anticoagulation <ul><li>Plasmin is generated by proteolytic cleavage of plasminogen, a plasma protein synthesized in the liver. </li></ul><ul><li>Prostacyclin (PGI2) is released by endothelium and activates platelet Gs protein-linked receptors. </li></ul><ul><li>Fibrinolysis </li></ul>
  7. 9. Testing of coagulation <ul><li>Common : </li></ul><ul><li>aPTT </li></ul><ul><li>PT </li></ul><ul><li>Fibrinogen testing </li></ul><ul><li>Platelet count </li></ul><ul><li>Platelet function testing </li></ul><ul><li>Other : </li></ul><ul><li>TCT </li></ul><ul><li>Bleeding time </li></ul><ul><li>Coagulation factor assays </li></ul><ul><li>Antiphosholipid antibodies </li></ul><ul><li>D - dimer </li></ul>
  8. 10. Influence of surgery trauma on hemostasis <ul><li>Damage to tissues exposes subendothelium proteins </li></ul><ul><li>Proteins in the blood plasma, called coagulation factors or clotting factors, respond in a complex cascade to form fibrin strands </li></ul><ul><li>Immobilization – slow down of the blood flow </li></ul>
  9. 11. Risk factors for postoperative thrombosis <ul><li>Perioperative, exposing factors affecting risk include: </li></ul><ul><li>Dehydration </li></ul><ul><li>Postoperative immobilisation </li></ul><ul><li>Need for transfusion </li></ul><ul><li>Patient-related, or predisposing, risk factors include: </li></ul><ul><li>Inherited thrombophilia </li></ul><ul><li>Advanced age </li></ul><ul><li>Obesity </li></ul><ul><li>Cancer </li></ul><ul><li>Prior VTE </li></ul><ul><li>Varicose veins </li></ul><ul><li>Use of estrogen-containing medications (such as oral contraceptives and hormone replacement therapy) </li></ul>
  10. 12. Measures of prophylactics of thrombosis <ul><li>low molecular weight heparins (LMWH) </li></ul><ul><li>Early and regular ambulation (walking) </li></ul><ul><li>Intermittent pneumatic compression (IPC) </li></ul><ul><li>150-300 mg of aspirin </li></ul>
  11. 14. <ul><li>DIC - is a complex systemic thrombohemorrhagic disorder involving the generation of intravascular fibrin and the consumption of procoagulants and platelets. The resultant clinical condition is characterized by intravascular coagulation and hemorrhage.  </li></ul>
  12. 15. Epidemiology <ul><li>½ of DIC cases result from complications of pregnancy. </li></ul><ul><li>1/3 result from carcinomatosis. </li></ul><ul><li>1/6 make up all other causes. </li></ul>
  13. 16. 2 forms of DIC <ul><li>Acute </li></ul><ul><li>Chronic </li></ul><ul><li>develops acutely when sudden exposure of blood to procoagulants occurs </li></ul><ul><li>Compensatory hemostatic mechanisms are quickly overwhelmed </li></ul><ul><li>Abnormalities of blood coagulation parameters are readily identified </li></ul><ul><li>organ failure frequently occurs </li></ul><ul><li>develops when blood is continuously or intermittently exposed to small amounts of tissue facto </li></ul><ul><li>Compensatory mechanisms in the liver and bone marrow are not overwhelmed </li></ul><ul><li>little obvious clinical or laboratory indication </li></ul><ul><li>observed in solid tumors and in large aortic aneurysms </li></ul>
  14. 17. Causes of DIC <ul><li>Acute vs Chronic </li></ul><ul><li>Systemic vs Localized </li></ul><ul><li>Single vs Multiple conditions </li></ul>
  15. 18. Acute DIC <ul><li>Infectious </li></ul><ul><li>Malignancy </li></ul><ul><li>Obstetric </li></ul>
  16. 19. Infectious <ul><ul><ul><li>Bacterial (eg, gram-negative sepsis, gram-positive infections, rickettsial) </li></ul></ul></ul><ul><ul><ul><li>Viral (eg, HIV, cytomegalovirus [CMV], varicella, hepatitis) </li></ul></ul></ul><ul><ul><ul><li>Fungal (eg, Histoplasma ) </li></ul></ul></ul><ul><ul><ul><li>Parasitic (eg, malaria) </li></ul></ul></ul>
  17. 20. Malignancy <ul><ul><ul><li>Hematologic (eg, acute myelocytic leukemias) </li></ul></ul></ul><ul><ul><ul><li>Metastatic (eg, mucin-secreting adenocarcinomas) </li></ul></ul></ul>
  18. 21. Obstetric <ul><ul><ul><li>Placental abruption </li></ul></ul></ul><ul><ul><ul><li>Amniotic fluid embolism </li></ul></ul></ul><ul><ul><ul><li>Acute fatty liver of pregnancy </li></ul></ul></ul><ul><ul><ul><li>Eclampsia </li></ul></ul></ul>
  19. 22. Acute DIC <ul><ul><li>Trauma </li></ul></ul><ul><ul><li>Burns </li></ul></ul><ul><ul><li>Motor vehicle accidents (MVAs) </li></ul></ul><ul><ul><li>Snake envenomation </li></ul></ul><ul><ul><li>Transfusion </li></ul></ul><ul><ul><li>Hemolytic reactions </li></ul></ul>
  20. 23. Acute DIC <ul><ul><li>Massive transfusion </li></ul></ul><ul><ul><li>Liver disease - Acute hepatic failure </li></ul></ul><ul><ul><li>Prosthetic devices </li></ul></ul><ul><ul><li>Shunts (Denver, LeVeen) </li></ul></ul><ul><ul><li>Ventricular assist devices </li></ul></ul>
  21. 24. Chronic DIC <ul><ul><li>Malignancies </li></ul></ul><ul><ul><ul><li>Solid tumors </li></ul></ul></ul><ul><ul><ul><li>Leukemia </li></ul></ul></ul><ul><ul><li>Obstetric </li></ul></ul><ul><ul><ul><li>Retained dead fetus syndrome </li></ul></ul></ul><ul><ul><ul><li>Retained products of conception </li></ul></ul></ul>
  22. 25. Chronic DIC <ul><ul><li>Hematologic </li></ul></ul><ul><ul><ul><li>Myeloproliferative syndromes </li></ul></ul></ul><ul><ul><ul><li>Paroxysmal nocturnal hemoglobinuria </li></ul></ul></ul><ul><ul><li>Vascular </li></ul></ul><ul><ul><ul><li>Rheumatoid arthritis </li></ul></ul></ul><ul><ul><ul><li>Raynaud disease </li></ul></ul></ul>
  23. 26. Chronic DIC <ul><ul><li>Cardiovascular </li></ul></ul><ul><ul><ul><li>Myocardial infarction </li></ul></ul></ul><ul><ul><li>Inflammatory </li></ul></ul><ul><ul><ul><li>Ulcerative colitis </li></ul></ul></ul><ul><ul><ul><li>Crohn disease </li></ul></ul></ul><ul><ul><ul><li>Sarcoidosis </li></ul></ul></ul>
  24. 27. Localized DIC <ul><ul><li>Aortic aneurysms </li></ul></ul><ul><ul><li>Giant hemangiomas (Kasabach-Merritt syndrome) </li></ul></ul><ul><ul><li>Acute renal allograft rejection </li></ul></ul><ul><ul><li>Hemolytic uremic syndrome </li></ul></ul>
  25. 28. Pathophysiology <ul><li>increased thrombin generation </li></ul><ul><li>a suppression of anticoagulant pathways </li></ul><ul><li>impaired fibrinolysis </li></ul><ul><li>inflammatory activation </li></ul>
  26. 29. The DIC process can be divided into four stages <ul><li>Hypercoagulable (Stage I) </li></ul><ul><li>Secondary fibrinolytic (Stage II) </li></ul><ul><li>Hypocoagulable (Stage III) </li></ul><ul><li>Reparation stage </li></ul>
  27. 30. Hypercoagulable (Stage I) <ul><li>release of tissue factor (TF) </li></ul><ul><li>FVIIa activation of the extrinsic pathway </li></ul><ul><li>deposition of thrombin in the microcirculation system </li></ul><ul><li>microthrombosis of the capillaries of major organs, leading to Acute Respiratory Distress Syndrome , multiple organ failure (MOF), miscarriage, clotted graft, pulmonary embolism (PE), acute myocardial infarct (AMI), stroke, and deep vein thrombosis (DVT). </li></ul>
  28. 31. Secondary fibrinolytic (Stage II) <ul><li>release of TPA by the endothelium system, which activates plasminogen to plasmin </li></ul><ul><li>Plasmin breaks down the clot, releasing fibrinogen degradation product (FDP) </li></ul><ul><li>release of TPA is an attempt to counterbalance the prothrombotic state into normal hemostasis and to prevent deposition of thrombi into the microcirculatory system </li></ul><ul><li>FDP, acts as an anticoagulant to inhibit platelet aggregation and prevent normal cross-linking of fibrin </li></ul>
  29. 32. Hypocoagulable phase (Stage III) <ul><li>leads to hemorrhage, but can be treated by FFP, cryo, and platelets to stop the bleeding </li></ul><ul><li>allogenic blood products, in addition to exposing the patient to donor blood products and the risk of blood-borne diseases, also initiates strong inflammatory reactions </li></ul>
  30. 33. Reparation phase <ul><li>Normalization of all body functions </li></ul><ul><li>Blood tests, condition of the patient are repairing to normal </li></ul>
  31. 34. Diagnosis <ul><li>Severe cases with haemorrhage </li></ul><ul><ul><li>PT and APTT are prolonged </li></ul></ul><ul><ul><li>fibrinogen level markedly reduced </li></ul></ul><ul><ul><li>High levels of fibrin degradation products, including D-dimer </li></ul></ul><ul><ul><li>severe thrombocytopenia </li></ul></ul><ul><ul><li>blood film may show fragmented red blood cells </li></ul></ul>
  32. 35. Diagnosis <ul><li>Mild cases without bleeding: </li></ul><ul><ul><li>increased synthesis of coagulation factors and platelets </li></ul></ul><ul><ul><li>PT, APTT, and platelet counts are normal </li></ul></ul><ul><ul><li>fibrin degradation products are raised </li></ul></ul>
  33. 36. Definitive diagnosis <ul><li>Thrombocytopenia </li></ul><ul><li>Prolongation of prothrombin time and activated partial thromboplastin time </li></ul><ul><li>low fibrinogen concentration </li></ul><ul><li>Increased levels of fibrin degradation products </li></ul>
  34. 37. Treatment <ul><li>Reversal of the underlying cause </li></ul><ul><li>Anticoagulants </li></ul><ul><li>Platelets </li></ul><ul><li>Fresh frozen plasma </li></ul><ul><li>Infusion with antithrombin </li></ul>