Infringements of coagulability of system of blood

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