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Management of coagulation and transfusion therapy
         in cardiothoracic anesthesia

                         Seminar
...
Summary

 Cell-based model of coagulation.
 Standard lab tests.
 CPB and haemostasis.
 Anticoagulation for CPB.
 Moni...
This presentation

 It’s not a lecture on Hematology.
 It’s not an academic review of main mechanisms of haemostasis.
 ...
Cell-based model of coagulation (1)




 Intrinsic, extrinsic and common
  pathways.
 Useful to understand laboratory
  ...
Cell-based model of coagulation (2)

 Cell-based model:
Cell-based model of coagulation (3)
Cell-based model of coagulation (4)

 Haemostasis starts with the interaction between TF and FVIIa on the
  surface of su...
Standard lab tests

 Good sampling technique.
 Time to form a fibrin clot in vitro.
 PT & INR (extrinsic path.): FVII...
CPB and haemostasis (1)

 Prevent clotting: heparine.
 Contact activation (bypass circuit).
 Exposure to air and TF (wo...
CPB and haemostasis (2)

 A. PO bleeding is a common complication of
 cardiac surgery but a surgical cause is only found
 ...
Anticoagulation for CPB (1)

 Unfractionated heparin.
 Rapid onset, clinical efficacy, rapid neutralization, safety, low...
Anticoagulation for CPB (2)

 Heparine resistance.
 Alternatives to unfractionated heparin.
 Heparin reversal: protamin...
Monitoring anticoagulation

 ACT, normal value 100-140 s.
 Activator: celite.
 Aprotinin: caolin.
 ACT↑ in thrombocyto...
Monitoring coagulation




 Low concentrations of heparin prolong APTT.
 PT↑ = clotting factor deficiency ⇒ FFP.
 Plate...
TEG (1)

 Monitoring coagulation to guide haemostatic blood transfusion.
 Reduction of transfusion of blood products.
 ...
TEG (2)

 Measures whole blood viscoelastic changes associated with fibrin
  polymerization.
 Fast: 10-20 min.
 Graphic...
Thromboelastography (3)
TEG (4)




          Anesth Analg 1999;88:312–9.
TEG (5)
TEG (6)

 Algorithm using point-of-care coagulation testing (TEG) reduce
  transfusion requirements.
 Cumulative costs f...
Antifibrinolytic therapy (1)

 Antifibrinolytic agents: aprotinin; synthetic: EACA, TA.
 Aprotinin high dose:↓ periop bl...
Antifibrinolytic therapy (2)

 Aprotinin ??.
 Mangano et al. N ENGL J MED
  Jan 2006.
 Eur J Anaesth 2007;24:6-14.
 Ci...
Antifibrinolytic therapy (3)

 In the current analysis, aprotinin dosage was not
  associated with increased adverse rena...
The new model of haemostasis
  In high doses rFVIIa binds to the surface of the locally activated
  platelets where it lea...
rFVIIa dosage

 Reconstitution and iv bolus injection over 2-5 min.
 Initial dose 90-120 mcg/kg.
 Repeat 2x or 3x (at 2...
Guidelines (1)
Guidelines (2)

 Institution-specific protocols should screen for high
  risk patients:
    1. Advanced age.
    2. Low p...
Guidelines (2)

 Preop interventions: EPO, limitation of antithrombotic
  drugs.
 Periop interventions:
    1. Use of an...
Thanks

Please, don´t forget the evaluation test!!.
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Management of coagulation and transfusion therapy in cardiothoracic anesthesia

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Management of coagulation and transfusion therapy in cardiothoracic anesthesia

  1. 1. Management of coagulation and transfusion therapy in cardiothoracic anesthesia Seminar By F. Javier Orellana July 2009
  2. 2. Summary  Cell-based model of coagulation.  Standard lab tests.  CPB and haemostasis.  Anticoagulation for CPB.  Monitoring anticoagulation.  Thromboelastography (TEG).  Antifibrinolytic therapy.  Guidelines.
  3. 3. This presentation  It’s not a lecture on Hematology.  It’s not an academic review of main mechanisms of haemostasis.  It’s a view of practical points in cardiac surgery concerning coagulation and blood transfusion (or other blood products).  It’s a review of literature on this subject.  It’s an update of present recommendations.
  4. 4. Cell-based model of coagulation (1)  Intrinsic, extrinsic and common pathways.  Useful to understand laboratory tests.  Not accurate representation of in vivo coagulation.
  5. 5. Cell-based model of coagulation (2)  Cell-based model:
  6. 6. Cell-based model of coagulation (3)
  7. 7. Cell-based model of coagulation (4)  Haemostasis starts with the interaction between TF and FVIIa on the surface of subendothelial cells.  The small amount of thrombin generated during the amplification phase activates platelets locally on whose surface the subsequent reactions take place.  The resulting thrombin burst results in the formation of a stable clot.
  8. 8. Standard lab tests  Good sampling technique.  Time to form a fibrin clot in vitro.  PT & INR (extrinsic path.): FVII, but also with FI, FII, FV and FX deficiencies, liver disease, vit. K deficiency, DIC, and high doses heparine.  APTT : all procoagulants except FVII and FXIII. Monitor: heparin therapy, haemophilia A /B, coagulation inhibitors.  TT: hypo/dysfibrinogenaemia, FDP (fibrinolytic therapy).  Fibrinogen level.  Near-patient tests of coagulation (NPT): Hemochron.  Platelet function analysing monitor.
  9. 9. CPB and haemostasis (1)  Prevent clotting: heparine.  Contact activation (bypass circuit).  Exposure to air and TF (wound) and recirculation.  Thrombin resistant + consumption of clotting factors and platelets.  Plasmin-platelets interaction.  Systemic inflammation state.  Hypothermia (< 35° C).  Haemodilution, preop platelets inhibitors, heparine itself, protamine.
  10. 10. CPB and haemostasis (2) A. PO bleeding is a common complication of cardiac surgery but a surgical cause is only found in 50% of re-explorations. B. Empiric transfusion of blood products is often inappropiate, carries the risk of adverse effects, and has been associated with an increase in wound infection. C. Rapid and accurate diagnosis of haemostasis is necessary to discriminate coagulopathic bleeding from surgical bleeding.
  11. 11. Anticoagulation for CPB (1)  Unfractionated heparin.  Rapid onset, clinical efficacy, rapid neutralization, safety, low cost.  Dose: 300-400 U/kg. + additional doses (ACT>480 s).
  12. 12. Anticoagulation for CPB (2)  Heparine resistance.  Alternatives to unfractionated heparin.  Heparin reversal: protamine.
  13. 13. Monitoring anticoagulation  ACT, normal value 100-140 s.  Activator: celite.  Aprotinin: caolin.  ACT↑ in thrombocytopenia or platelet dysfunction (GpIIbIIIa inhibitors).  Also with haemodilution and hypothermia. Once CPB is established, ACT ceases to correlate with heparin concentration.  Heparin concentration monitoring. ACT is simple, familiar, cheaper and remains the standard monitor.
  14. 14. Monitoring coagulation  Low concentrations of heparin prolong APTT.  PT↑ = clotting factor deficiency ⇒ FFP.  Platelet count.  Fibrinogen↓ ⇒ cryoprecipitate.
  15. 15. TEG (1)  Monitoring coagulation to guide haemostatic blood transfusion.  Reduction of transfusion of blood products.  Improve outcome and reduce costs.  Laboratory tests are of no value during CPB.
  16. 16. TEG (2)  Measures whole blood viscoelastic changes associated with fibrin polymerization.  Fast: 10-20 min.  Graphical representation.
  17. 17. Thromboelastography (3)
  18. 18. TEG (4) Anesth Analg 1999;88:312–9.
  19. 19. TEG (5)
  20. 20. TEG (6)  Algorithm using point-of-care coagulation testing (TEG) reduce transfusion requirements.  Cumulative costs for treatment of perioperative coagulation disorders can be reduced by ‘bedside’ ROTEM analysis to achieve a selective substitution management.  Cost-effective: YES.
  21. 21. Antifibrinolytic therapy (1)  Antifibrinolytic agents: aprotinin; synthetic: EACA, TA.  Aprotinin high dose:↓ periop blood loss & transfusion requirements.  High, low (1/2, 1/4) dose aprotinin >> placebo.  Synthetic antibrinolytics >> placebo (↓ markers of fibrinolysis, blood/sparing properties).  Aprotinin >> synthetic (reduces blood loss).  Aprotinin (not synthetic) attenuates the inflammatory response to CPB. Also steroids.  Thrombotic complications?.
  22. 22. Antifibrinolytic therapy (2)  Aprotinin ??.  Mangano et al. N ENGL J MED Jan 2006.  Eur J Anaesth 2007;24:6-14.  Circulation 2007;115:2801-2813.
  23. 23. Antifibrinolytic therapy (3)  In the current analysis, aprotinin dosage was not associated with increased adverse renal outcome. In regard to renal outcome, this analysis did not demonstrate an essential detrimental influence of aprotinin dosage on renal function.
  24. 24. The new model of haemostasis In high doses rFVIIa binds to the surface of the locally activated platelets where it leads to the formation of a thrombin ¨burst¨.
  25. 25. rFVIIa dosage  Reconstitution and iv bolus injection over 2-5 min.  Initial dose 90-120 mcg/kg.  Repeat 2x or 3x (at 2-3 h intervals).  Patient 70 kg: 19 mg.  Novoseven 1.2 mg 664,72 £.  Novoseven 2.4 mg 1.329,44 £.  Novoseven 4.8 mg 2.658,88 £.  Cost 1 patient: 10.635,52 £.
  26. 26. Guidelines (1)
  27. 27. Guidelines (2)  Institution-specific protocols should screen for high risk patients: 1. Advanced age. 2. Low preop red blood cell volume. 3. Preop antiplatelet or antithrombotic drugs. 4. Redo, complex procedures. 5. Emergency operations. 6. Non cardiac patient comorbidities.
  28. 28. Guidelines (2)  Preop interventions: EPO, limitation of antithrombotic drugs.  Periop interventions: 1. Use of antifibrinolytics. 2. Selective use of off-pump CABG. 3. Routine use of cell-saving device. 4. Autologous predonation and normovolemic hemodilution.  Consensus, institution-specific blood transfusion algorithms supplemented with point-of-care testing.  Multimodality approach to blood conservation combining all of the above.
  29. 29. Thanks Please, don´t forget the evaluation test!!.

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