This document summarizes key points about managing coagulation and transfusion therapy in cardiothoracic anesthesia. It discusses the cell-based model of coagulation and standard lab tests. It describes how cardiopulmonary bypass can impact hemostasis and outlines approaches to anticoagulation for bypass including heparin and its monitoring. It also discusses thromboelastography for monitoring coagulation to guide transfusion, use of antifibrinolytic therapy, and guidelines for managing perioperative coagulation and reducing transfusion requirements.
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Management of coagulation and transfusion therapy in cardiothoracic anesthesia
1. Management of coagulation and transfusion therapy
in cardiothoracic anesthesia
Seminar
By F. Javier Orellana July 2009
2. Summary
Cell-based model of coagulation.
Standard lab tests.
CPB and haemostasis.
Anticoagulation for CPB.
Monitoring anticoagulation.
Thromboelastography (TEG).
Antifibrinolytic therapy.
Guidelines.
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. Cell-based model of coagulation (1)
Intrinsic, extrinsic and common
pathways.
Useful to understand laboratory
tests.
Not accurate representation of
in vivo coagulation.
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. 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. 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. 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.
12. Anticoagulation for CPB (2)
Heparine resistance.
Alternatives to unfractionated heparin.
Heparin reversal: protamine.
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.
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. TEG (2)
Measures whole blood viscoelastic changes associated with fibrin
polymerization.
Fast: 10-20 min.
Graphical representation.
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.
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. 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. 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. 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 £.
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. 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.