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Basic Clinician Training Module 3

Basic Clinician Training Module 3. Basic bleeding profiles. Introduction to bleeding. Causes of bleeding Mechanical – vascular injury Pathophysiological – imbalance between the anticoagulant/antithrombotic and prothrombotic forces of the hemostatic system

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Basic Clinician Training Module 3

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  1. Basic Clinician TrainingModule 3 Basic bleeding profiles

  2. Introduction to bleeding • Causes of bleeding • Mechanical – vascular injury • Pathophysiological – imbalance between the anticoagulant/antithrombotic and prothrombotic forces of the hemostatic system • Monitoring hemostasis – finding where the imbalance resides

  3. Monitoring bleeding with the TEG • TEG analysis – monitoring hemostatic components and their interactions. • Mechanical – Normal TEG parameters • Pathophysiological • R: enzymatic pathway abnormality • Angle (a): fibrinogen deficiency • MA: platelet abnormality • LY30: fibrinolysis (See Module 6)

  4. Decision Tree EPL > 15% No or Yes LY30 > 7.5% C.I. Hemorrhage C.I. > 3.0 No Yes < 1.0 > 3.0 R > 10min R < 3min No Yes Primary fibrinolysis Secondary fibrinolysis No Yes Fibrinolysis Low clotting factors Platelet hypercoagulability MA > 73mm MA < 55mm No Yes Yes No Low platelet function Enzymatic hypercoagulability Enzymatic & platelet hypercoagulability a < 45º i Yes Hypercoagulable Low fibrinogen level

  5. Mechanical bleeding • Characterized by bleeding patient with a normal TEG tracing. • Probable cause: Surgical injury to blood vessel with insufficient repair of the blood vessel. • Other possible explanations • Clot development not confined to injury site – suggests vWF deficiency • Presence of platelet inhibitors

  6. Patient status: bleeding • Probable cause (3): • Vessel injury • vWF deficiency • Presence of platelet inhibitor

  7. Patient status: bleeding • Probable cause  Common treatment: • Vessel injury  Suture • vWF deficiency  DDAVP • Presence of platelet inhibitor  Run Platelet Mapping

  8. Enzymatic pathway abnormalities • Characterized by a bleeding patient and a TEG tracing with an abnormally long R value. • Factor deficiency may also cause abnormalities in other TEG parameters (angle, MA) • Probable causes: • Coagulation factor(s) deficiency • Coagulation factor dysfunction • Presence of anticoagulant (i.e. residual heparin) • Effect: • Slow rate of thrombin generation leading to slow clot development • Insufficient thrombin generation leading to insufficient clot development

  9. Causes of enzymatic pathway abnormalities • Coagulation factor deficiency • Hemodilution • Liver disease or liver congestion • Trauma with significant blood loss and/or blood salvage • Congenital – i.e. hemophilia • Factor consumption > synthesis • Cardiopulmonary bypass, ECMO • Disseminated intravascular coagulation (DIC) • Coagulation factor dysfunction • Vitamin K deficiency • Warfarin treatment • Presence of anticoagulant • Residual heparin

  10. Enzymatic pathway abnormality:Coagulation factor deficiency Patient status: bleeding Patient condition: bleeding Probable cause: factor deficiency Probable cause: Factor deficiency

  11. Enzymatic pathway abnormality:Coagulation factor deficiency Patient status: bleeding • Probable cause(s): • Factor deficiency • Platelet deficiency/dysfunction

  12. Enzymatic pathway abnormality:Coagulation factor deficiency Patient status: bleeding • Probable cause(s)  Common treatment(s) • Factor deficiency  FFP • Platelet deficiency/dysfunction  platelets

  13. Enzymatic pathway abnormality:Residual heparin • Characterized by a bleeding patient and a TEG tracing with an abnormally long R value (non-heparinase sample) • Probable causes: • Residual heparin after protamine administration due to insufficient protamine dose. • Heparin rebound – reappearance of heparin in circulation after initial reversal with protamine • Release of endogenous sources of heparin (i.e. reperfusion of transplanted liver) • Effect: inhibition of thrombin action resulting in reduced fibrin formation and clot development.

  14. Enzymatic pathway abnormality:Residual heparin Post Protamine Patient status: Bleeding • Probable cause(s): • Residual heparin • Factor deficiency First TEST for residual heparin

  15. Testing for residual heparin with the TEG analyzer • Run blood sample on two channels simultaneously • K = kaolin activated (clear cup) • KH = kaolin with heparinase (blue cup) • Results: • If R for K  KH, long R is not due to heparin • If R for K is long and for KH is normal, heparin is present in blood sample

  16. Testing for residual heparin with the TEG analyzer R for K > KH suggests presence of heparin

  17. Fibrinogen deficiency • Characterized by a bleeding patient and a TEG tracing with only an abnormally low angle (a). • Probable cause: low fibrinogen levels • Effect: slow rate of clot development • Note: The angle parameter is influenced by the enzymatic and platelet pathways, thus correcting a deficiency or defect in these pathways will typically correct the angle.

  18. Causes of fibrinogen deficiency • Liver disease or congestion • Disseminated intravascular coagulation (DIC) – hypocoagulable stage • OB-GYN complications – placental abruption • Hemodilution • Excessive consumption

  19. Fibrinogen deficiency Patient status: bleeding Probable cause: fibrinogen deficiency

  20. Fibrinogen deficiency Patient status: Bleeding Probable cause: Fibrinogen deficiency Common treatment: Cryoprecipitate or FFP

  21. Platelet abnormality • Characterized by a bleeding patient and a TEG tracing with an abnormally low MA value • A low MA value may also be associated with an elongated R and/or a low angle values • Probable causes: • Low platelet number • Low platelet function • Note: The TEG cannot distinguish between a low platelet count and low platelet function • Effect: formation of a clot with low clot strength that is insufficient to stop vascular bleeding.

  22. Platelet abnormality:A note on low platelet counts • In certain disease states platelet counts may be reduced, but the remaining platelets may be hyperfunctional and hypersensitive, resulting in normal or high clot strength (normal to high MA). • Example: cancer patients

  23. Platelet abnormalityLow platelet counts - causes • Bone marrow disorders (i.e. leukemia) • Chemotherapy • Congenital disorder • Lupus • Trauma with significant blood loss and/or blood salvage • Hemodilution • Cardiac valve dysfunction – regurgitation • Consumption and/or sequestration • Platelet antibodies - HITT

  24. Platelet abnormalityPlatelet dysfunction - Mechanisms • Activation – inhibition or dysfunction of platelet receptors • Adhesion – inhibition or dysfunction of GPIb receptor preventing adhesion of platelet to endothelium • Aggregation – inhibition or dysfunction of GPIIb/IIIa receptors preventing the development of a platelet plug • Secretion – inhibition or dysfunction of secretory pathways resulting in reduced platelet activation • Procoagulant activity – reduction of thrombin generation on platelet surface

  25. Platelet abnormalityLow platelet function - causes • Cardiopulmonary bypass • Antiplatelet therapies • Platelet antibodies • Congenital disorders • Liver disease • Uremia • Consumption

  26. Platelet abnormality Patient status: bleeding • Probable cause(s): • Low platelet count +/or • Low platelet function

  27. Platelet abnormality Patient status: bleeding • Probable cause(s)  Common treatments: • Low platelet count  platelet transfusion • Low platelet function  platelet transfusion

  28. Platelet abnormality Patient status: bleeding • Probable cause(s): • Low platelet count +/or • Low platelet function

  29. Platelet abnormality Patient status: bleeding • Probable cause(s)  Common treatment • Low platelet count  platelet transfusion • Low platelet function  platelet transfusion

  30. Platelet abnormality Patient status: bleeding • Probable cause(s): • Factor deficiency +/or • Low platelet count +/or • Low platelet function

  31. Platelet abnormality Patient status: bleeding • Probable cause(s)  Common treatment(s): • Factor deficiency  FFP +/or • Low platelet count  platelet transfusion • Low platelet function  platelet transfusion

  32. Platelet abnormalitiesSpecial considerations • The inhibition of platelets by platelet inhibitors may not be revealed by the TEG using a kaolin activated sample. This is due to thrombin generation in the blood sample which results in maximum activation of platelets which overrides other activation pathways. • An important factor to consider in induced platelet dysfunction (i.e., treatment with antiplatelet drugs) is the monitoring of platelet inhibition. • PlateletMapping™ assays measure the degree of inhibition at the ADP receptor and arachadonic acid pathways as well as provide a reference point against which to interpret the inhibition (See Module 6)

  33. Interpretation Exercises Hemorrhage

  34. Exercise 1 Black tracing: Kaolin Green tracing: Kaolin with heparinase • Using the TEG Decision Tree, what is your interpretation of this TEG tracing? • [Select all that apply] • Factor deficiency • Platelet deficiency or dysfunction • Low fibrinogen level • Fibrinolysis • Normal • Has heparin been reversed in this patient? Yes or No. Answer Next

  35. Exercise 2 Post-protamine Patient status: bleeding • Using the TEG Decision Tree, what is your interpretation of this TEG tracing? • [Select all that apply] • Factor deficiency • Platelet deficiency or dysfunction • Low fibrinogen level • Fibrinolysis • Normal • What treatment(s) would you consider for this patient? Answer Next

  36. Exercise 3 Patient status: Bleeding • Using the TEG Decision Tree and the available information from the TEG tracing: • Is it likely the patient will require more protamine as a treatment for bleeding? Yes or No. • Is it likely the patient will require FFP as a treatment for bleeding? Yes or No. Next Answer

  37. Exercise 4 Patient status: Bleeding • Using the TEG Decision Tree what is a likely cause(s) of bleeding in this patient? • [Select all that apply] • Factor deficiency • Platelet deficiency or dysfunction • Low fibrinogen level • Fibrinolysis • Surgical bleeding • What treatment(s) would you consider for this patient? Answer Next

  38. Exercise 5 • Using the TEG Decision Tree what is your interpretation of this TEG tracing? • [Select all that apply] • Factor deficiency • Platelet deficiency or dysfunction • Low fibrinogen level • Fibrinolysis • Normal • If this patient was bleeding, what treatment(s) would you consider? Answer Next

  39. Exercise 6 Post-protamine Patient status: bleeding • Using the TEG Decision Tree what is your interpretation of this TEG tracing? • [Select all that apply] • Factor deficiency • Anticoagulant effect • Platelet deficiency or dysfunction • Low fibrinogen level • Surgical bleeding • What treatment(s) would you consider for this patient? Answer Next

  40. Exercise 7 Black tracing: Kaolin Green tracing: Kaolin with heparinase Patient status: bleeding • Using the TEG Decision Tree what is your interpretation of this TEG tracing? • [Select all that apply] • Factor deficiency • Anticoagulant effect • Platelet deficiency or dysfunction • Low fibrinogen level • Surgical bleeding • How would you treat this patient? Answer Next

  41. Exercise 8 Post-protamine • - The above patient is bleeding after administration of protamine. What are the possible • causes of bleeding (select all that apply)? • - For each selection, identify one treatment consideration. • Surgical bleeding • Factor deficiency • Residual platelet inhibitor effect • Diminished platelet adhesion • Anticoagulant effect Answer Next

  42. Exercise 9 • The above is the baseline TEG (post-induction) of a female patient (70 yr, 54kg) requiring • CABG with CPB. The patient has not been taking aspirin for 7 days (81 mg/d). • Based on this TEG and the patient history, is this patient at risk for bleeding post-CPB? Yes or No. • If so, what will be the most likely cause(s) of bleeding? • Surgical bleeding • Factor deficiency • Platelet deficiency/dysfunction • Fibrinolysis • Anticoagulant effect Answer Next

  43. Exercise 10 Green: Post-protamine Black: ICU • The above patient has started bleeding approximately 1 hr post-op. What is the most likely • cause(s) of bleeding? • Surgical bleeding • Factor deficiency • Platelet deficiency/dysfunction • Fibrinolysis • Anticoagulant effect • How would you treat this patient? Answer END

  44. Exercise 1 Black tracing: Kaolin Green tracing: Kaolin with heparinase • Using the TEG Decision Tree what is your interpretation of this TEG tracing? • Factor deficiency • Platelet deficiency or dysfunction • Low fibrinogen level • Fibrinolysis • Normal – all parameters are within normal range • Has heparin been reversed in this patient?Yes or No. Since the R values for both • the kaolin and kaolin with heparinase samples are the same suggests that the • heparin has been reversed. Back

  45. Exercise 2 Post-protamine Patient status: bleeding • Using the TEG Decision Tree what is your interpretation of this TEG tracing? • [Select all that apply] • Factor deficiency • Platelet deficiency or dysfunction • Low fibrinogen level • Fibrinolysis • Normal • What treatment(s) would you consider for this patient? After completion of protamine • administration, consider treating with platelets first. Repeat TEG. If R value is still • elongated and the patient is bleeding, consider treating with FFP. Back

  46. Exercise 3 Patient status: Bleeding • Using the TEG Decision Tree and the available information from the TEG tracing: • Is it likely the patient will require more protamine as a treatment for bleeding? Yes or No. • This is a tracing from a kaolin activated sample. The presence of heparin in a kaolin sample • would result in an elongated R value. An R within normal range suggests heparin is not present, • thus additional protamine is not required. • Is it likely the patient will require FFP as a treatment for bleeding? Yes or No. • An R value within normal range suggests that factor deficiency is not the cause • of bleeding in this patient. Back

  47. Exercise 4 Patient status: Bleeding • Using the TEG Decision Tree what is a likely cause(s) of bleeding in this patient? • [Select all that apply] • Factor deficiency • Platelet deficiency or dysfunction • Low fibrinogen level • Fibrinolysis • Surgical bleeding • A slightly elongated R may suggest factor deficiency, however surgical bleeding cannot • be ruled out. • What treatment(s) would you consider for this patient? The R value is less than the • trigger point for FFP transfusion. If patient is oozing, wait an hour and repeat the • TEG. If R is still elongated and the patient is still oozy, consider treating with FFP. Back

  48. Exercise 5 • Using the TEG Decision Tree what is your interpretation of this TEG tracing? • [Select all that apply] • Factor deficiency • Platelet deficiency or dysfunction • Low fibrinogen level • Fibrinolysis • Normal • If this patient was bleeding, what treatment(s) would you consider? • Cryoprecipitate or FFP Back

  49. Exercise 6 Post-protamine Patient status: bleeding • Using the TEG Decision Tree what is your interpretation of this TEG tracing? • [Select all that apply] • Factor deficiency • Anticoagulant effect • Platelet deficiency or dysfunction • Low fibrinogen level • Surgical bleeding • What treatment(s) would you consider for this patient? Platelet transfusion Back

  50. Exercise 7 Black tracing: Kaolin Green tracing: Kaolin with heparinase Patient status: bleeding • Using the TEG Decision Tree what is your interpretation of this TEG tracing? • [Select all that apply] • Factor deficiency (cannot rule out) • Anticoagulant effect (incomplete reversal of heparin) • Platelet deficiency or dysfunction (cannot rule out) • Low fibrinogen level • Surgical bleeding • How would you treat this patient? A common treatment protocol would likely • include administration of additional protamine to reverse the heparin effect. • If the patient continues to bleed, repeat the TEG to determine the probable • cause. Most likely platelet deficiency/dysfunction. Back

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