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Description : a report on coagulation monitoring and ROTEM, Why the need for monitoring?

Tags : coagulation, ROTEM,monitoring

Published on : Nov 17, 2023 | Views : 630 | Downloads : 0

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Slide 1-

Coagulation Monitoring and ROTEM Roberto Enrico S. Imperial
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Why the need for monitoring? Requirement for cardiopulmonary bypass Often necessary in cardiac surgery Inflammatory response  stimulation of coagulation and fibrinolytic cascade Necessitates use of anticoagulant  heparin Hemostatic changes are seen even after heparin has been reversed
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Hemostasis Components: Vascular endothelium Platelets - primary hemostasis Coagulation cascade – secondary hemostasis
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Anticoagulation for CPB Needed in preparation for blood contact with the extracorporeal circuit Ideal agent Easy to administer Rapid onset Titratable Predictable Measurable in timely fashion Reversible
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Monitoring Heparin Clotting time
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Activated Clotting Time Activators Celite/Kaolin Normal value: 80-120 seconds Modification with heparinase Monitor coagulation status during CPB with heparin eliminated Use in CPB Allows easier titration of heparin and protamine doses Reduced blood loss and transfusion requirements
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Activated Clotting Time Factors that alter ACT Hemodilution - ↑ ACT Hypothermia - ↑ ACT Thrombocytopenia < 30k-50k/uL - ↑ ACT Platelet lysis - ↓ ACT
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Heparin Resistance Inability to increase the ACT despite adequate dose and plasma concentration of heparin Patients receiving preoperative heparin treatment require larger doses of heparin intraop Treatment: AT III concentrate Increased heparin dose FFP
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Heparin-Induced Thrombocytopenia Occurs 5-14 days after heparin administration Mediated by antibodies binding to the heparin-PF4 complex Causes platelet activation and subsequent thrombocytopenia Associated with 30% risk for thrombosis  50% mortality rate Treatment Use LMWH instead Pharmacologic platelet inhibition – prostacyclin, iloprost, aspirin Plasmapheresis
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Measurement of Heparin Sensitivity Responses to heparin are extremely variable Due to different concentration of various endogenous heparin binding proteins (i.e vitronectin and PF4)  interpatient variation in heparin responsiveness Heparin dose response curve
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High-Dose Thrombin Time TT - clotting time that measures the conversion of fibrinogen to fibrin Prolonged in presence of heparin, hypo/dysfibrinogenemia Advantage Not altered by hemodilution and hypothermia (unlike ACT)
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Heparin Neutralization Protamine Binds to positively charged groups on heparin Recommended dose: 1-1.3 mg protamine per 100 IU/1 mg of heparin *often results in protamine excess Adverse hemodynamic effects Type I – hypotension Type II (immunologic) IIA anaphylaxis IIB anaphylactoid IIC noncardiogenic pulmonary edema Type III hypotension and pulmonary hypertension leading to right heart failure Adverse effects on coagulation
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Monitoring for Heparin Rebound Heparin rebound – re-establishment of heparinized state after heparin has been neutralized with protamine Rapid distribution and clearance of protamine shortly after protamine administration Release of heparin from heparin storage sites (endothelium, connective tissue) Monitoring Protamine titration assay Heparin-neutralized thrombin time assay Heparinase ACT
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Heparin Neutralization Monitors Ideal to measure concentration of remaining circulating heparin present Give the corresponding protamine dose only Optimal protamine dose Underdose = unneutralized heparin  bleeding Overdose = possible coagulopathy Tests Thrombin time Protamine titration assay
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Other heparin neutralizing agents Platelet factor 4 Binds and inactivates heparin Released from platelets, binds heparin, and promotes thrombin and clot formation Inhibits factor Xa and IIa inhibition of heparin Devoid of adverse hemodynamic effects Heparinase Degrades heparin by cleavage of the saccharide bonds in the molecule 5 – 7 mg/kg No hemodynamic effects No platelet depressive effects
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Tests of Coagulation Activated partial thromboplastin time (aPTT) Measures intrinsic and common coagulation pathway F IX and X most sensitive to heparin NV 28-32 seconds Prothrombin time (PT) Measures extrinsic and common coagulation pathway NV 12-14 seconds Standardized with INR
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Tests of Coagulation Fibrinogen level Clotting time is inversely related to fibrinogen concentration NV 180-220 mg/dL
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Monitoring Fibrinolysis Fibrinolysis Ensures that coagulation does not proceed unchecked Dissolves clot when local endothelial healing occurs Mediated by plasmin Monitoring Viscoelastic tests (TEG, ROTEM) End products of fibrin degradation (D-dimers)
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Monitoring Thrombin Inhibitors Selective thrombin inhibitors Viable alternative to heparin for CPB Hirudin, agratroban, bivalirudin Inhibit clot-bound thrombin independently of AT-III Associated with less bleeding, better platelet counts compared to heparin Monitoring ACT, aPTT, TT
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Monitoring Platelet Function Platelet count Thrombocytopenia Common during cardiac surgery (hemodilution, sequestration, destruction by non-endothelial surfaces) Platelet size and volume Larger, younger platelets are more active Bleeding time Make a skin incision and measuring the time to clot formation by platelet plug NV 4-10 minutes Aggregometry Objective measure of platelet activation
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Effects of Heparin on Platelets
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Thromboelastography Useful in obtaining information about clot formation and clot dissolution Coagulation cascade Platelet function Platelet-fibrin interaction Fibrinolysis
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Thromboelastography
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Thromboelastography
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Rotational Thrombelastometry (ROTEM)
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ROTEM Assays INTEM INTEM – contact phase activation, F XII, XI, IX, VIII, II, I, platelets and fibrinolysis HEPTEM – INTEM + heparinase – to detect residual heparin EXTEM EXTEM – Tissue factor activation, F VII, X, V, II, I, platelets and fibrinolysis FIBTEM – EXTEM + cytochalasin D (platelet blocking) – to assess fibrinogen APTEM – EXTEM + aprotinin, rule out fibrinolysis compared to EXTEM
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Point of care tests of platelet response to agonists Tests platelet function in response to agonists
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Summary Hemostatic insults during CPB Heparin effect Platelet dysfunction Fibrinolysis defects Coagulation factors defects Appropriate tests for management Better use of blood products/medications
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Reference: Kaplan’s Cardiac Anesthesia: for Cardiac and Noncardiac Surgery 7th edition Thank you