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Anticoagulation for PCRRT

Anticoagulation for PCRRT. Dr. Peter Skippen, PICU. BC Children’s Hospital, Vancouver. CANADA. Outline. Normal Coagulation Anticoagulation: Options Heparin Citrate Others Conclusions. Ca ++. Ca ++. Ca ++. Ca ++. Ca ++. Ca ++. Mechanisms of Filter Thrombosis.

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Anticoagulation for PCRRT

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  1. Anticoagulation for PCRRT Dr. Peter Skippen, PICU. BC Children’s Hospital, Vancouver. CANADA.

  2. Outline • Normal Coagulation • Anticoagulation: Options • Heparin • Citrate • Others • Conclusions

  3. Ca++ Ca++ Ca++ Ca++ Ca++ Ca++ Mechanisms of Filter Thrombosis TISSUE FACTOR TF:VIIa CONTACT PHASE XII activation XI IX monocytes / platelets / macrophages X Va VIIIa Ca++ platelets Xa Phospholipid surface prothrombin THROMBIN NATURAL ANTICOAGULANTS (APC, ATIII) FIBRINOLYSIS ACTIVATION FIBRINOLYSIS INHIBITION fibrinogen CLOT

  4. Coagulation in Critically Ill Child • Pre-existing inflammatory states • sepsis • trauma • shock • hypercoagulable / thrombohemorrhagic states • Organ failure states • liver / renal (2˚ coagulation abnormalities) • blood oncology / marrow failure • Perioperative • cardiopulmonary bypass • Medications • platelet effects • immunosuppressive / oncologic • thrombogenic / fibrinolytic

  5. Factors Affecting Filter Life • Pre-existing condition of patient’s coag /anticoag system • Treatment characteristics • A-V vs. V-V • vascular access • diffusion vs. convection • filtration fraction • blood flow • membrane material and geometry • circuit alarms

  6. Sites of Thrombus Formation • any blood surface interface • hemofilter • bubble trap • catheter • areas of turbulence / resistance • very high blood flow rates • luer lock connections / 3 way stopcocks

  7. Technical aspects cannulae cannulation site circuitry blood flow rate FF predilution? No anticoagulation Saline flush? Hemodilution? Heparin unfractionated LMWH Citrate Others prostacyclin danaparoid hirudin nafamostate mesylate Anticoagulation: Options

  8. Unfractionated Heparin

  9. Ca++ Ca++ Ca++ Ca++ Ca++ Ca++ Sites of Action of Heparin LMWH TISSUE FACTOR TF:VIIa CONTACT PHASE XII activation XI IX monocytesplatelets macrophages X Va VIIIa Ca++ platelets Xa Phospholipid surface ATIII prothrombin UF HEPARIN THROMBIN NATURAL ANTICOAGULANTS (APC, ATIII) FIBRINOLYSIS ACTIVATION FIBRINOLYSIS INHIBITION fibrinogen CLOT

  10. Heparin - Problems • bleeding • unable to inhibit thrombin bound to clot • unable to inhibit Xa bound to clot • ongoing thrombin generation • direct activation of platelets • thrombocytopenia • extrinsic pathway unaffected

  11. No Heparin Systemically Heparinized NO surface - heparinized NO surface - no heparin Compliments of Dr. Gail Annich, University of Michigan

  12. Unfractionated Heparin Hoffbauer R et al. Kidney Int. 1999;56:1578-1583.

  13. LMWH: Theoretic Advantages • Reduced risk of bleeding • Less risk of HIT

  14. LMWH Hoffbauer R et al. Kidney Int. 1999;56:1578-1583.

  15. LMWH • no difference in filter life • no difference in risk of bleeding • no quick antidote • need to monitor levels • risk of accumulation • renal clearance • minimal filter clearance • increased cost

  16. Citrate

  17. Citrate: Mechanism of Action • Binds calcium - essential coagulation co-factor

  18. Citrate: Clinical Data

  19. Ca++ Ca++ Ca++ Ca++ Ca++ Ca++ Sites of Action of Citrate TISSUE FACTOR TF:VIIa CONTACT PHASE XII activation XI IX monocytes / platelets / macrophages X Va VIIIa Ca++ platelets Xa Phospholipid surface prothrombin CITRATE THROMBIN NATURAL ANTICOAGULANTS (APC, ATIII) FIBRINOLYSIS ACTIVATION FIBRINOLYSIS INHIBITION fibrinogen CLOT

  20. Citrate: Advantages • No need for heparin • Less bleeding risk • Simple to monitor

  21. Citrate Hoffbauer R et al. Kidney Int. 1999;56:1578-1583.

  22. Citrate: Technical Considerations • ensure catheter patency • establish desired blood flow • pre-filter infusion • initial citrate flow = x 2 (mls/hr) BFR (mls/min) • systemic calcium infusion • aim for pre-filter ionized Ca++ < 0.4mmol/L • adjust dialysate as needed • anticipate alkalosis • adjust electrolyte replacements as necessary • Na+ / PO4-- / Ca++ / Mg++

  23. Citrate: Problems • metabolic alkalosis • metabolized in liver / skeletal muscle / other tissues • electrolyte disorders • hypernatremia • hypocalcemia • hypomagnesemia • sugar load • “citrate lock”? • hepatic failure • ?cardiac toxicity • neonatal hearts

  24. Citrate: Clinical Data

  25. Citrate: Caution? • Congenital metabolic diseases? • ? mitochondropathies • Severe liver disease / hepatic failure • Excessive calcium requirements • Massive blood transfusions

  26. Hirudin • Highly selective / specific thrombin inhibitor • Minimal non-renal clearance • Long acting • No specific antagonist

  27. Nafamostate Mesylate • Synthetic protease inhibitor • Inhibits thrombin, Xa, XIIa, TF-VIIa complex • Low MW  high EC clearance • ACT for monitoring • No antidote but short half life

  28. Conclusions • Wide range of practice • UF heparin most commonly used anticoagulant • Citrate may be agent of choice in most situations?

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