Laboratory Monitoring of Warfarin Therapy - Pathology

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Warfarin Monitoring Table I Clinical Management of the Supratherapeutic INR* *Data from Ansell, 2004 and other sources. The purpose of this table is to convey general guidelines for the treatment of a supratherapeutic INR. Clinical judgment is required for the individual patient. Warfarin Risks and Side Effects 6
Warfarin Monitoring tient is actively bleeding and the INR needs to be corrected acutely, fresh frozen plasma can be administered with vitamin K and in extreme 12cases prothrombin complex concentrates can be given. When a patient is found to have a markedly elevated PT without active bleeding, a more conservative approach is warranted such as simply skipping dosages until the INR returns to the appropriate range (Table I). Warfarin-induced skin necrosis is a rare but significant side effect. It follows administration by one to ten days, is heralded by parasthesia and an erythematous flush, which is followed by petechiae and hemorrhage which leads to skin necrosis. Skin necrosis is most commonly associated with proctein C deficiency and occasionally protein S deficiency. Protein C has a very short half-life and a rapid decline in activity from over 50% to less than 5% apparently initiates the development of skin necrosis in these patients. Therefore, screening for protein C and S deficiencies in patients with deep venous thrombosis may help to identify those with an increased risk of skin necrosis. Ansell, J. et al. The Pharmacology and Management of the Vitamin K Antagonists: The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 126: 204- 233, 2004. DeLoughery, T.G. “Oral anticoagulants” in Disorders of Hemostasis and Thrombosis, a Clinical Guide, Second Edition. Eds Goodnight, S.H. Jr. & Hathaway, W.E.. The McGraw- Hill Companies, New York, pp. 553-566, 2001. Fairweather, R.B., Ansell, J., van den Besselaar, A.M.H.P., Brandt, J.T., Bussey, H.I., Poller, L., Triplett, D.A. & White, R.H. College of American Pathologists Conference XXXI on laboratory monitoring of anticoagulant therapy. Laboratory monitoring of oral anticoagulant therapy. Arch. Pathol. Lab. Med. 122:768-781, 1998. Gage, B.F. et al. Management and dosing of warfarin therapy. Am. J. Med. 109:481– 488, 2000. Hirsh, J. Oral anticoagulants: Mechanism of action, clinical effectiveness, and optimal therapeutic range. Chest 119: 8S-21S, 2001. Jaffer, A.K. et al. Low–Molecular-Weight- Heparins as Periprocedural Anticoagulation for Patients on Long-Term Warfarin Therapy: A Standardized Bridging Therapy Protocol. J. Thromb. Thrombolysis. 20:11-16, 2005. Mueller, R.L. First-generation agents: aspirin, heparin and coumarins. Best Pract. Res. Clin. Haematol. 17:23-53, 2004. Riley, R.S., Fisher, L.M., and Rowe, D. Clinical utilization of the International Normalized Ratio (INR). J. Clin. Lab. Anal. 14:101-114, 2000. Sconce, E.A. The impact of CYP2C9 and VKORC1 genetic polymorphism and patient characteristics upon warfarin dose requirements: proposal for a new dosing regimen. Blood. 106:2329-2333, 2005. Tie, J.K., Nicchitta, C., von Heijne, G. & Stafford, D.W. Membrane topology mapping of vitamin K epoxide reductase by in vitro translation/cotranslocation. J. Biol. Chem. 280: 16410-16416, 2005. Wallin, R. and Hutson, S.M. Warfarin and the Vitamin K-Dependent !-Carboxylation System. Trends Mol. Med. 10: 299-302, 2004. References 7
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