Patient Care Hematology & Oncology - October 2007 - (Page 9)

Bridge anticoagulation I ly 4 days before surgery and withholding any type of anticoagulation until the postoperative period • Lowering the warfarin dosage by approximately one-third and performing the invasive procedure when the INR is approximately 1.5 or less • Using bridge therapy by stopping warfarin 4 to 5 days before the procedure and starting UFH or LMWH 2 days before the procedure.1 The evidence for supporting one of these options over another for a given procedure is weak. The American College of Chest Physicians (ACCP) graded periprocedural bridging evidence as 2C (riskbenefit unclear, observational studies, very weak recommendations; other alternatives may be equally reasonable). Clinicians judge the bleeding risks associated with proposed surgery and the thrombotic risks inherent in the patient’s condition in deciding which periprocedural path to follow. Every decision needs to be individualized. Several reviews of the literature address the question of bridge therapy.3-5 Procedures identified as requiring no interruption of OAC included most dental and ophthalmic procedures (excluding retinal surgery), joint and soft tissue injections, and upper endoscopy with or without biopsy. More invasive procedures requiring interruption of OAC included pacemaker insertion, major abdominal surgery, thoracic surgery, GU surgery, cancer surgery, and neurosurgery. It is important to consider that in addition to the bleeding risk from the type of procedure, factors such as location and extent of surgery and the accessibility of the bleeding site to compression independently affect the risk of bleeding. Conditions that place patients at the highest risk of thromboembolism are shown in Table 1 (page 10). There is general agreement that patients with these conditions require periprocedural bridge therapy. FIGURE 1 Intrinsic pathway Surface contact XII XI IX XIIa XIa IXa VIII Extrinsic pathway Tissue damage VII VIIa X Common pathway Prothrombin (II) Xa Thrombin Fibrinogen (I) Fibrin This simplified coagulation cascade illustrates the sites of action of warfarin, which depletes the factors shown in blue, and of unfractionated and low-molecular-weight heparins, which enhance antithrombin III, thus inhibiting the factors shown in red. Options for bridge therapy UFH has been the anticoagulation of choice in hospitalized patients for many years, and it has been used as the standard of care in patients who require bridge therapy before and after a surgical procedure. Figure 1 illustrates heparin’s enhancing effect on antithrombin III, an enzyme primarily responsible for the inhibition of thrombin and factor Xa. The anticoagulant effects of heparin are complicated by the chemical and pharmacologic heterogeneity of the product. Since UFH has a relatively short half-life, it has to be given as a continuous infusion when therapeutic levels are needed. This requires continuous laboratory monitoring of the activated partial thromboplastin time (aPTT) to provide effective doses without increasing the risk of bleeding. As a result, UFH bridging requires hospi- OCTOBER 2007 PATIENT CARE HEMATOLOGY & ONCOLOGY 9

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Patient Care - Hematology & Oncology - October 2007 Research Digest Contents Information for Authors Medicine in the News Strategies for Bridge Anticoagulation Therapy How to Integrate the New Cervical Cancer Guidelines into Practice Dermatology Case Challenge Clinical Clips Classified Advertising

Patient Care Hematology & Oncology - October 2007

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