A 62-year-old man is evaluated in the ER for sudden onset of swelling of the right calf with pain for past 2 days. The patient noticed the swelling after he woke up from sleep and had pain while walking. He cannot recollect any history of trauma, denies any recent travel, and has never had a blood clot in the past His medical history is remarkable for hypertension, adequately controlled with lisinopril, and stage-III squamous cell carcinoma of the lung for which he recently completed six cycles of chemotherapy. On physical examination, there is tender swelling of the right calf without erythema. His D-dimer is 640 ng/mL. Venous Doppler of the right leg reveals occlusive thrombi in the deep veins. A plan is made to initiate anticoagulation and to extend the treatment for 6 months.What will be the drug of choice for anticoagulation for this patient?
Malignancy is a recognized risk factor for venous thromboembolism (VTE), and VTE is the second leading cause of death in cancer patients. Procoagulant molecules expressed both by cancer cells and host tissue contribute to this condition. Low-molecular-weight heparin (LMWH) is the preferred anticoagulant for long-term treatment in patients with cancer. When compared with warfarin, LMWH reduces the rate of recurrent VTE without significant risk of bleeding. Newer anticoagulants such as rivaroxaban have not been adequately tested for cancer-induced VTE yet.Young patients with unprovoked VTE, a history of unexplained VTE, or family history of VTE raise the suspicion of an inherited hypercoagulable disorder. The common inherited hypercoagulable disorders are Factor V Leiden mutation, prothrombin gene mutation, protein S deficiency, protein C deficiency, antithrombin III deficiency, dysfibrinogenemia, and antiphospholipid antibody syndrome. When inherited hypercoagulable disorders are strongly suspected, tests for above mentioned disorders can be ordered. In the event of an acute thrombosis, however, it is not recommended to test for protein C, protein S, and anti-thrombin III since active coagulation can reduce the plasma concentration of these proteins resulting in false-positive result. To avoid confusion, it is recommended to order only Factor V Leiden mutation, prothrombin gene mutation, and antiphospholipid antibody with acute VTE or when patients are on warfarin.Warfarin-induced skin necrosis results from a transient hypercoagulable state. Warfarin initially affects all the vitamin K-dependent clotting proteins (Factors II, VII, IX, X, and proteins C and S). Since Protein C has a short half-life (8-12 hours), the serum protein C concentration drops quickly to 50% of normal in first 24 hours. Since circulating levels of other vitamin K-dependent proteins are still high, this gives rise to a hypercoagulable state which may cause microthrombi in the dermal and subcutaneous vessels, resulting in skin necrosis. The risk is particularly high in case of congenital protein C deficiency; nearly one-third cases of warfarin-induced skin necrosis are associated with congenital protein C deficiency.
Rivaroxaban
Low-molecular-weight heparin
Warfarin
Low dose aspirin (81 mg/d)
Oncology