Upper extremity deep venous thrombosis (UEDVT) makes up approximately 1-4% of all episodes of deep venous thrombosis (DVT). Risk factors for UEDVT include central venous catheterization, strenuous upper extremity exercise or anatomic abnormalities causing venous compression, inherited thrombophilia, and acquired hypercoagulable states including pregnancy, oral contraceptive use, and cancer. Unexplained or recurrent UEDVT should prompt a search for inherited hypercoagulable states or underlying malignancy. Clinical presentations include arm, neck, and shoulder pain; edema; skin discoloration; tenderness; and venous distension. Because UEDVT is frequently asymptomatic until complications ensue, a high index of suspicion is required for patients with one or more risk factors for thrombosis. Pulmonary embolism and post-thrombotic syndrome are the most common sequelae of UEDVT. Early detection and treatment of UEDVT decrease complications, morbidity, and mortality. Compressive ultrasonography is an effective and economical means of confirming the clinical diagnosis in most patients. Traditional anticoagulant therapy of UEDVT is giving way to a multimodal approach involving transcatheter thrombolytic therapy followed by a minimum of 3 months of warfarin sodium anticoagulant therapy, venous decompression as needed, and balloon angioplasty with stenting for treatment of residual stricture. Low-dose anticoagulant therapy can safely and effectively mitigate the increased risk of UEDVT associated with the use of central venous catheters.

From injury through healing, thrombin has several important functions in blood clotting, subsequent clot lysis, and tissue repair. These include edema, inflammation, cell recruitment, cellular releases, transformations, mitogenesis, and angiogenesis. Thrombin also participates in disease states, such as venous thrombosis, coronary thrombosis, stroke, and pulmonary emboli, among others and is implicated in atherosclerosis, the growth and metastasis of certain cancers, Alzheimer's disease, and perhaps other conditions. Thrombin must be continually generated to sustain normal and pathogenic processes. This is because of a variety of consumptive mechanisms. Unlike other activated factors in thrombotic and fibrinolytic pathways, and because thrombin promotes its own generation (feedback and cellular activation), thrombin is a primary target for therapeutics. Besides recombinant hirudins, Argatroban (Novastan) and Bivalirudin (Hirulog) are promising thrombin-directed inhibitors for antithrombotic intervention.

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