In the United States, it is estimated that roughly 100 per 100,000 people per year experience a first-time venous thromboembolism (VTE). Of these cases, two thirds are caused by deep venous thrombosis (DVT).1 Much literature has been devoted to the occurrence of VTE in hospitalized patients who are ill or recovering from a surgical procedure. However, many patients present as outpatients to the emergency room with symptoms related to their VTE. This chapter focuses on the current practices for evaluation and diagnosis of DVT and hopes to help guide the emergency physician through the current evidence-based clinical practice guidelines for antithrombotic and thrombolytic therapy.2
Lower extremity DVT is subdivided into proximal (thigh) and distal (calf) vein thrombosis. Proximal DVT is considered of more clinical importance since it is more commonly associated with serious disease and potentially fatal outcomes.
Venous thrombi are composed mainly of fibrin and red blood cells, with the number of platelets and leukocytes being variable. The development, progression, and breakdown of venous thromboemboli reflect a balance between thrombogenic stimuli and protective mechanisms. In the 19th century, Virchow identified and described thrombogenic stimuli. Virchow is credited with outlining the now classic triad of hypercoagulability, endothelial injury, and stasis in association with VTE.3 The presence of the above factors alters the balance between endogenous fibrinolysis and fibrin formation that contributes to the formation and proliferation of a thrombus.1 The protective mechanisms against thromboembolic formation are inactivation of activated coagulation factors by circulating inhibitors such as antithrombin and activated protein C, clearance of activated coagulation factors and soluble fibrin polymer complexes by mononuclear phagocytes and the liver, and plasma and endothelial cell–derived fibrinolytic enzyme lysis of fibrin.4
Using Virchow's triad as a framework, one can better understand the factors that predispose the development of venous thrombosis and the protective mechanisms that counter thrombogenic stimuli. This allows for a better understanding of the various risk factors and treatments for venous thrombi.
The activated clotting factors in blood are regulated by inhibitors on the surface of endothelial cells and circulating antiproteinase. Hypercoagulable states offset the balance and tip the natural clotting cascade in the direction of fibrin production and clot formation. This can be seen as a result of reduced levels of inhibitors or an increase in activated clotting factors. Activation of coagulation may result from the contact of factor XII with collagen on the damaged vessels' exposed subendothelium.5 Malignant cells contain a cysteine protease that can directly activate factor X. This may be one mechanism by which malignancy can induce thrombosis.6 Fibrin formation is enhanced by acquired states of hypercoagulability. Genetic thrombophilias and neoplastic abnormalities increase fibrin formation or decrease fibrinolysis.
The processes that initiate a venous thrombosis are less certain and felt to be much different from those that initiate an arterial ...