39: Deep Vein Thrombosis

INTRODUCTION

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 vein 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.^2,3

This second edition update focuses on the following four areas: further literature supporting the use of point-of-care ultrasonography by the emergency medicine physician; diagnosis and management of the upper extremity DVT; the updated 2012 American College of Chest Physicians (ACCP) guidelines regarding diagnosis and treatment of VTE diseases; and oral direct thrombin inhibitors or oral factor Xa inhibitors for the treatment of DVT.

ANATOMY AND PATHOPHYSIOLOGY

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, the number of platelets and leukocytes being variable. The development, progression, and breakdown of VTE 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.⁴ The presence of these factors alters the balance between endogenous fibrinolysis and fibrin formation, which contributes to the formation and proliferation of a thrombus.¹ The protective mechanism 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 cells derived fibrinolytic enzyme lysis of fibrin.⁵

Using Virchow's triad as 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.

Hypercoagulability

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 ...