Venous thromboembolism (VTE), which includes both deep venous thrombosis (DVT) and pulmonary embolism (PE), represents one of the most common preventable causes of hospital death and is associated with substantial long-term morbidity and mortality. The incidence of DVT exceeds 250,000 patients a year while more than 200,000 patients a year develop PE.1,2 The total incidence of VTE is estimated between 300,000 and 600,000 individuals in the United States per year.3 The widespread impact of VTE on healthcare spending ranges in the order of billions of dollars.4 Therefore, the incidence, prevalence, cost, morbidity, and mortality from VTE represent a significant public health burden. As such, understanding the underlying risk factors, diagnostic approaches, and factors that affect prophylaxis and treatment of DVTs and PEs is paramount.
Epidemiology and Risk Factors for DVT
The annual incidence of DVT in the United States has remained constant since the 1980s at approximately 50 per 100,000 person-years, However, the incidence varies with the comorbidities of each population studied, and this fact highlights the influence of genetic, environmental, and socioeconomic factors in predisposing to DVT formation. There are racial differences with African Americans having the highest incidence of VTE, Whites having an intermediate incidence, and Hispanics and Asian/Pacific Islanders having the lowest incidence.1,5 Patient factors that predispose to the increased risk of DVT formation include trauma and malignancy. Pregnancy results in uterine compression of venous outflow, contributing to an increased VTE risk. Hospitalization is a particularly potent risk factor for DVT formation with hospitalized patients displaying an increased risk of DVT as compared to matched outpatients. Events occurring during hospitalization, such as surgery and immobilization, increase the risk for DVT, with patients undergoing elective neurologic and orthopedic surgeries demonstrating the greatest risk. When considering hospitalized patients and outpatients alike, risk factors such as increasing age, obesity, certain disease states (e.g., inflammatory bowel disease, systemic lupus erythematosus, malignancies), inherited thrombophilias and hypercoagulability syndromes, the presence of varicose veins, and estrogen hormone therapies (oral contraceptives or hormone replacement therapy) further independently predispose patients to DVT formation.6 Analysis of these factors has enabled the development of risk assessment models, such as the Padua (for medial patients) or Caprini (for surgical patients) scores, which employ these factors to risk-stratify patients and guide their thromboprophylaxis during hospitalization.
The pathophysiologic underpinnings of DVT formation were first proposed by Virchow approximately 150 years ago as a triad of venous stasis, hypercoagulability, and endothelial injury. The specific mechanisms of each component and how they interact with one another is not completely understood and remains the subject of ongoing studies. As such, it is not surprising that disease processes that serve to impede venous outflow (e.g., immobility), favor blood clot formation (e.g., inherited thrombophilias), and alter endothelial integrity (e.g., sepsis and infection) greatly increase DVT formation risk. Furthermore, certain disease states such as malignancy ...