Ufuk Çobanoğlu

*The University of Yuzuncu Yil Turkey* 

#### **1. Introduction**

Pulmonary embolism (PE) is a common disease with high morbidity and mortality, yet it is a disorder that is difficult to diagnose (Stein & Matta, 2010). 90% of the clinical PE originates from the proximal deep veins of the lower extremities. An ultrasonographic study involving patients diagnosed with pulmonary embolism detected thrombus in 29% of the deep veins (Anderson et al., 1991). Failure to demonstrate the presence of deep vein thrombosis (DVT) in many patients with pulmonary embolism results from the detachment of the emerging blood clot or the inability of ultrasonography to show minor clots (Anderson et al., 1991). Besides DVT, immobilization after fracture or surgical procedures, pregnancy, delivery and usage of estrogen containing oral contraceptives are the other predisposing factors for pulmonary emboli (Quinn et al., 1992). The predisposing factors were first described by Virchow in 1856 as consisting of three major phenomena (Table 1) (Anderson et al., 1991; Quinn et al.,1992): the "Virchow triad", that is, the triad of the three factors that induce the process of vascular clotting: endothelial injury, hypercoagulability and lower extremity stasis (Carson et al., 1992).

In 75% of pulmonary embolism cases, the acquired and/or hereditary factors that lead to one of these predisposing factors are detected; in half of the hereditary thrombophilia cases, an accompanying acquired risk factor is also present (White, 2003). Stasis in the lower extremities usually results from slow blood flow occurring in the patient groups with decreased mobility. In patients with endothelial injury, causes such as trauma and surgery trigger this process while hypercoagulation is a mechanism observed in cases of hereditary thrombophilia (White, 2003). Table 2 presents the acquired and hereditary risk factors.
