Preface

Pulmonary embolism is a serious, potentially life-threatening cardiopulmonary disease that occurs due to partial or total obstruction of the pulmonary arterial bed. Pulmonary embolism constitutes 5-25% of in-hospital deaths, and mortality is decreased from 30% to 8% with early treatment. Therefore, risk factors should be identified and treatment should be planned to decrease the risk of mortality. Clinical findings, routine laboratory data, electrocardiogram, chest X-ray, and arterial blood gases are not sufficient to diagnose or rule out pulmonary embolus. The presence of some nonspecific findings such as dyspnea, pleuritic chest pain, tachypnea, and tachycardia, and one or more risk factors for venous thromboembolism raise suspicion for pulmonary embolus. However, it is not possible to diagnose pulmonary embolus with these factors. Recently, new improvement occurred in the diagnosis and treatment of the disease. The aim of this disease is to re-review pulmonary embolism in the light of new developments. In this book, in addition to risk factors causing pulmonary embolus, a guide for systematic approaches to lead the risk stratification for decision making is also presented. In order to provide a maximum length of active life and continuation of functional abilities as the aim of new interventional gerontology, the risk factors causing pulmonary embolus in elderly individuals are evaluated, and the approach to prevention and treatment is defined. The risk of the development of deep vein thrombosis and pulmonary embolism, combined with obesity due to immobility, the disease of this era, irregular and excessive eating, and treatment management are highlighted. Non-thrombotic pulmonary emboli are also covered and an attempt is made to constitute an awareness of this picture that can change the treatment and prognosis of the disease to a considerable extent. In addition to the pathophysiological definition of pulmonary embolus, the priority goal of quick and definitive diagnosis is emphasized, and diagnostic strategies are discussed in the book. A numerical analysis of the vena cava filters, which is a current approach to prevent pulmonary emboli recurrences, is presented in the last chapter.

I would like to thank the authors of all chapters for their intense labor and efforts in the preparation of this book. It is our belief that the new opinions and approaches presented will be beneficial to the readers.

> **Dr. Ufuk Çobanoğlu** Yüzüncü Yl University, School of Medicine Chief of Department of Thoracic Surgery Turkey

**1** 

*Turkey* 

Ufuk Çobanoğlu

*The University of Yuzuncu Yil* 

**Risk Factor for Pulmonary Embolism** 

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

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.

Among the hereditary risk factors leading to a predisposition to thrombosis, antithrombin deficiency was first shown to create predisposition to thrombosis in 1965, followed by the description of protein C deficiency in 1981 and protein S in 1984. These three deficiencies represent only 15% of hereditary thrombophilias. The description of the active protein C (APC) resistance by Dahlback et al in 1993 (Dahlback, 1995) and of the factor V Leiden mutation by Bertina in 1994 (Bertina, 1999) enabled elucidation of the etiology in 20% of patients with thrombosis and in 50% of families with thrombophilia. Similarly, hyperhomocysteinemia and a mutation in the prothrombin gene were shown to cause hereditary thrombophilia in 1994 and 1996, respectively (Makris et al., 1997). In patients with genetic thrombophilia, the predisposition to thrombotic and recurrent venous

thromboembolism (VTE) in the early stages of life is increased.

**1. Introduction** 

stasis (Carson et al., 1992).

**2. Genetic risk factors** 
