DEFINITION AND NATURAL HISTORY
Venous thromboembolism (VTE) includes both deep-vein thrombosis (DVT) and pulmonary embolism (PE). DVT results from blood clot formation within large veins, usually in the legs. PE results from DVTs that have broken off and traveled to the pulmonary arterial circulation. Isolated calf vein thrombi have much lower risk of PE. Although DVTs are typically related to thrombus formation in the legs and/or pelvis, indwelling venous catheters, pacemakers, and internal cardiac defibrillators have increased the occurrence of upper extremity DVT. In the absence of PE, the major complication of DVT is postthrombotic syndrome, which causes chronic leg swelling and discomfort due to damage to the venous valves of the affected leg. In its most severe form, postthrombotic syndrome causes skin ulceration. PE is often fatal, usually due to progressive right ventricular failure. Chronic thromboembolic pulmonary hypertension is another long-term complication of PE.
Some genetic risk factors, including factor V Leiden and the prothrombin G20210A mutation, have been identified, but they account for only a minority of venous thromboembolic disease. Medical conditions that increase the risk of VTE include cancer and antiphospholipid antibody syndrome. A variety of other risk factors have been identified, including immobilization during prolonged travel, obesity, smoking, surgery, trauma, pregnancy, estrogen-containing contraceptives, postmenopausal hormone replacement, and inflammatory diseases (e.g., inflammatory bowel disease, psoriasis).
Massive PE, with thrombosis affecting at least half of the pulmonary vasculature, often includes dyspnea, syncope, hypotension, and cyanosis. Submassive PE includes RV dysfunction in the setting of normal systemic arterial pressure. Low-risk PE, which includes normal RV function and systemic arterial pressure, has an excellent prognosis.
DVTs often present with progressive lower calf discomfort. For PE, unexplained dyspnea is the most common presenting symptom. Chest pain, cough, or hemoptysis can indicate pulmonary infarction with pleural irritation. A substantial fraction of pts hospitalized for syncope have PE.
Tachypnea and tachycardia are common in PE. Low-grade fever, neck vein distention, and a loud P2 on cardiac examination can be seen. Hypotension and cyanosis suggest massive PE. Physical examination with DVT may be notable only for mild calf tenderness. However, with massive DVT, marked thigh swelling and inguinal tenderness can be observed.
Normal D-dimer level essentially rules out PE in pts with low-to-moderate likelihood of PE, although hospitalized pts often have elevated D-dimer levels due to other disease processes. Although hypoxemia and an increased alveolar-arterial O2 gradient may be observed in PE, arterial blood gases are rarely useful in diagnosing PE. Elevated serum troponin, plasma heart-type fatty acid-binding protein, and brain natriuretic peptide levels can be seen in PE. The electrocardiogram can show an S1Q3T3 sign in PE, but that finding is not frequently observed.