Deep Vein Thrombosis and Pulmonary Embolism

Etiology and Pathogenesis

Venous thromboembolism (VTE) is common and has an annual incidence of approximately 0.1% in the general population. VTE is a broad term used to include patients with both deep venous thromboembolism (DVT) and pulmonary embolism (PE). These conditions warrant consideration together because up to 90% of PEs are secondary to DVT in the iliac, femoral, or popliteal venous systems. Less common sources of PE include calf vein thrombosis, pelvic vein thrombosis, thrombus formation from right heart abnormalities, upper extremity thrombosis, invasive tumors (renal cell carcinoma), and fat embolism secondary to trauma.

Venous thrombosis occurs when there is stasis of blood flow, endothelial injury, and hypercoagulability (commonly known as Virchow triad). Stasis of blood flow can occur when venous outflow is obstructed (e.g., May-Thurner Syndrome, which is left iliac venous obstruction secondary to an overlying right common iliac artery) or situations that lead to immobility ( Fig. 63.1 ). Any travel resulting in immobility for >4 hours increases the risk of DVT by at least twofold, and this risk can persist for several weeks after travel. Although all hospitalized patients who are immobile are at increased risk of DVT, those in the postoperative setting have an additional risk. Surgery and trauma affect each element of the Virchow triad by decreasing venous flow in the setting of immobilization, allowing the exposure of tissue factor through endothelial damage, and increasing hypercoagulability via depletion of endogenous anticoagulants. Hypercoagulability can be inherited or acquired. Factor V Leiden mutation, prothrombin gene mutation, protein S deficiency, protein C deficiency, and antithrombin III deficiency are inherited conditions that account for approximately 10% of DVTs. Of these conditions, patients with protein S deficiency are most likely to have a DVT in their lifetime. Acquired hypercoagulable conditions include antiphospholipid syndrome, nephrotic syndrome, inflammatory bowel disease, heparin-induced thrombocytopenia, pregnancy, oral contraceptive pills, hormone replacement therapy, myeloproliferative disorders, and malignancy.

The pathogenesis of PE begins with the embolization of DVT ( Fig. 63.2 ). PE results in a ventilation and/or perfusion (V/Q) mismatch by obstructing perfusion of pulmonary alveoli that have normal ventilation, leading to impaired gas exchange and/or hypoxemia, and possibly even infarction of the lung. An inflammatory process can contribute to atelectasis, which leads to intrapulmonary shunting and stimulation of the respiratory drive and respiratory alkalosis with hypocapnia. PE can also lead to acute pulmonary infarction if small emboli occlude the distal segmental and subsegmental vessels. The resulting parenchymal necrosis and pleural inflammation can cause pleuritic chest pain. Finally, PE can lead to obstructive shock and cardiovascular collapse if the thrombus burden is large enough to obstruct cardiac output from the right ventricle ( Fig. 63.3 ). Large PEs can cause increased pulmonary vascular resistance, pulmonary hypertension, acute right ventricular (RV) failure, and RV dilatation. Due to the RV dilatation and reduced RV output, the left ventricular (LV) preload decreases and the cardiac output decreases, leading to systemic hypotension and obstructive shock.

Clinical Presentation

When evaluating patients with possible DVT and/or PE, it is important for the clinician to be familiar with risk factors for VTE. The most important risk factors are immobilization or prolonged bedrest, recent surgery, tobacco use, obesity, previous VTE, lower extremity trauma, malignancy, hormone or oral contraceptive use, pregnancy or postpartum status, and stroke. A history of DVT and malignancy are the strongest predictors of VTE.

Pulmonary Embolism

Patients with PE can have a variety of different presentations that range from no symptoms to shock and/or hemodynamic collapse. The most common presenting symptoms, in order of prevalence, are dyspnea, pleuritic chest pain, leg pain and/or swelling due to DVT, cough, orthopnea, wheezing, and hemoptysis. Less common presentations include arrhythmias, presyncope, syncope, and shock. Dyspnea, especially due to proximal infarction of a proximal vessel, is typically sudden in onset, with patients noticing worsening breathlessness over a matter of seconds. Distal vessel infarction can cause pleural inflammation and pleuritic chest pain. It is important to note that the preceding symptoms may be absent, even in the setting of significant amount of thrombus burden, and up to 25% of patients will not report the presence of dyspnea. Signs of PE, in order of prevalence, include hypoxemia, tachypnea, lower extremity pain and/or swelling, tachycardia, rales, decreased breath sounds, loud pulmonic component of the second heart sound, jugular venous distention, and fever ( Fig. 63.4 ).

Differential Diagnosis