Pulmonary Embolism & Deep Vein Thrombosis

Pulmonary embolism occurs when the pulmonary arteries are obstructed. This is most often due to emboli that travel from the deep veins of the thighs/pelvis. Because deep vein thrombosis and pulmonary embolism so often occur together, we have a term for their combined condition: venous thromboembolism. Nonthrombotic sources of pulmonary embolism include: air, fat, amniotic fluid, bacterial (septic), foreign bodies, and, tumors. Pulmonary embolism is a leading cause of cardiovascular-related death; denote that key complications of pulmonary embolism include pulmonary hypertension, right heart failure, and pulmonary infarction. Supportive therapy, which includes administration of oxygen, saline, and vasopressors. Anti-coagulation therapies, which can include heparin or fondaparinux for short-term treatment, and warfarin for longer-term treatment. In some cases, embolectomy or clot dissolution is required to restore blood flow through the pulmonary arteries. Leading cause of Pulmonary embolism. The "Virchow Triad" comprises three factors that predispose an individual to deep vein thrombosis; each of the three elements of the Virchow Triad contribute to the formation of clots in the blood vessels. Endothelial injury promotes clotting – endothelial injury can be due to fracture, surgery, trauma, or even previous deep vein thrombosis. Upon injury, the endothelium responds by triggering the clotting cascade (review of hemostasis). If this process goes unchecked, and the clots are not ultimately dissolved, they can be problematic. Venous stasis is another predisposing factor – venous stasis can be caused by immobility (if a person is bed-ridden or on a long flight, for example), elevated central venous pressure, heart failure, and obesity. To prevent DVT in hospitalized patients, we use SCD's (sequence compression devices), which prevent venous stasis in the legs. In select patients, we use prophylactic anticoagulants, which includes low doses of enoxaparin or heparin. Note that heparin-induced thrombocytopenia is a worrisome complication of anticoagulant, but, overall, in the correct population, prophylactic anticoagulants can be an important way of preventing DVT. Hypercoagulation states – Pregnancy (which is also associated with inferior vena cava stasis) – The post partum period – Smoking (which is also associated with endothelium damage) – Cancer – Medications, including combined hormonal contraceptives and some hormonal replacement therapies – Coagulation disorders, such as Factor V Leiden disorder. Be aware that individuals with multiple predisposing factors (i.e., pregnant women who are put on bed rest, for example), are at higher risk for developing deep vein thrombosis. Symptoms When present, symptoms of deep vein thrombosis tend to arise unilaterally in the legs, leaving them swollen, tender, and with signs of venous dilation. Deep vein thrombosis can occur in the upper body, too, but this is less common. Post thrombotic syndrome occurs when the venous valves are damaged. Diagnosis of deep vein thrombosis: Wells Score for Deep Vein Thrombosis, which gives points based on several factors including the presence of swelling, edema, and the likelihood of alternative diagnosis. (see the link in our notes for a full description of the Wells Score for Deep Vein Thrombosis). D-dimer level is an important way to try to rule out low-probability DVTs. If deep vein thrombosis is highly suspected, imaging with contrast venography or venous ultrasonography with compression can verify the presence of thrombus. Pathogenesis We'll begin by showing how a clot can reach the lungs and become lodged in the pulmonary arteries. First, show a clot in a deep vein of the thigh: show red blood cells, platelets, white blood cells, and fibrin. Then, indicate that a piece of this clot can break off and travel to the inferior vena cava. From here, the clot can pass through the right atrium and ventricle, and be pumped through the pulmonary trunk and arteries to reach the pulmonary blood supply. This clot blocks blood flow so that downstream alveoli will not be perfused and gas exchange will be impaired. Symptoms As a result of pulmonary artery obstruction and impaired gas exchange, show that patients may experience dyspnea, tachypnea (rapid breathing), and chest pain. Hypoxemia, ventilation to perfusion mismatch, and respiratory alkalosis can develop. Tachycardia and right heart failure are possible. We also look for ***altered mental state in elderly patients. Classifications We can classify PE by risk level: pulmonary embolisms are considered massive (high risk), intermediate (submassive), and low risk. Risk is determined by assessing hemodynamic instability (i.e., the presence of hypotension). Emboli can also be classified by their location: Saddle emboli are located where the pulmonary trunk bifurcates. Other emboli may become lodged in the lobar, segmental, or subsegmental arteries. Diagnosis of pulmonary embolism can be difficult due to the nonspecific symptoms and signs. The Pulmonary Embolism Wells Score gives points based on a variety of factors, including heart rate, presence of signs/symptoms, and likelihood of an alternative diagnosis. Wells score of 4 or greater indicates that pulmonary embolism is likely. Some calculators say less than 2 is low probability, 2-6 is moderate probability, and higher than 6 is highly probable. We can also measure D-dimer in the blood to rule out pulmonary embolism. D-dimer is a product of fibrin degradation, and levels greater than 500 nanograms per milliliter indicate that pulmonary embolism is possible and more tests are needed. Additional tests for pulmonary embolism:

• Ventilation to perfusion scan is a noninvasive test that can indicate the presence of a blood clot.

– Chest CT w/angiography is perhaps the most widely used assessment for Pulmonary Embolism. With this, we can actually visualize disruption of blood flow within the pulmonary arteries. – Chest X-Rays may show signs of: Atelectasis Hampton hump, which is indicative of pulmonary infarction; we'll learn more about in a moment) Westermark sign, which is indicative of oligemic areas; show that this appears as an area of poor perfusion of pulmonary arteries. Pulmonary effusion – ECG: may show sinus tachycardia; some patients may show an S wave in lead 1 with inverted Q and T waves in lead III (S1Q3T3 sign). – Thrombi formed premortem display lines of Zahn, which are formed by layers of fibrin, red blood cells, and platelet deposition. Additional Diagnostic Images Pulmonary infarction is most often due to small emboli that obstruct blood flow and cause tissue ischemia. – As mentioned, these patients' x-rays may show the wedge-shaped "Hampton Hump," most often in the lower lobes.