Talal Dahhan, MD, Christian Castillo, MD and Victor F. Tapson, MD

1. Who first described pulmonary embolism?

    Pulmonary embolism (PE) was probably first reported in the early 1800s clinically, but Rudolf Virchow elucidated the mechanism by describing the connection between venous thrombosis and PE in the late 1800s. He also coined the term embolism.

2. What is Virchow’s triad?

    Virchow’s triad comprises the three broad categories of risk factors that contribute to thrombosis, including:

3. What percentage of patients with acute PE have clinical evidence of lower extremity deep vein thrombosis (DVT)?

    In the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) II study of 192 patients with angiographically documented PE, 47% had evidence of DVT by physical examination. The majority of patients with proven PE do have residual DVT present proven by imaging. More than 90% of emboli originate in the deep veins of the legs and thighs.

4. What percentage of patients with proximal DVT will develop PE?

    Approximately 50% of patients with proximal DVT will develop PE.

5. What is the usual cause of death in subjects with PE?

    It is well established that right ventricular (RV) failure is the cause of cardiovascular collapse and death in acute massive PE. Registry data have also suggested that patients with RV dysfunction on echocardiogram are at increased risk of all-cause mortality at 3 months.

6. What are the major risk factors for venous thromboembolism (VTE)?

    Risk factors are crucial in raising suspicion for acute VTE, although the disease may be idiopathic. Previous thromboembolism, immobility, cancer, advanced age, major surgery, trauma, acute medical illness, and certain thrombophilias impart significant risk. A list of risk factors for VTE is shown in Box 57-1.

7. How commonly are recommended VTE prevention measures used?

    Recent data suggest that worldwide, prophylaxis is underused. A recent study including more than 67,000 patients, the Epidemiologic International Day for the Evaluation of Patients at Risk for Venous Thromboembolism in the Acute Hospital Care Setting (ENDORSE) registry, indicated that in many countries less than half of patients deemed appropriate candidates for prophylaxis measures actually received them.

8. How should a patient with suspected DVT be initially evaluated?

    The symptoms and signs of DVT are nonspecific, and although clinical prediction rules can be useful, there should be a low threshold to proceed to compression ultrasonography. D-dimer testing may be useful; the diagnosis of DVT can be excluded without the need for ultrasound if the patient has a combination of a low or moderate clinical probability estimate and a negative D-dimer result. If the patient falls into the moderate or high clinical pretest probability or has a positive D-dimer test, further evaluation with ultrasound is advised. The enzyme-linked immunosorbent assay (ELISA)–based D-dimer tests have superior sensitivity (96% to 98%). DVT is discussed further in Chapter 50.

9. What are the symptoms and signs of acute PE?

    The symptoms and signs of PE are generally nonspecific but most commonly include dyspnea and chest pain, and may include the following:

If PE is associated with pulmonary hypertension, then elevated neck veins, a loud P2, RV heave, or a right-sided gallop may be noted.

10. What are four clinical syndromes seen with acute PE?

11. What is the Wells score for suspected acute PE?

    First described in 1998, the Wells score is a clinical prediction score based on simple, noninvasive clinical parameters. It has evolved over the years, has been validated, and is useful in determining pretest probability for suspected acute PE. Pretest probability can be defined based on the calculated score from the modified Wells score (Table 57-1). PE has ultimately been classified as “unlikely” if the clinical decision score was 4 or less, and “likely” with a score of more than 4 points. This cutoff was chosen because it has been shown to give an acceptable VTE diagnostic failure rate of 1.7% to 2.2% when in combination with a normal D-dimer test result. Moreover, with a score of 4 or less and a negative D-dimer test, no further testing appears to be necessary. A score greater than 4 requires further evaluation, and computed tomographic angiography (CTA) is usually performed. High clinical suspicion, however, should always take precedence, even if the Wells score is low.