1 . Classification of pulmonary embolism (PE) typically categorizes the disease as
| A) | | left or right. |
| B) | | acute or chronic. |
| C) | | massive or supermassive. |
| D) | | hemodynamically stable or unstable. |
Classification of PE typically categorizes the disease as
hemodynamically stable or unstable. The most common type is hemodynamically stable, which can
range from small, mildly symptomatic or asymptomatic PE (previously referred to as low-risk PE
or small PE) to those who present with right ventricular dysfunction but who are
hemodynamically stable (previously referred to as submassive or intermediate-risk PE) [3,4]. While PE characterized by right ventricular dysfunction can be
hemodynamically stable, more severe (unstable) disease is characterized by the presence of
systemic arterial hypotension, which indicates at least half of the pulmonary vascular tree is
affected [4,5]. Hemodynamically unstable PE (previously referred to as massive or
high-risk PE) will result in significant hypotension. Hemodynamic instability is defined as
the presence of cardiac arrest requiring resuscitation, or obstructive shock or persistent
hypotension not caused by other pathologies [36].
2 . The annual incidence of PE is difficult to pinpoint but is estimated to be about
| A) | | 6 to 7 cases per 100,000 population. |
| B) | | 26 to 37 cases per 100,000 population. |
| C) | | 60 to 70 cases per 100,000 population. |
| D) | | 160 to 170 cases per 100,000 population. |
The annual incidence of PE is difficult to pinpoint but is estimated to be about 60 to 70 cases per 100,000 population [6]. General autopsy studies from all-cause mortality have found PE, variable in number and age, to be present in 30% to 45% of cases [6,7,8,9].
3 . The majority of patients who die from PE do so
| A) | | within 60 minutes of presentation. |
| B) | | within two hours of presentation. |
| C) | | after more than two days of treatment. |
| D) | | more than two weeks after presentation. |
Behind only stroke and coronary artery disease, PE is one of the most common types of cardiovascular disease. It is more common in patients 60 to 70 years of age, with the highest incidence in patients 70 to 80 years of age. Although death following a diagnosis of PE is relatively common, as high as 30%, many of these patients have coexisting serious conditions, such as cancer, recent surgery, or sepsis. The direct mortality associated with undiagnosed/untreated PE during the course of diagnosis and treatment is about 5% to 8%. An estimated 10% of patients with acute PE die suddenly; approximately two-thirds of patients who die from PE do so within two hours of presentation. The mortality rate for those treated for hemodynamically unstable PE is about 20%, and those with cardiogenic shock have a mortality rate of 25% to 30%. Those with a hemodynamically stable PE have a mortality rate of 1% to 25%, depending on the degree of right ventricular dysfunction [2,4,5,10].
4 . Most commonly, a PE occurs when
| A) | | a portion of a malignant tumor enters into the pulmonary circulation. |
| B) | | a deep vein thrombus detaches and embolizes into the pulmonary circulation. |
| C) | | nitrogen bubbles form in the blood vessels and embolize into the pulmonary circulation. |
| D) | | air enters the systemic venous circulation and travels to the right ventricle and pulmonary circulation. |
Most commonly, a PE occurs when a deep vein thrombus detaches and migrates, or embolizes, into the pulmonary circulation. This can lead to blockage of the pulmonary vasculature, causing a ventilation-perfusion (VQ) mismatch and impairing gas exchange and circulation. PE is more common in the lower lung fields, compared with the upper ones, and both lungs are typically involved. Peripheral PE, as opposed to central PE, can lead to a pulmonary infarction coupled with alveolar hemorrhage. As further obstruction of the pulmonary artery occurs, there is an increase in dead space ventilation and elevation of pulmonary arterial pressure by increasing pulmonary vascular resistance. This further worsens VQ mismatch, with vascular occlusion of the arteries.
5 . The differential diagnosis of PE includes all of the following, EXCEPT:
| A) | | Pneumonia |
| B) | | Heart failure |
| C) | | Pneumothorax |
| D) | | Hyperthyroidism |
A strict (confirmatory) diagnosis of PE would require direct anatomic evidence of pulmonary artery obstruction, which by modern imaging technique (e.g., computed tomography [CT] angiography) would involve invasive measures and exposure to radiation. As the size and distribution (severity) of PE are variable, the preferred strategy for selecting diagnostic testing relies on degree of clinical suspicion, clinical judgment, and assessment of pre-test probability. Selection of noninvasive testing to rule out the diagnosis, based on the assessed clinical probability of PE, has proved effective in reducing the use of CT imaging, thereby minimizing lung and breast-tissue exposure to irradiation [27]. The differential diagnosis includes heart failure, pneumothorax, pneumonia, sepsis, acute chest syndrome, chronic obstructive pulmonary disease (COPD) exacerbation, and anxiety or other psychotropic illnesses. A systematic review and meta-analysis found that a history of sudden dyspnea, syncope, thrombophlebitis, previous deep vein thrombosis, leg swelling, active cancer, or recent surgery was associated with an increased probability of PE [54]. An inability to increase alveolar oxygen pressure (PaO2) greater than 8.0 kPa (60 mm Hg) despite high-flow oxygen should also raise suspicion for PE.
6 . Which of the following statements regarding D-dimer testing in patients with suspected PE is TRUE?
| A) | | A normal D-dimer level effectively rules out PE. |
| B) | | Assessment of D-dimer levels should never be used for screening. |
| C) | | In the event that the D-dimer is low, planar VQ scanning is essential. |
| D) | | The specificity of D-dimer increases with age and is most useful in patients older than 50 years of age. |
Assessment of D-dimer levels can be used for screening purposes and to rule out PE if the pretest probability is intermediate or low. D-dimer is a byproduct of intrinsic fibrinolysis. It is considered to be a highly sensitive test for the absence of PE and has a very high negative predictive value. A normal D-dimer level effectively rules out PE or deep vein thromboembolism. In the event that the d-dimer is elevated, further testing (e.g., computed tomography [CT] angiography, planar VQ scanning) can be performed [10; 14; 15; 16]. Because the test is not specific, an elevated finding is not diagnostic. The specificity of D-dimer decreases with age, and the use of age-adjusted cut-offs is recommended for patients older than 50 years of age. The formula is age (years) x 10 mcg/L for patients older than 50 years of age.
7 . What is the imaging modality of choice when evaluating patients with suspected PE and normal chest x-ray for whom CT angiography is contraindicated?
| A) | | MRI |
| B) | | A VQ scan |
| C) | | Ultrasound |
| D) | | Fluoroscopy |
VQ scans visualize areas that are ventilated but not perfused (i.e., VQ mismatch). This testing requires more time, is less specific than CT angiography, and should be done with clinical correlation. However, it is the imaging modality of choice for patients with suspected PE and normal chest x-ray for whom CT angiography is contraindicated, including those with impaired kidney function and pregnant patients. Normal ventilation is 4 L air/minute, and normal perfusion is 5 L blood/minute; thus, a normal VQ ratio is 0.8. A high VQ ratio (>0.8) indicates that the patient's ventilation is exceeding perfusion, while a low VQ ratio indicates a VQ mismatch caused by poor ventilation. When blood is diverted away from the occluded section, overperfusion can occur in the normally ventilated regions. The modified Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED-II) criteria score the probability of PE based on VQ scan findings (Table 1).
8 . In the primary management of PE, the dose of apixaban is
| A) | | 5 mg once daily for most patients. |
| B) | | 10 mg twice daily for seven days, followed by 5 mg twice daily. |
| C) | | 15 mg twice daily with food for 21 days, followed by 20 mg once daily with food. |
| D) | | once-daily oral 60 mg for patients who weigh more than 60 kg or 30 mg for patients 60 kg of less. |
ORAL ANTICOAGULATION THERAPY
| Agent | Dosage |
|---|
| Vitamin K Antagonist |
| Warfarin | 5 mg once daily for most patientsa |
| Direct Thrombin Inhibitor |
| Dabigatran etexilate | After at least 5 days of initial therapy with a parenteral anticoagulant,
transition to oral 150 mg twice daily. |
| Factor Xa Inhibitors |
| Apixaban | 10 mg twice daily for 7 days, followed by 5 mg twice daily |
| Edoxaban | After at least 5 days of initial therapy with a parenteral anticoagulant,
transition to once-daily oral 60 mg for patients >60 kg or 30 mg for patients
≤60 kg. |
| Rivaroxaban | 15 mg twice daily with food for 21 days, followed by 20 mg once daily with
food |
| aFor patients who are
expected to be more sensitive to warfarin, a starting dose of 2.5 mg daily is
recommended. After three days of treatment, dosage should be adjusted based on INR
values. |
9 . Patients who have chronic provoked factors for PE, such as active cancer, a hypercoagulable state, or chronic immobility, should continue anticoagulation therapy
| A) | | for three months. |
| B) | | for six months. |
| C) | | for one year. |
| D) | | indefinitely. |
As noted, the duration of anticoagulation therapy for secondary prevention is dependent on a variety of factors, such as bleeding risk and risk factors for PE, and can range from three months to lifelong therapy [3,28,32]. If the patient experienced PE following a transient risk factor (i.e., a provoked event), such as immobilization or recent surgery or trauma, at least three months of treatment is warranted, after which therapy should be reassessed. However, those who have chronic provoked factors for PE, such as active cancer, a hypercoagulable state, or chronic immobility, may benefit from long-term (indefinite) anticoagulation therapy. When creating the treatment plan, the goal is to weigh the benefits of PE and deep vein thrombosis prevention with the risk of anticoagulation events (e.g., bleeding). Risk factors for bleeding include age 65 years or older, frequent falls, alcohol abuse, renal failure, previous stroke, diabetes, and anemia.
10 . According to the HESTIA exclusion criteria, a patient with which of the following would be ineligible for outpatient PE treatment?
| A) | | Pregnancy |
| B) | | PE diagnosed during anticoagulant treatment |
| C) | | Severe pain requiring IV pain medication for more than 24 hours |
| D) | | Any of the above |
PE IN THE OUTPATIENT SETTING
HESTIA EXCLUSION CRITERIA FOR OUTPATIENT TREATMENT
| Criteria | Pointsa |
|---|
| Hemodynamically unstable | 1 |
| Thrombolysis or embolectomy needed | 1 |
| Active bleeding or high risk of bleeding | 1 |
| More than 24 hours on supplemental oxygen needed to maintain oxygen saturation
>90% | 1 |
| PE diagnosed during anticoagulant treatment | 1 |
| Severe pain requiring IV pain medication for more than 24 hours | 1 |
| Medical or social reason for hospital treatment for more than 24 hours (e.g.,
infection, malignancy, no support system) | 1 |
| Creatinine clearance of <30 mL/min | 1 |
| Severe liver impairment | 1 |
| Pregnancy | 1 |
| History of heparin-induced thrombocytopenia | 1 |
| aA score of 1 or more is
defined as high risk and rules out outpatient treatment. |
