Clinical features
Most frequently, pulmonary embolism develops in the setting of one of the risk factors mentioned earlier. Commonly, the embolus produces no significant symptoms, and the entire episode may go unnoticed by the patient and physician. When the patient does have symptoms, acute onset of dyspnea is the most frequent complaint. Less common is pleuritic chest pain or hemoptysis. Syncope is an occasional presentation, particularly in the setting of a massive pulmonary embolism, defined as acute pulmonary embolism causing hemodynamic instability and sustained hypotension (systolic blood pressure <90 mm Hg for at least 15 minutes or requiring inotropic support).
On physical examination, the most common findings are tachycardia and tachypnea. The chest examination may be entirely normal or may reveal a variety of nonspecific findings such as decreased air entry, localized crackles, or wheezing. With pulmonary infarction extending to the pleura, a pleural friction rub may be detected, and evidence of a pleural effusion may be found. Cardiac examination may reveal acute right ventricular overload (i.e., acute cor pulmonale), in which case the pulmonic component of the second heart sound (P2) is increased, a right-sided S4 is heard, and a right ventricular heave may be present. If the right ventricle fails, a right-sided S3 may be heard and jugular veins may be distended. Examination of the lower extremities may reveal changes suggesting a thrombus, including tenderness, swelling, or a cord (palpable clot within a vessel). However, only a minority of patients (approximately 10%) with emboli arising from leg veins have clinical evidence of deep venous thrombosis, so the absence of these findings should not be surprising or overly reassuring.
Common symptoms of pulmonary embolism:
1.Dyspnea
2.Pleuritic chest pain
3.Hemoptysis
4.Syncope
Diagnostic evaluation
Diagnosis of acute pulmonary embolism can be challenging, and the approach depends on the clinician’s level of suspicion, or pretest probability, of pulmonary embolism. As an example, for patients in whom the diagnosis is considered less likely, the clinician may start with a D-dimer assay (discussed later).
Most patients who present with acute dyspnea or chest pain will have a chest radiograph and oxygen saturation checked by pulse oximetry. The radiographic findings in an acute pulmonary embolism are quite variable. Usually, the chest radiograph is normal. When it is not, the abnormalities often are nonspecific, including areas of atelectasis or elevation of a hemidiaphragm, indicating volume loss. Volume loss may be related to decreased ventilation to the involved area due to small airways constriction and possibly loss of surfactant. If pleuritic chest pain is present, the patient may try to reduce pain by breathing more shallowly, which contributes to atelectasis.
Occasionally, the chest radiograph reveals a localized area of decreased lung vascular markings corresponding to the region where the vessel has been occluded. This finding is called the Westermark sign, but it is often difficult to read unless prior radiographs are available for comparison. With a large proximal embolus, enlargement of a pulmonary artery near the hilum occasionally occurs secondary to distention of the vessel by the clot itself. An apparent abrupt termination of the vessel may occur, although
this is usually difficult to see on a plain chest radiograph.
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Both infarction and pulmonary hemorrhage may appear as an opacified region on the radiograph. Classically, the density is shaped like a truncated cone, fanning out toward and reaching the pleural surface. This finding, called a Hampton hump, is relatively infrequent. Pleural effusions may be seen as an accompaniment of pulmonary embolic disease. Pleural effusions associated with pulmonary embolism may be either exudative or transudative and contain a variable number of red blood cells.
Arterial blood gas values typically show a widened alveolar-arterial difference in partial pressure of oxygen (PAO2−PaO2 [AaDO2]), a low PaO2, and respiratory alkalosis, with hypocapnia occurring in more than 80% of cases. As PCO2 is decreased, arterial PO2 is higher than it would be if hyperventilation was not present. Occasionally, PO2 is normal, so the presence of a normal PO2 does not exclude the diagnosis of pulmonary embolism. Unfortunately, because of the variability in values, arterial blood gases are not very useful in determining the likelihood of pulmonary embolism.
Characteristic arterial blood gas values in pulmonary embolic disease:
1.Decreased PO2 and widened AaDO2
2.Decreased PCO2
3.Increased pH
The measurement of plasma D-dimer levels is commonly used as part of the diagnostic strategy for venous thromboembolic disease, especially in patients who are less likely to have a pulmonary embolism. D-dimer is a degradation product of cross-linked fibrin; therefore, levels are increased in the setting of thrombosis of any type. Plasma levels of D-dimer typically are increased in the setting of venous thrombosis but also are increased in many other conditions including trauma, surgery, pregnancy, cancer, and inflammation. Thus, D-dimer testing for venous thrombosis or pulmonary embolism is very sensitive, but the test is quite nonspecific. Previously, the interpretation of D-dimer testing was complicated by the use of different assays with varying sensitivity and specificity. However, the superior sensitivity and high negative predictive value of the quantitative enzyme-linked immunosorbent assay (ELISA) have established it as the standard D-dimer test. When the D-dimer measurement is used in clinical practice, normal levels are considered as strong evidence against thromboembolic disease. Thus, a normal D-dimer level is helpful in excluding the diagnosis, especially in the patient with a low pretest probability of having a pulmonary embolus, but an elevated level is considered nonspecific and therefore does not establish the diagnosis definitively.
Recommendations for the best radiologic test to diagnose pulmonary embolism have shifted in the last three decades. Traditionally, the major screening test for pulmonary embolism had been the perfusion lung scan (described in Chapter 3), but contrast computed tomographic angiography (CTA) is now used either instead of, or in addition to, perfusion lung scanning. Evaluation of the large veins in the lower extremities, typically using ultrasound techniques, is another commonly used diagnostic strategy. Identification of a clot in a vein above the popliteal fossa warrants the same treatment acutely as a documented pulmonary embolus and often obviates the need for further evaluation.
The technique of CTA (discussed in Chapter 3) is the most commonly used modality in the diagnosis of pulmonary embolism (Fig. 13.1). CTA offers the significant advantage of high-quality visualization of the lung parenchyma, which is helpful in considering the likelihood of competing diagnoses, such as pneumonia. In addition, in many centers, CTA can be performed more quickly and is more readily available than ventilation-perfusion scanning. However, the radiation dose associated with CTA, especially to the breast and chest, is significantly higher than with ventilation-perfusion scanning, so
despite its advantages CTA has not completely replaced perfusion scanning as a diagnostic modality. The clinician must weigh the risks and benefits, as well as the practical issues of test availability and interpretation, for each patient in whom the diagnosis of pulmonary embolism is being considered.
FIGURE 13.1 Chest computed tomographic angiography shows pulmonary
embolus in the midsized vessel in the left lung. A, Standard cross-sectional view
shows a blood vessel (seen on end) filled by a clot rather than radiopaque contrast
dye (arrow). B, Image displayed in a reformatted oblique view shows the same
vessel in its longitudinal course. The arrow marks the absence of radiopaque dye in
the vessel at the edge of the clot. Source: (Courtesy Dr. Phillip Boiselle.)
A perfusion lung scan is performed by injecting radiolabeled macroaggregated albumin particles into a peripheral vein. In areas of normal blood flow in the lungs, the albumin particles lodge in a fraction of the small vessels that have been perfused. When blood flow is obstructed by a clot within the pulmonary arterial system, perfusion lung scanning demonstrates no labeled albumin and, therefore, an absence of perfusion to the region of lung supplied by the occluded vessel (Fig. 13.2). If the results of the scan are normal, pulmonary embolism can be excluded. However, perfusion abnormalities do not automatically indicate the presence of embolic disease. False-positive lung scans are common because local decreases in blood flow may result from primary disease of the lung parenchyma or the airways. A ventilation scan, which involves inhalation of a xenon radioisotope, is often added because if regions of decreased blood flow are secondary to airway disease, corresponding abnormalities should be seen on the ventilation scan. If a defect in perfusion is due to a pulmonary embolism, ventilation still will be present in the area, and the perfusion defect will be mismatched (i.e., will not have a corresponding ventilation defect). If parenchymal disease (e.g., pneumonia) is the cause of a perfusion defect, the corresponding abnormality should be seen on the chest radiograph.
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FIGURE 13.2 Positive perfusion scan shows multiple perfusion defects in a patient
with pulmonary emboli. Six views of complete scan are shown: right lateral (R
LAT), anterior (ANT), left lateral (L LAT), right posterior oblique (RPO), posterior
(POST), and left posterior oblique (LPO). Compare with normal scan results in Fig.
3.12. a, anterior; l, left; p, posterior; r, right. Source: (Courtesy Dr. Henry Royal.)
Interpretation of the perfusion lung scan is a complicated process that depends on the clinical setting, results of the chest radiograph, and frequently the findings on a ventilation lung scan. As the perfusion scan often is not definitive, a probability is placed on the likelihood of pulmonary embolism, taking into account the size and number of defects and the presence or absence of corresponding abnormalities on the radiograph and ventilation lung scan. The scan results are analyzed in conjunction with the pretest probability of pulmonary embolism, the term used to represent the clinician’s assessment of the likelihood of pulmonary embolism based on the patient’s clinical presentation.
When the lung scan is inconclusive, it is critical that additional diagnostic evaluation be performed. Different options for further investigation are available, focusing either on the veins of the lower extremities or on the pulmonary vasculature itself. However, because lower extremity studies are often negative even in the presence of documented pulmonary embolism, a negative lower extremity study does not preclude the need for further evaluation of the pulmonary arteries if there is a reasonably high suspicion of pulmonary thromboembolism.
Major techniques for the diagnosis of pulmonary emboli include chest computed tomographic angiography (CTA), ventilation–perfusion lung scanning, and conventional pulmonary angiography.
Long considered the gold standard for confirmation of pulmonary embolism, conventional pulmonary