The clinical setting, including risk factors such as family history or personal prior history of venous thromboembolism, can help suggest the diagnosis of PE. Semi-quantitative clinical scoring systems such as the Wells Diagnostic Scoring System are beginning to replace "gestalt" estimates of clinical likelihood (Table 244-1). Clinical Syndromes Patients with massive PE present with systemic arterial hypotension and usually have anatomically widespread thromboembolism. Primary therapy with thrombolysis or embolectomy offers the greatest chance of survival. Those with moderate to large PE have right ventricular hypokinesis on echocardiography but normal systemic arterial pressure. Optimal management is controversial; such patients may benefit from thrombolysis or embolectomy rather than anticoagulation alone. Patients with small to moderate PE have both normal right heart function and normal systemic arterial pressure. They have a good prognosis with either adequate anticoagulation. The presence of pulmonary infarction usually indicates a small PE, but one that is exquisitely painful, because it lodges peripherally, near the innervation of pleural nerves. However, larger, more central PEs can occur concomitantly with peripheral pulmonary infarction. Nonthrombotic pulmonary embolism may be easily overlooked. Possible etiologies include fat embolism after blunt trauma and long bone fractures, tumor embolism, or air embolism. Intravenous drug users may inject themselves with a wide array of substances, such as hair, talc, or cotton. Amniotic fluid embolism occurs when fetal membranes leak or tear at the placental margin. The pulmonary edema seen in this syndrome is probably due primarily to alveolar capillary leakage. Symptoms and Signs Dyspnea is the most frequent symptom of PE, and tachypnea is its most frequent sign. Whereas dyspnea, syncope, hypotension, or cyanosis indicates a massive PE, pleuritic pain, cough, or hemoptysis often suggests a small embolism located distally near the pleura. On physical examination, young and previously healthy individuals may simply appear anxious but otherwise seem deceptively well, even with an anatomically large PE. They may only have dyspnea with moderate exertion. They often lack "classic" signs such as tachycardia, low-grade fever, neck vein distention, or an accentuated pulmonic component of the second heart sound. Sometimes, a paradoxical bradycardia occurs. In older patients who complain of vague chest discomfort, the diagnosis of PE may not be apparent unless signs of right heart failure are present. Unfortunately, because acute coronary ischemic syndromes are so common, one may overlook the possibility of life-threatening PE and may inadvertently discharge these patients from the hospital after the exclusion of myocardial infarction with serial blood tests to detect cardiac injury and serial electrocardiograms. Differential Diagnosis The differential diagnosis of PE is broad (Table 244-2). Although PE is known as "the great masquerader," quite often other illnesses simulate PE. For example, when the proposed diagnosis of PE is supposedly confirmed with a combination of dyspnea, chest pain, and an abnormal lung scan, the correct diagnosis of pneumonia might become apparent 12 h later when an infiltrate blossoms on chest x-ray, purulent sputum is first produced, and high fever and shaking chills develop. Some patients have PE and a coexisting illness such as pneumonia or heart failure. In such circumstances, clinical improvement will often fail to occur despite standard medical treatment of the concomitant illness. This situation can serve as a clinical clue to the possible coexistence of PE. Nonimaging Diagnostic Modalities These are generally less expensive but also less specific than diagnostic modalities that employ imaging. Blood Tests The quantitative plasma D-dimerenzyme-linked immunosorbent assay (ELISA) level is elevated (>500 ng/mL) in more than 90% of patients with PE, reflecting plasmin's breakdown of fibrin and indicating endogenous (though clinically ineffective) thrombolysis. However, the D-dimer assay is not specific and therefore has no useful role among patients who are already hospitalized. Levels increase in patients with myocardial infarction, sepsis, or almost any systemic illness. The plasma D-dimer ELISA has a high negative predictive value and can be used to help exclude PE. In a prospective 1-year evaluation, the Emergency Department at Brigham and Women's Hospital mandated obtaining a D-dimer ELISA in all 1106 patients suspected of PE. It served as an excellent screening test, with a sensitivity of 96.4% and negative predictive value of 99.6%. Data from the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) indicate that, contrary to classic teaching, arterial blood gases lack diagnostic utility for PE, even though the PO2 and PCO2 will often both decrease. Among patients suspected of PE, neither the room air arterial PO2 nor calculation of the alveolar-arterial oxygen gradient can reliably differentiate or triage patients who actually have PE at angiography. Electrocardiogram Classic abnormalities include sinus tachycardia; new-onset atrial fibrillation or flutter; and an S wave in lead I, a Q wave in lead III, and an inverted T wave in lead III (Chap. 210). Often, the QRS axis is greater than 90°. T-wave inversion in leads V1 to V4, perhaps the most frequent but least publicized change, reflects right ventricular strain. Noninvasive Imaging Modalities Chest Roentgenography A normal or near-normal chest x-ray in a dyspneic patient suggests PE. Well-established abnormalities include focal oligemia (Westermark's sign), a peripheral wedged-shaped density above the diaphragm (Hampton's hump), or an enlarged right descending pulmonary artery (Palla's sign). Venous Ultrasonography Confirmed DVT is usually an adequate surrogate for PE. Ultrasonography of the deep venous system relies upon loss of vein compressibility as the primary criterion for DVT. About one-half of patients with PE have no imaging evidence of DVT, probably because the clot has already embolized to the lung or is in the pelvic veins, where ultrasonography is usually inadequate. Therefore, the workup for PE should continue if there is high clinical suspicion, despite a normal ultrasound examination. Chest CT Computed tomography (CT) of the chest with intravenous contrast (ordinarily, 100 mL administered at 3 to 4 mL/s via an antecubital vein) is superseding lung scanning (see below) as the principal imaging test for the diagnosis of PE. Chest CT effectively diagnoses large, central PE (Fig. 244-1). New generation multislice scanners image the entire thorax with 1-mm thin sections during a single 12- to 15-s breath-hold and can detect peripherally located thrombi in fifth order branches. In patients without PE, the lung parenchymal images may establish alternative diagnoses not apparent on chest x-ray that explain the presenting symptoms and signs, such as pneumonia, emphysema, pulmonary fibrosis, pulmonary mass, or aortic pathology. | | Figure 244-1 Bilateral "saddle" pulmonary thromboembolism computed tomography scan of the chest. The arrows outline the "saddle" (Courtesy of Philip Costello, MD.) |
Lung Scanning See also Chap. 235. Small particulate aggregates of albumin labeled with a gamma-emitting radionuclide are injected intravenously and are trapped in the pulmonary capillary bed. The perfusion scan defect indicates absent or decreased blood flow, possibly due to PE. Ventilation scans, obtained with radiolabeled inhaled gases such as xenon or krypton, improve the specificity of the perfusion scan. Abnormal ventilation scans indicate abnormal nonventilated lung, thereby providing possible explanations for perfusion defects other than acute PE. A high probability scan for PE is defined as having two or more segmental perfusion defects in the presence of normal ventilation (Fig. 244-2). | | Figure 244-2 Three views of the pulmonary perfusion scan illustrating multiple segmental perfusion defects in both lung fields. The ventilation scan, which is normal, is not shown. The marked mismatch between normal ventilation and abnormal perfusion makes this lung scan high probability for pulmonary thromboembolism. LPO, left posterior oblique; POST, posterior; RPO, right posterior oblique. |
The diagnosis of PE is very unlikely in patients with normal and near-normal scans but is about 90% certain in patients with high-probability scans. Unfortunately, most patients have nondiagnostic scans, and fewer than half of patients with angiographically confirmed PE have a high-probability scan. Importantly, as many as 40% of patients with high clinical suspicion for PE and "low-probability" scans do, in fact, have PE at angiography. Magnetic Resonance (MR) (Contrast-Enhanced) MR pulmonary angiography utilizes gadolinium contrast agent, which unlike iodinated contrast agents used in CT angiography, is not nephrotoxic. The risk of a contrast reaction with gadolinium is very low, and no ionizing radiation is used. When compared with first-generation chest CT scanning, results are similar. MR also assesses right ventricular function, thus making it a promising single test for both diagnosis of PE and assessment of hemodynamic effect. Echocardiography More than half of patients with PE will have normal echocardiograms. Nevertheless, this imaging test helps with the rapid triage of extremely ill patients who may have PE. Bedside echocardiography can usually reliably differentiate among illnesses that have radically different treatment, including acute myocardial infarction, pericardial tamponade, dissection of the aorta, and PE complicated by right heart failure. McConnell's sign, i.e., right ventricular free wall hypokinesis with normal right ventricular apical motion, appears to be specific for PE. Detection of right ventricular dysfunction due to PE helps to stratify the risk, delineate the prognosis, and plan optimal management. Invasive Diagnostic Modalities Pulmonary Angiography Selective pulmonary angiography is the most specific examination available for establishing the definitive diagnosis of PE and can detect emboli as small as 1 to 2 mm. A definitive diagnosis of PE depends upon visualization of an intraluminal filling defect in more than one projection. Secondary signs of PE include abrupt occlusion ("cut-off") of vessels; segmental oligemia or avascularity; a prolonged arterial phase with slow filling; or tortuous, tapering peripheral vessels. Chest CT scanning is replacing diagnostic pulmonary angiography, because it is less invasive. In the current era of chest CT with contrast, pulmonary angiography is reserved for (1) patients with technically inadequate CT scans, (2) scans performed on older machines that cannot image fourth- and fifth-order pulmonary arteries, and (3) patients who will undergo interventions such as catheter embolectomy or catheter-directed thrombolysis. Contrast Phlebography Venous ultrasonography has virtually replaced contrast phlebography, which is costly, uncomfortable, and occasionally results in contrast allergy or contrast-induced phlebitis. Integrated Diagnostic Approach We advocate an integrated diagnostic approach to streamline the workup of PE (Fig. 244-3). This strategy combines the clinical likelihood of PE with the results of noninvasive testing, especially D-dimer ELISA, venous ultrasonography, and chest CT or lung scanning to determine whether pulmonary angiography is warranted. | | Figure 244-3 Diagnosis strategy for pulmonary thromboembolism: An integrated diagnostic approach. ED, emergency department; ELISA, enzyme-linked immunosorbent assay; CT, computed tomography; U/S, ultrasound; DVT, deep vein thrombosis; PA gram, pulmonary arteriogram. |
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