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If acute PE is suspected, a careful assessment of the patient is necessary, including a history, a physical examination, a risk factor assessment, and laboratory/imaging studies (Table 38-4). Clinical features that may suggest DVT are leg pain, warmth, swelling, or redness.24 Clinical features suggestive of acute PE are acute onset of dyspnea, pleuritic chest pain, tachycardia, and hypoxemia. Massive acute PE should be considered if the patient has acute-onset hypotension, severe hypoxemia, or cardiac arrest. The presence of clinical features of both DVT and PE is highly suggestive of the diagnosis, but is not specific.24 Thus, further studies need to be done to make a final diagnosis.
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Additional studies should be considered whenever acute PE is suspected. Electrocardiography (ECG) may reveal unexplained tachycardia, which is common in PE, but is nonspecific. An S1Q3T3 pattern, right bundle branch block, or right-axis deviation on ECG might suggest massive PE, but these findings are nonspecific.25 Arterial blood-gas analysis might show hypoxemia and/or respiratory alkalosis, although arterial Po2 levels might be normal in patients with a PE.
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D-Dimer assay can also be helpful to diagnose venous thrombosis and PE, but it is nonspecific. It can also be positive in cancer, trauma, infection, or other inflammatory states.26 It is used mainly in the emergency department to rule out PE in low-risk patients.26 The diagnostic value of the d-dimer assay in neurocritical care is not well established.
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Other biomarkers may also provide valuable information in terms of severity of PE. Levels of cardiac troponins are often increased in massive PE and can be used for risk stratification, but they are not sensitive or specific and should not be used as the sole diagnostic tool.27 Elevated levels of B-natriuretic peptide (BNP) may be seen in massive PE in response to ventricular stretching,28 but these, too, are not sensitive or specific enough to be used as a diagnostic tool.
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Chest radiography is routinely obtained in patients with acute shortness of breath and is typically normal in patients with PE.
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Lately, multidetector CT angiography (MDCTA) of the chest has become the initial test of choice for diagnosis of acute PE (Figure 38-2). Sensitivity of helical CT angiography in the diagnosis of PE has been reported to be from 57% to 100%, and its specificity has been reported from 78% to 100%.29, 30 A recent study using MDCTA performed in outpatients with suspected PE has reported its sensitivity as 83% and specificity as 96%.31 Sensitivity and specificity of MDCTA also depend on pretest clinical probability and location of the embolus. Patients with a high clinical suspicion of PE and negative MDCTA will require further testing to rule out PE. Advantages of MDCTA over ventilation/perfusion V̇/Q̇ scanning or conventional angiography include ease of performance, speed, and characterization of the right ventricle and pulmonary parenchyma. Given its advantages and high sensitivity and specificity, MDCTA has become the gold standard to diagnose or rule out PE. MDCTA does require administration of intravenous contrast, which can lead to nephrotoxicity in patients with elevated creatinine and needs to be kept in mind. There are no randomized controlled trials conducted in specific neurologic conditions to evaluate the efficacy of MDCTA in the diagnosis of PE. But we do believe that findings from studies done in other patient populations can be extrapolated to neurologic patients.
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Ventilation/perfusion scanning (V̇/Q̇ scan) had a major role in the diagnosis of PE a few years ago, but it has been largely replaced by MDCTA in recent years. It has good sensitivity and specificity. A normal V̇/Q̇ scan essentially rules out PE.32 But there are some logistical issues with V̇/Q̇ scanning: patients are required to have a normal chest radiograph, and most of the patients in the ICU have an abnormal chest radiograph, thus limiting the value of the V̇/Q̇ scan as a diagnostic tool for PE in critical care setting.
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Duplex ultrasonography of the lower extremity is often done, as most of the pulmonary emboli originate from lower extremities. It is positive in 10% to 20% of patients without any clinical features of DVT, and in 50% of patients with clinical features of DVT.33 Thus, a negative duplex ultrasonography of lower extremities with high clinical suspicion does not rule out PE.33
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Pulmonary angiography is the gold standard for diagnosis of PE, but it is an invasive procedure. Because the sensitivity and specificity of MDCTA have been similar to those of pulmonary angiography, MDCTA has largely replaced pulmonary angiography as a diagnostic tool for PE.
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Echocardiography is a useful tool for risk stratification of massive and submassive PE. Some recent studies have suggested that right ventricular strain on echocardiography in normotensive patients puts these patients at higher risk of death. Signs of right ventricular strain on echocardiography include right ventricle dilation and right ventricle hypokinesis (Figure 38-3). Administration of thrombolytics has been suggested in this subgroup of patients but is debatable.34, 35 Echocardiography requires some training and can be done by intensivists.
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Figure 38-4 shows general approach to a patient with suspected PE with CT angiography as the initial test.
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