Imaging of Pulmonary Embolism and Nontraumatic Aortic Pathology

In the two preceding chapters we discussed chest imaging in patients without a history of injury and in the setting of trauma. In this chapter, we focus on imaging of three particularly life-threatening conditions: pulmonary embolism (PE), spontaneous aortic dissection, and spontaneous thoracic aortic aneurysm rupture. These conditions share computed tomography (CT) as their primary diagnostic modality today. For each of these, we briefly review pathophysiology, pretest probability assessment, and the limited role of chest x-ray in diagnosis. We discuss the role of CT in detail, comparing CT to other imaging modalities, including the historical criterion standards, pulmonary angiography and aortography, which are more rarely performed today. We consider the role and diagnostic accuracy of alternative imaging modalities, including ventilation–perfusion (VQ) scan, magnetic resonance imaging (MRI), and echocardiography. We consider challenging clinical scenarios, such as the patient with contraindications to intravenous (IV) contrast, the unstable patient who may be at risk during imaging tests outside of the emergency department, the patient requiring exclusion of both PE and aortic pathology, and the pregnant patient with suspected PE. Along the way, we review critical imaging findings that may allow you to diagnose these important conditions before radiologist interpretation, allowing earlier initiation of therapy. In the chapter on interventional radiology ( Chapter 16 ), interventions for PE and aortic disease are described, with a critical review of the evidence for these treatments.

Brief Guide to Figures in This Chapter

Figures in this chapter are grouped according to clinical case so that x-rays, CT scans, and other imaging studies from a single patient are clustered together for teaching purposes. This means that sometimes you are directed to a figure later in the chapter, illustrating a related imaging finding in a different patient. These cross-references to later figures are marked by the words see also. In addition, a summary of the figure content is listed in Table 7-1 for quick reference. We highly recommend looking at all figures corresponding to a given patient case. They are arranged to illustrate pearls and pitfalls of imaging.


Guide to Figures in This Chapter

Content Figure Numbers
Pulmonary embolism figures 7-1 to 7-59

  • Chest x-ray findings of pulmonary embolism

7-2, 7-3, 7-34, 7-38, 7-41, 7-51, 7-52

    • Westermark sign


    • Hampton’s hump (visible pulmonary infarct)

7-3, 7-34, 7-38, 7-41, 7-51, 7-52

  • CT findings of pulmonary embolism

7-8 to 7-33, 7-35 to 7-37, 7-39, 7-40, 7-42, 7-47, 7-55

    • Contrast timing for CT pulmonary angiography

7-11, 7-12

    • Saddle or central pulmonary emboli

7-13 to 7-27, 7-33, 7-39

    • Cardiac thrombus and dilatation secondary to pulmonary emboli

7-16, 7-17

    • Segmental and peripheral pulmonary emboli

7-28, 7-29, 7-36, 7-42

    • Lung window findings of pulmonary infarction

7-30 to 7-32, 7-35, 7-37, 7-42

    • Distinguishing pulmonary embolism from artifacts and adenopathy

7-39, 7-40, 7-47

  • VQ findings of pulmonary embolism

7-43 to 7-46, 7-48 to 7-50, 7-53, 7-54

  • Angiographic findings of pulmonary embolism

7-4, 7-5

  • Tumor emboli

7-56 to 7-59
Aortic disease figures 7-60 to 7-102

  • Chest x-ray findings of aortic disease

7-60, 7-65, 7-67, 7-69, 7-70, 7-73, 7-75, 7-78, 7-85, 7-88, 7-92, 7-95, 7-98, 7-99

    • Classic chest x-rays of aortic aneurysm or dissection

7-60, 7-65, 7-67, 7-69, 7-70, 7-73, 7-75, 7-92, 7-95

    • Normal x-ray despite aortic dissection

7-67, 7-78, 7-85, 7-88, 7-92

    • Mediastinal abnormalities on chest x-ray unrelated to aortic dissection or aneurysm

7-98, 7-99

  • CT scan findings of aortic disease

7-61 to 7-64, 7-66, 7-68, 7-69, 7-71, 7-74, 7-76, 7-77, 7-79 to 7-84, 7-86, 7-87, 7-89 to 7-91, 7-93, 7-94, 7-96 to 7-98, 7-100

    • Contrast timing for CT aortography

7-80, 7-81

    • Aortic branch vessel involvement

7-80, 7-82, 7-83 (brachiocephalic)

    • Iliac artery


    • Brachiocephalic artery

7-80, 7-82, 7-83

    • Renal artery

7-84, 7-91

    • Coronary artery


    • Mesenteric artery


    • Imaging for concurrent PE and aortic pathology


    • Aortic endovascular repair and endoleak

7-74, 7-93, 7-94

  • Angiographic findings of aortic disease


We begin our discussion with PE. This discussion sets the stage for our review of aortic imaging, which has many features similar to those of PE.

Pulmonary Embolism

PE occurs when thrombus, usually from lower extremity or pelvic veins, migrates to the pulmonary arteries, resulting in partial or complete obstruction of blood flow in the affected vessel. The lung segment supplied by this vessel may become infarcted, and atelectasis or pleural effusion may occur. Pulmonary embolism is a life-threatening condition, although the range of reported mortality is very wide. In a large US emergency department sample of patients diagnosed with acute PE, 30-day mortality attributed to acute PE was only 1.1%, but all-cause mortality was 5.4%. Other studies suggest 30-day death rates of 15% in initially hemodynamically stable patients and almost 60% in patients presenting with hemodynamic instability, demonstrating the wide range of clinical severity.

Which Patients Require Imaging for Pulmonary Embolism? How Does Pretest Probability Influence Imaging Decisions?

Pretest probability assessment is a key part of planning for diagnostic imaging in emergency department patients with suspected PE. Pretest probability assessment first determines whether a patient requires imaging of any kind to assess for PE. Next, pretest probability strongly determines the reliability of the available diagnostic imaging modalities, influencing both the choice of modality and the clinical application of a negative or positive imaging test. As we discuss in detail later in the sections on VQ scan and CT, when imaging test results are at odds with clinical pretest probability, additional testing is warranted because of the possibility of false-positive and false-negative imaging results.

PE can be challenging to diagnosis clinically, as it can present with a variety of symptoms, including chest pain, dyspnea, and syncope. Let’s consider how clinical risk assessment tools should be applied to patients with suspected PE. First, ask the binary question: Is PE a possible cause of the patient’s presentation? If the answer is unequivocally “no,” (for example, in a patient with pleuritic chest pain immediately after blunt chest trauma), further risk assessment is not needed and may trigger unnecessary testing. If the answer is “yes” (including “likely not,” “possibly so,” or “likely yes”), “ further clinical risk stratification is needed. Several clinical assessment schemes exist, but they share the ability to sort patients into low-risk categories (not requiring imaging) and higher-risk categories (requiring imaging). Some risk stratification schemes incorporate lab testing (D-dimer

D-dimer is a fibrin degradation product present in blood after a clot is degraded by fibrinolysis. Its presence or absence can be used as a screening tool for the presence of clot.

), whereas others rely solely on clinical history and physical exam. We consider two risk stratification tools or clinical decision rules: Wells score and pulmonary embolism rule-out criteria (PERC).

Clinical decision rules are important guides to imaging decisions once the diagnosis of PE has been considered based on clinical gestalt. This last statement is important, because the two clinical rules we discuss here could lead to unnecessary imaging if applied indiscriminately to patients with clinical presentations not suggestive of PE. For example, a 60-year-old patient presenting with fever, abdominal pain, heart rate of 120 beats per minute, and history of appendectomy 10 days prior may be an obvious clinical case of postoperative abscess but scores 3 points by Wells criteria (discussed later), falling into a moderate risk group for PE. Clearly, the patient should not be evaluated for PE solely based on these criteria, unless clinical signs and symptoms suggest PE. By the same concept, the patient would fail several of the PERC, but these should not be applied if the clinician does not suspect PE. Figure 7-1 demonstrates appropriate use of risk-stratification for PE, and also shows how inappropriate use of risk-stratification rules could lead to unnecessary imaging.

Figure 7-1

Two strategies for application of clinical risk stratification for pulmonary embolism (PE). Strategy A first asks the binary question: Could PE be the cause of the patient’s presentation? Then it applies specific clinical risk scores. This avoids unnecessary testing of patients with presentations not compatible with PE. Strategy B applies a clinical scoring system first and may lead to inappropriate testing of patients who have no clinical signs or symptoms of PE but have risk factors. Indiscriminate use of D-dimer testing without clinical risk stratification leads to the same type of error.

Wells criteria ( Table 7-2 ) are validated criteria to identify patients with a low clinical risk for PE. Wells and colleagues have investigated multiple cutoffs, including a low–moderate–high categorization, and a PE unlikely–likely categorization (see Table 7-2 ). In Wells’ validation set, patients with a score less than 2 (low risk) had an overall PE rate of only 2.0%, regardless of D-dimer result. However, the confidence intervals were broad, with an upper limit of 7.1%, which would be unacceptably high for most clinicians. Ironically, low-risk patients with a negative D-dimer had a higher rate of PE (2.7%) than those with positive D-dimer testing (0%) in Wells’ study, though no statistical difference between the groups existed. When the Wells Criteria are dichotomized into PE “unlikely” (score ≤ 4) and “likely” (score > 4) categories, an unlikely score plus a negative SimpliRed D-dimer predicts a PE risk for around 2% with an upper 95% CI of 6%. Other studies suggest that the SimpliRed D-Dimer is not sufficiently sensitive and that ELISA D-dimer assays are superior. More recently, a simplified dichotomized Wells Criteria has been described, although this rule requires additional prospective validation. Under this paradigm, each criterion is assigned only 1 point, and a score of no more than 1 combined with a normal D-dimer predicts a 3-month incidence of venous thromboembolism (VTE) of 0%, with a 95% confidence interval (CI) of 0% to 1.6%. Using this strategy, 26% of patients could avoid diagnostic imaging for PE. The use of Wells criteria, in conjunction with D-dimer testing, to screen patients for possible PE is widely accepted and was endorsed by the American College of Emergency Physicians (ACEP) in its 2003 clinical policy on evaluation of adult patients with suspected PE, now retired.


Wells Criteria for Pulmonary Embolism

Criterion Score
Clinical signs and symptoms of DVT 3.0
PE is No. 1 diagnosis or equally likely 3.0
Heart rate > 100 bpm 1.5
Immobilization at least 3 days or surgery in past 4 weeks 1.5
Previous objectively diagnosed PE or DVT 1.5
Hemoptysis 1.0
Malignancy with treatment within 6 months, or palliative 1.0

Total score: <2 gives low (1.3%) risk of PE, 2-6 gives moderate (16.2%) risk, >6 gives high (37.5%) risk. Score ≤ 4 plus negative D-dimer predicts a 2% risk for venous thromboembolic disease. When each criterion is assigned only 1 point, a score ≤ 1 plus a normal D-dimer gives a 0% rate of VTE at 3 months.

Data from Douma RA, Gibson NS, Gerdes VE, et al. Validity and clinical utility of the simplified Wells rule for assessing clinical probability for the exclusion of pulmonary embolism. Thromb Haemost 101:197-200, 2009; Wells PS, Anderson DR, Rodger M, et al. Derivation of a simple clinical model to categorize patients’ probability of pulmonary embolism: Increasing the models utility with the SimpliRED D-dimer. Thromb Haemost 83:416-420, 2000.

The PERC are a prospectively derived and validated system to exclude PE without D-dimer testing. The advantage of such a system is the avoidance of unnecessary imaging prompted by false-positive D-dimer results, a problem often encountered with highly sensitive D-dimer tests. The criteria ( Box 7-1 ) are meant to be applied only to patients judged to be at low risk for PE based on physician gestalt. Imaging decisions in patients not judged by gestalt to be at low risk of PE should not be based on PERC. In a prospective study of more than 8100 patients, the rate of 45-day VTE or death was less than 2% in PERC-negative patients. The rule can eliminate the need for diagnostic imaging in about 20% of patients with a low pretest probability (defined as <15%) based on physician gestalt. Multiple other clinical probability scores exist including the Charlotte Rule and Geneva Rule, with similar overall accuracy. These and experienced clinician gestalt can be used to determine pretest probability.

Formulating a pretest probability assessment of PE should be routine practice before the decision to perform a diagnostic imaging test for PE. In patients whose pretest probability assessment suggest a need for imaging to evaluate for PE, multiple imaging tests are available, but the usual first imaging step is chest x-ray.

How Is Chest X-ray Useful in the Evaluation of Pulmonary Embolism? What Is the Importance of Classic Abnormalities Such as Hampton’s Hump and the Westermark Sign? Do Any Chest X-ray Findings Confirm or Exclude Pulmonary Embolism?

Chest x-ray plays a limited role in the diagnosis of PE, as an embolism is not directly visible on plain x-ray. The greatest importance of chest x-ray in assessment for PE is in evaluation of the differential diagnosis, which can include pneumonia, pneumothorax, malignancy, pleural effusion, pericardial disorders, and aortic or other mediastinal abnormalities. Chest x-ray is inexpensive, rapid to obtain, and exposes the patient to minimal radiation in comparison with CT and VQ scan. Consequently, it is an appropriate initial imaging test in virtually every patient with suspected PE, as it explores the differential diagnosis of complaints such as chest pain, dyspnea,

Box 7-1

  • Age <50 years

  • Pulse <100 beats per minute

  • Sa o 2 >94%

  • No unilateral leg swelling

  • No hemoptysis

  • No recent trauma or surgery (with general anesthesia) in past 4 weeks

  • No prior PE or DVT

  • No hormone use

In a patient classified as “low risk” by clinician gestalt, PE is unlikely if all of the preceding criteria are fulfilled. Sensitivity is 97.4% (95% CI = 95.8%-98.5%), and specificity is 21.9% (95% CI = 21.0%-22.9%); likelihood ratio negative is 0.12 (95% CI = 0.07-0.19). The score is meant to be used without D-dimer testing.

Pulmonary Embolism Rule-Out Criteria

From Kline JA, Courtney DM, Kabrhel C, et al. Prospective multicenter evaluation of the pulmonary embolism rule-out criteria. J Thromb Haemost 6:772-780, 2008; Kline JA, Mitchell AM, Kabrhel C, et al. Clinical criteria to prevent unnecessary diagnostic testing in emergency department patients with suspected pulmonary embolism. J Thromb Haemost 2:1247-1255, 2004.
and syncope. Chest x-ray also provides information that can predict the diagnostic utility of VQ scan or in some cases can even substitute for the ventilation portion of the VQ scan, reducing cost and radiation exposure. Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) I, a multicenter trial from 1983 to 1989 that provided methodologically rigorous evaluation of diagnostic tests for PE, provides a rich source of information on the diagnostic value of chest x-rays in patients with and without PE. Normal chest x-rays occurred in only 12% of patients in this study published in 1990—although this was a high-risk patient population with a high incidence of PE. Normal chest x-rays may be more common in a lower-risk cohort, more typical of emergency department patients undergoing testing today. The most common chest x-ray findings in patients with PE were atelectasis, parenchymal areas of increased opacity, or both, but these findings occurred with similar frequency in patients without PE and therefore cannot be used to differentiate PE. Several classically described chest x-ray findings of PE were specifically investigated but found to have little diagnostic value (see Table 7-3 ). The Westermark sign (oligemia distal to a large vessel occluded by PE) ( Figure 7-2 ) was found to be relatively specific but highly insensitive, found in only 8% to 14% of patients with PE. “Classic” findings that proved nonspecific and insensitive included the Fleischner sign (a prominent central artery caused by distension of a vessel by a large clot or by pulmonary hypertension from distal embolization) and Hampton’s hump (a wedge-shaped pleural-based peripheral density with a convex medial border, representing parenchymal infarction) ( Figure 7-3 ; see also chest x-rays in Figures 7-34, 7-38, 7-41, 7-51, and 7-52 and CT findings in Figures 7-30, 7-31, 7-32, 7-35, 7-37, 7-42, and 7-55 ). Findings such as these should not be used to exclude or confirm PE, because they have excessively high false positive and false negative rates.


Chest X-ray Findings and Pulmonary Embolism Diagnosis

Chest X-ray Finding Sensitivity Specificity
Normal 12% 82%
Oligemia (Westermark sign) 8%-14% 92%-96%
Prominent central pulmonary artery (Fleischner sign) 20% 80%
Pleural-based area of increased opacity (Hampton’s hump) 22%-24% 82%
Vascular redistribution 9%-10% 85%-87%
Pleural effusion 35%-36% 70%
Elevated diaphragm 14%-20% 85%-90%

From Worsley DF, Alavi A, Aronchick JM, et al. Chest radiographic findings in patients with acute pulmonary embolism: Observations from the PIOPED Study. Radiology 189:133-136, 1993.

Figure 7-2

Pulmonary embolism (PE), chest x-ray with the Westermark sign.

This 57-year-old female with ovarian cancer presented with worsening dyspnea and leg pain. She underwent ventilation–perfusion scan that was high probability for PE.

Her chest x-ray shows an area in the right upper thorax with decreased pulmonary vascular markings compared with the left. This is consistent with the Westermark sign, an indication of a proximal PE blocking distal flow of blood to a lung segment. The Westermark sign is very insensitive but relatively specific, according to data from the Prospective Investigation of Pulmonary Embolism Diagnosis study. Occasionally, an abnormal region of lung parenchyma that is poorly ventilated because of bronchospasm or emphysema may have physiologic vasoconstriction, giving a similar appearance.

Figure 7-3

Pulmonary embolism (PE): Chest x-ray showing Hampton’s hump.

A, Posterior–anterior chest x-ray. B, Lateral chest x-ray. This 62-year-old female presented with sudden onset right pleuritic back pain awakening her at 2 am . Her initial vital signs were pulse oximetry 96% on room air, blood pressure 153/70, heart rate 69 bpm, and temperature 38.0°C (100.4°F). This is an example of PE resulting in a peripheral wedge-shaped pleural-based infarction—Hampton’s hump. Note how the density stops abruptly at the minor fissure (a pleural boundary) inferiorly. This was interpreted in the radiology report as “right axillary subsegment pneumonia, right upper lobe.” Pneumonia and pulmonary infarction can appear identical on chest x-ray. Although neither sensitive nor specific for PE, Hampton’s hump should be recognized as a possible finding of PE to avoid misdiagnosis of a patient with pneumonia. PE was strongly suspected in this patient because of sudden onset and recent hospitalization, and computed tomography confirmed the diagnosis (see Figure 7-32 ).

Several key points about chest x-ray bear emphasis:

  • Chest x-ray abnormalities including pleural effusion, atelectasis, lung mass, and parenchymal densities can coexist with or be a consequence of PE. Chest x-ray findings must be considered carefully in the context of the patient’s presentation and overall risk profile for PE. For example, a chest x-ray finding of parenchymal opacity can represent pneumonia or pulmonary infarction. In the context of fever and productive cough, the chest x-ray may provide sufficient information to diagnose pneumonia. However, in the setting of abrupt pleuritic pain and dyspnea, the same finding should be considered compatible with PE and should not prevent further testing for PE.

  • No chest x-ray finding is sensitive enough to rule out PE.

  • With the exception of the rare finding of oligemia (Westermark sign), no chest x-ray finding appears to be specific enough to rule in PE. If the diagnosis is seriously suspected, additional testing is warranted to confirm PE, regardless of suggestive chest x-ray findings such as Hampton’s hump.

  • A normal or near-normal chest x-ray is generally a prerequisite for VQ scan. As described in more detail later in this chapter, chest x-ray abnormalities often predict a nondiagnostic VQ scan, in which case CT may be a better choice.

A variety of chest x-rays from patients with pulmonary emboli are shown throughout the chapter, along with corresponding CT and VQ scans. The take-home point regarding chest x-ray is to avoid being misled by chest x-ray findings into inappropriately abandoning the hunt for pulmonary embolism in an at-risk patient.

What Modalities Can Be Used to Detect Pulmonary Embolism? How Does Pulmonary Angiography Diagnose Pulmonary Embolism?

As we discussed earlier, chest x-ray plays a limited role in the diagnosis of PE, as an embolism is not directly visible on plain x-ray. Instead, indirect or associated findings of PE may sometimes be visible, including pleural effusions and pulmonary parenchymal opacities associated with infarction. In general, these findings are neither sensitive nor specific for PE, so the major role of chest x-ray is in evaluation for other pathologic processes in the differential diagnosis. Common imaging tests for PE include VQ scan and CT pulmonary angiography, with niche roles for MRA and echocardiography in the evaluation of selected patients, as discussed later. The historical criterion standard diagnostic test was fluoroscopic pulmonary angiography ( Figures 7-4 and 7-5 ). In this test, a catheter is inserted through a central vein and advanced through the right heart to the pulmonary artery. Contrast is injected through the catheter, filling the pulmonary arterial tree, which is then visible under fluoroscopy. A pulmonary embolus is visible as a filling defect within the stream of contrast. A fully occlusive PE may completely block flow of contrast distally, whereas a partially occlusive thrombus or small peripheral thrombus may be subtler. As we discuss later, CT pulmonary angiography uses the same principles to detect thrombus and shares many of the advantages and pitfalls. Although pulmonary angiography is used as the “gold standard” diagnostic test in many studies evaluating other imaging modalities, angiography is itself imperfect. Based on animal models, autopsy studies, and follow-up studies using subsequent diagnosis of PE to identify false-negative angiography results, pulmonary angiography is likely only about 87% sensitive (95% CI = 79%-93%), which as we discuss is comparable to CT sensitivity. Pulmonary angiography is rarely performed today as a primary diagnostic test for PE because of its invasive nature and morbidity. Its role has largely been relegated to secondary investigation in cases in which other diagnostic modalities are inconclusive or when invasive therapy is needed for massive PE. The chapter on interventional radiologic techniques ( Chapter 16 ) discusses pulmonary angiography in detail.

Figure 7-4

Pulmonary arteriogram: Schematic.

This schematic of a pulmonary angiogram depicts a normal examination (A) and an examination consistent with pulmonary embolism (PE) (B). During pulmonary angiography, radiopaque contrast material is directly injected into the main pulmonary arteries, using a pulmonary arterial catheter. The pulmonary arterial tree is then visible under fluoroscopy. A, Contrast injected through a catheter in a main pulmonary artery completely fills the arterial tree, indicating that no obstructing pulmonary emboli are present. B, A branch of the tree does not fill (outlined here in dashed line). In addition, a filling defect in the stream of contrast is visible in another section of the arterial tree, although contrast does flow distal to the partially obstructing PE.

Figure 7-5

Pulmonary arteriogram.

Pulmonary arteriography is the historical criterion standard diagnostic imaging test for pulmonary embolism—although recent studies suggest that computed tomography may be comparable in sensitivity and specificity. Today, the study is rarely performed unless other diagnostic imaging tests are inconclusive or an invasive therapy such as mechanical clot disruption or catheter thrombolysis is planned. In pulmonary angiography, a catheter is advanced through a central vein into the right heart and then into the right and left pulmonary arteries. Contrast is injected, and the pulmonary arterial tree becomes visible under fluoroscopy. Filling defects may be seen directly, or a branch of the tree may fail to fill, indicating a thrombus blocking flow of contrast to that region. A, The patient’s right pulmonary arterial tree appears to be missing a major branch. Filling defects representing pulmonary emboli are also present. B, The left pulmonary arterial tree appears normal.

Next, we discuss the theory behind other common tests for PE, starting with CT.

CT Pulmonary Angiography

CT was independently invented in 1972 by British physicist Godfrey N. Hounsfield and American Allan M. Cormack, who in 1979 shared the Nobel Prize in medicine and physiology for their contributions. CT was a breakthrough technology, because it allowed depiction of cross-sectional anatomy with soft-tissue detail unobtainable by conventional x-ray, discovered in 1895 by Wilhelm Roentgen. The first CT scanner could accommodate only the human head and required more than 7 minutes to acquire a single image (slice). Early CT scanners used a single x-ray emitter and detector to acquire image data. Data was acquired one slice at a time, with the emitter and detector circling the patient once, and then the table moving a small distance between each image acquisition ( Figure 7-6 ). The consequence was not only poor image resolution but also data gaps, because anatomic information between slices was unavailable. The ability of CT to diagnose subtle pathology, such as small pulmonary emboli, was limited by both resolution and data gaps. Initially CT was used to demonstrate not the PE but the infarcted lung segment, and it had a sensitivity of less than 50%.

Figure 7-6

Single detector, nonhelical computed tomography.

Individual slices were acquired by rotating a single, paired x-ray source and detector around the patient.

Computed Tomography Scan Characteristics

Two innovations known as “helical” and “multislice” technology improved CT image and data quality, enhancing diagnostic capability. Because of these improvements in CT technology, older studies on the diagnostic characteristics of single-slice CT do not apply to most CT scanners now in clinical use. CT scanners with helical or “spiral” capability acquire data continuously as the patient moves through the gantry ( Figure 7-7 ). Although depending on the CT protocol some data gaps may remain, the amount of missing data is substantially reduced by this technology. All modern scanners can acquire image data in this fashion. In the early years of CT, spiral CT for the diagnosis of PE was an important distinction, because nonhelical scanners were still in use at many institutions. Multislice CT introduces additional x-ray detectors. In scanners of this type, as the patient moves through the CT gantry, the emitter and detectors rotate around the patient in a circular path. The combination of continuous table motion and circular motion of the x-ray source and detectors results in a helical pattern of data acquisition. Data is acquired as a three-dimensional volume. Slices may be reconstructed in any plane, or three-dimensional reconstructions can be generated using sophisticated software. This technology offers substantial improvements in resolution, allowing structures less than a millimeter in size to be seen (the minimum slice thickness on most commercial CT scanners today is 0.625 mm). A tradeoff continues to exist between detail (resolution and signal-to-noise ratio) and radiation exposure. A high-resolution CT of the chest or abdomen exposes a patient to a radiation dose equivalent to approximately 400 chest x-rays. A common misconception is that a higher “slice number” of a CT scanner indicates higher resolution. Instead, the slice number (4 slice, 16 slice, 64 slice, etc.) refers to the number of x-ray detectors, which determines the number of slices that can be acquired simultaneously. This is independent of the slice thickness, which determines resolution. A higher slice number does allow a body region such as the chest to be scanned more quickly, minimizing motion artifact and thus improving test performance. Chapter 8 discusses some technical aspects of CT in more detail in the context of cardiac CT.

Figure 7-7

Multidetector, helical computed tomography (CT).

An x-ray source and multiple x-ray detectors rotate helically around the patient to acquire a volume of image data. All modern scanners use this technology, so requesting a spiral CT for diagnosis of pulmonary embolism is not necessary. A 4-detector CT is shown, but CT scanners with 16, 32, 64, or 256 detectors are commonly available today.

On CT, the density of tissues is measured in Hounsfield units (HU). Air has a density of −1000 HU, water 0 HU, and bone + 1000 HU. Fat, being less dense than water but denser than air, has a value of approximately −50 HU. Soft tissues such as muscle are somewhat denser than water and have an approximate value of +40 HU to +100 HU. A gray scale is then assigned spanning the range of densities, with the densest structures appearing white and the least dense appearing black. This gray scale can be shifted to accentuate tissues of interest. For example, if the user is interested in viewing details of bone, the computer reassigns the entire gray scale to values just below +1000 HU, allowing differentiation of subtle detail within bone. Detail of other structures is not visible on this setting, because all soft-tissue structures appear a fairly uniform gray whereas air remains black. If the user is interested in viewing lung detail, the gray scale is assigned to values near −1000 HU to accentuate details of low-density lung. Details of bone would be obscured on this setting, because all structures that are significantly denser than air would appear white. Most modern computerized picture archiving and communication systems (PACSs) allow the user to select from a list of useful preset variations in the gray scale, or windows. Typical window settings are lung, soft tissue (sometimes called vascular, chest–abdomen, or mediastinal), and bone. Most findings described in this chapter are seen best on soft tissue window settings, because these highlight detail of soft tissues and blood vessels. Some findings are seen best on lung windows, and these are specifically pointed out in the text and figure legends. Examples of window settings are shown in Figure 7-8 .

Figure 7-8

Window settings highlight pathology: CT pulmonary angiography.

All images are from same patient with pulmonary embolism (PE) and pulmonary infarct. The PE is easily visible on soft tissue window (A) but not on lung window (B). The parenchymal changes of the resulting infarcted lung are visible on lung window (C) but not on soft tissue window (D). These findings are described further in later figures.

How Does CT Pulmonary Angiography Detect Pulmonary Embolism?

As described earlier, traditional pulmonary angiography uses contrast material injected through a catheter in the main pulmonary artery to fill the pulmonary arterial tree. A filling “defect,” or location where contrast fails to fill a vessel lumen, marks the presence of a PE (see Figures 7-4 and 7-5 ). CT pulmonary angiography relies on the same principle of filling defects in a stream of injected contrast ( Figures 7-9 and 7-10 ). The technique can be augmented by acquiring additional CT images of the pelvis and lower extremities to assess for clot in these locations, a test called CT venography (discussed later in this chapter). Contrast material is injected, usually peripherally through a catheter in the antecubital fossa. For CT pulmonary angiography, the CT acquisition is timed in an attempt to coincide with the arrival of the contrast bolus in the pulmonary arteries, after it has first traversed veins of the upper extremity, the subclavian vein, the superior vena cava, and the right atrium and ventricle ( Figure 7-11 ). An ideal scan is achieved with a rapid contrast bolus and perfect timing of the scan. A poor contrast bolus may fail to fill the pulmonary arteries, limiting diagnostic accuracy. A poor contrast bolus may cause either a false-negative or a false-positive result. In some cases, a vessel that is partially filled with contrast may simulate the filling defect of a PE, causing a false-positive result. More often, PEs may be missed because they are not visible unless surrounded by a bright bolus of contrast ( Figure 7-12 ) (a noncontrast chest CT is therefore not useful to assess for PE). A poorly timed scan may result in an image in which the pulmonary arteries are poorly opacified with contrast, because the contrast bolus has not yet reached or has already passed through the pulmonary arteries. Today, automated bolus tracking software improves the timing of the bolus. A technician injects a small test bolus of contrast, and CT images at the level of the main pulmonary artery are acquired over a few seconds. Enhancement of the pulmonary artery is measured over this time interval, allowing selection of the optimal timing of the full contrast injection and complete CT scan (see Fig. 7-12 ).

Figure 7-9

Computed tomography (CT) pulmonary angiography: Schematic of axial CT images.

Pulmonary embolism (PE) is detected on CT scan by rapid injection of contrast. The dense contrast fills the pulmonary arteries, except where PE creates a “filling defect.” Filling defects in the central pulmonary arteries are relatively easy to recognize, whereas distal branch vessels can be more difficult to evaluate because of their small size. Noncontrast CT is not useful for detection of PE, because liquid blood and thrombus share the same soft-tissue density. A, Noncontrast CT shows the aorta and main pulmonary artery filled with liquid blood, which has a dark gray appearance. B, Contrast has been injected, and the main pulmonary artery fills completely with contrast, eliminating the possibility of a thrombus in this location. C, A filling defect is present, where no contrast has filled the right pulmonary artery because of the presence of thrombus—a PE. Thrombi can have almost any shape, from irregular “blobs” to well-formed casts of the vessels from which they originate. It is common for some contrast to flow around thrombi, although in some cases they fully occlude the vessel in which they come to rest.

Figure 7-10

Computed tomography (CT) pulmonary angiography: Axial images.

Compare these images with the schematic in Figure 7-9 . A, A normal pulmonary artery fills completely with contrast. There are no filling defects to suggest pulmonary embolus. B, The stream of contrast is interrupted by a filling defect. This fully obstructs the right pulmonary artery and crosses through the left pulmonary artery—a “saddle” pulmonary embolus. An unenhanced CT cannot be used to identify pulmonary emboli, as the densities of thrombus and liquid blood are nearly identical without the use of injected contrast (see Figure 7-12 ).

Figure 7-11

Contrast timing for computed tomography (CT) pulmonary angiography.

Coronal CT image, demonstrating the effect of contrast timing on scan quality. In this patient, a contrast bolus (white) is present in the left subclavian vein and has reached the right atrium. The ascending aorta is not as well opacified with contrast. An optimal scan for aortic pathology or pulmonary embolism is timed so that the contrast bolus is in the vessel of interest at the time of the scan.

Figure 7-12

Contrast timing for computed tomography (CT) pulmonary angiography.

This image dramatically displays why contrast is essential for the detection of pulmonary embolism (PE) and why timing of contrast is critical. A, No contrast has been given, and the pulmonary artery appears uniform. B, Contrast fills the pulmonary artery, and a huge saddle PE becomes visible. Automated contrast bolus tracking software is used to determine the optimal timing of the CT image acquisition, relative to the moment of contrast injection. A small test bolus of contrast is injected, and the intensity of enhancement in the pulmonary artery is measured over several seconds. In the bottom half of the figure, the software displays a graph and table of the Hounsfield unit enhancement versus time. The full CT scan is then performed using the time interval that produced the desired degree of enhancement. Studies in the radiology literature have clarified the degree of enhancement needed for a diagnostic scan.

Small-caliber catheters and distally placed catheters (in the hand, wrist, or forearm) may result in a suboptimal contrast bolus and a nondiagnostic scan. A discussion of flow rates through peripheral catheters is given in Chapter 4 in the context of cervical CT angiography. An optimal contrast bolus requires an automated pressure injector, with an injection rate of around 4 to 5 mL per second. Phantom studies show that peripheral catheters as small as 20 gauge allow adequate contrast injection rates without exceeding safe pressure limits. Many institutions bar the use of central venous catheters with power injectors because of theoretical concerns of embolization of catheter fragments. Embolization has also been described with peripheral venous catheters, but this appears to be a much rarer event. Embolization occurs because of mechanical fragmentation of a catheter subjected to high pressures. Central venous catheters may be subject to fragmentation more than are peripheral catheters because of their length, which causes a linear increase in resistance to flow. In addition, a central catheter’s tip usually lies in the superior vena cava, with little obstruction to embolization of a fragment. In contrast, a peripheral catheter fragment may be prevented from embolizing because of valves in peripheral veins. Despite these concerns, a number of studies suggest that pressure injection through central venous catheters is safe. Some newer permanent and emergency devices are designed for high-pressure, rapid infusion. Examples include PowerPort and PowerLine, Bard Access Systems, which can tolerate 300 psi with a 5 mL per second maximum infusion rate (information from the manufacturer’s website).

What Are the Diagnostic Findings of Pulmonary Embolism on CT Pulmonary Angiography?

Large pulmonary emboli may be recognized easily by familiarity with a few basic points. Box 7-2 outlines a simple approach to CT interpretation for PE. Figures 7-9 and 7-10 depict classic findings of PE on CT scan. On CT, a normal pulmonary artery fills with contrast and appears bright white when viewed with soft-tissue windows. A PE within the vessel displaces contrast, creating a filling defect, which appears as a dark gray region within the vessel. The majority of pulmonary emboli occur within a few bifurcations of the main pulmonary artery, so inspection of the central pulmonary arteries may allow detection of PE in many cases. In one study, 51% of pulmonary emboli were found in central or lobar vessels, and 27% were in segmental vessels. In only 22% were isolated subsegmental vessels involved. More distal vessel branches may be more difficult to interpret because of their small size and the quality of the contrast bolus. Start your interpretation with inspection of the main pulmonary artery and its branches, because emboli in this location are both common and easily recognized ( Figures 7-13 through 7-28 ). Inspect for saddle pulmonary emboli (see Figures 7-10, 7-13, and 7-15 ) and right atrial and ventricular abnormalities (see Figures 7-16 and 7-17 ).

Figure 7-13

Pulmonary embolism (PE): Saddle embolus on CT pulmonary angiography.

The main pulmonary arteries are a simple place to start when interpreting computed tomography (CT) for PE, as the anatomy is easily recognized and large clots are readily seen. A, B, Two axial CT images through the level of the main pulmonary artery. This 66-year-old female with a previous history of PE became short of breath while grocery shopping. Her vital signs were stable on emergency department arrival (blood pressure 143/75, heart rate 109 bpm, oxygen saturation 100% on 2 L). Her CT shows a remarkable saddle PE, with perfectly formed casts of the vessels from which the clots originated. Some of these are seen in long axis and have a tubular shape. Others are seen in cross section and appear circular.

Figure 7-14

Pulmonary embolism: Multiple and bilateral emboli on CT pulmonary angiography.

This 51-year-old female with metastatic ovarian cancer presented with dyspnea and pleuritic chest pain. A large filling defect is present in the right main pulmonary artery, surrounded by a thin stream of contrast. A large thrombus is also visible in a branch of the left pulmonary artery, again surrounded by contrast. A, C, Axial computed tomography images. B, Close-up from A. D, Close-up from C.

Figure 7-15

Pulmonary embolism (PE): Saddle embolus with enlarged right ventricle on CT pulmonary angiography.

This 73-year-old female had recently undergone total knee arthroplasty when she experienced syncope and was found to have a systolic blood pressure of 80 mm Hg with tachycardia and hypoxia to 80% on room air. Her CT shows a large saddle PE. The patient underwent pulmonary angiography (see Figure 7-5 ) and thrombectomy. Her CT also showed right ventricular enlargement (See Figure 7-16 ).

Figure 7-16

Pulmonary embolism (PE): Saddle embolus with enlarged right ventricle on CT pulmonary angiography.

Same patient as Figure 7-15 . Her CT showed a large saddle PE (prior figure). In addition, sections through the right atrium and ventricle showed enlargement of these chambers and filling defects suggesting thrombus in these chambers. Note the tubular and rounded cross sections, which could correspond to thrombus casts of lower extremity veins. A, B, Same slice with window settings adjusted to highlight clot and cardiac chamber anatomy.

Figure 7-17

Pulmonary embolism: Large bilateral PE with right ventricular enlargement on CT pulmonary angiography and echocardiogram.

This 79-year-old male with a history of pancreatic cancer experienced sudden dyspnea and presyncope while in the shower. Paramedics found the patient to be hypoxic to 80% oxygen saturation on room air with a systolic blood pressure of 80 mm Hg. The patient was noted to have bilateral large pulmonary emboli on CT ( A; B, close-up). In addition, the right atrium and ventricle were noted to be dilated (C), concerning for right heart strain. This was confirmed on echocardiogram. C, The CT window has been adjusted to allow the internal structure of the heart to be better appreciated—the setting is closer to a normal bone window. Note the massive right atrium. The right ventricle is as large as the left.

Figure 7-18

Right main pulmonary artery embolus: Axial CT pulmonary angiography image.

A, A filling defect representing a pulmonary embolus obstructs contrast flow in the right main pulmonary artery. B, Close-up.

Figure 7-19

Pulmonary embolism: Emboli in main pulmonary arteries on CT pulmonary angiography.

This 68-year-old male with esophageal cancer presented with an acute syncope episode and less acutely worsening dyspnea. A to C, Consecutive axial images through the level of the main pulmonary artery. These computed tomography slices show multiple filling defects characteristic of pulmonary emboli. Although these appear somehow suspended in the middle of the lumen of the pulmonary artery, remember that you are looking at individual slices through a larger three-dimensional structure. The thrombus may be caught on a vessel bifurcation and dangling like a streamer in the current. Learn the appearance of these large main pulmonary artery clots. These are easiest to recognize, but peripheral clots share the same features. These thrombi are dark filling voids within a contrast-filled vessel. They are not fully occlusive, more like pieces of Jell-O than like a cork in a wine bottle. It is common to see contrast outlining the margins of a thrombus. This will help you confirm that the filling defect is within the vessel, not outside of a vessel that is leaving the plane of the image.

Figure 7-20

Pulmonary embolism in main pulmonary arteries on CT pulmonary angiography.

Same patient as Figure 7-19 . Look in closer detail at the main pulmonary artery, which is nicely seen with both major branches in this image. In the right main pulmonary artery, a large thrombus is visible. Just distal to this, the artery curves anteriorly and another thrombus is seen, outlined with a thin ribbon of contrast on each side. This is called “railroad tracking” and is a common feature of pulmonary emboli. In the left main pulmonary artery, a strand of thrombus is caught at a major bifurcation. The embolus winds in and out of the plane of the image and appears as several filling defects. Inspection of adjacent image slices would prove these to be part of the same long segment of clot. Again, railroad tracking surrounds the anterior portion of the clot.

Figure 7-21

Artifacts on CT pulmonary angiography.

Same patient as Figure 7-20 . Look in closer detail at the main pulmonary artery and its neighboring structures. The superior vena cava is visible as a bright kidney bean shape. It is so bright because of the continued injection of intravenous contrast that it is creating “beam-hardening artifact,” which produces a sunburst pattern emanating from the superior vena cava. This sunburst is slightly overlapping the adjacent structures, interfering with their visualization. The pulmonary artery is well opacified with contrast, which has traveled through the superior vena cava, mixed with blood in the right atrium, and then been ejected by the right ventricle into the main pulmonary trunk and its branches. A moderate amount of contrast fills the ascending aorta, while less has reached the descending aorta. For the purposes of this imaging study, which seeks to evaluate filling defects in the pulmonary arteries, this is fine—but this would be a suboptimal study for evaluation of aortic dissection.

Figure 7-22

Pulmonary embolism (PE) in bilateral main pulmonary arteries on CT pulmonary angiography.

This 50-year-old female developed acute dyspnea, pleuritic right chest pain, and syncope after a 3-day prodrome of left leg pain. A single image complete image (A) is shown for orientation, which is the same as usual for CT (patient’s right is on left side of image). Coned-in views of the main pulmonary artery are also shown to allow you to follow the thrombus from slice to slice. The close-up corresponding to the complete computed tomography slice is number 21. Although it cannot be seen in its entirety in a single slice, a saddle PE occludes much of the left pulmonary artery and extends across to the right. Arrows point out the thrombus in some images.

Figure 7-23

Pulmonary embolism in left main pulmonary artery on CT pulmonary angiography.

This 58-year-old male with metastatic lung cancer presented with acute chest tightness and dyspnea. The patient described himself as “gasping for air.” Again, a large central pulmonary embolus is seen as a filling defect, lodged at a bifurcation of the left main pulmonary artery. B, Close-up.

Figure 7-24

Pulmonary embolism (PE) in left main pulmonary artery on CT pulmonary angiography.

Same patient as Figure 7-23 . Some institutions routinely perform multiplanar reconstructions to further characterize PE. In equivocal cases, these may help to delineate true thrombus from various artifacts. In this patient, the diagnosis of PE is unequivocal, but additional reconstructions are shown to illustrate their capabilities. This oblique coronal view shows the left pulmonary artery, filled with an amorphous clot. As in other figures, the clot is seen to partially occlude the vessel with a thin rim of surrounding contrast.

Figure 7-25

Pulmonary embolism (PE) in left main pulmonary artery on CT pulmonary angiography, sagittal view.

Same patient as Figure 7-24 . This sagittal view shows the left pulmonary artery, again with clot partially occluding the vessel. A circular rim of contrast surrounds the clot in some locations. This is a common appearance that should be recognized.

Figure 7-26

Railroad track sign of pulmonary embolism: Axial CT pulmonary angiography images.

Pulmonary emboli often do not fully occlude a vessel. Contrast may be seen leaking around the periphery of a thrombus, helping to identify a true filling defect within a pulmonary artery. A, A filling defect representing a pulmonary embolus obstructs contrast flow in a segmental pulmonary artery. Contrast can be seen leaking around the thrombus, sometimes called the railroad track sign. B, Close-up.

Figure 7-27

Right main pulmonary artery embolus: Coronal CT pulmonary angiography image.

A, Coronal view of the same patient as in Figure 7-26 . Multiplanar images can clarify the diagnosis when a filling defect is suspected on axial images. Sometimes the additional images will reveal the suspected thrombus to be a structure outside the blood vessel—for example, an adjacent lymph node. Here, a filling defect representing a pulmonary embolus obstructs contrast flow in the right main pulmonary artery. Contrast can be seen leaking around and through the thrombus, a variation of the railroad track sign. B, Close-up. The window setting has been adjusted to decrease the brightness of the contrast bolus from that seen with soft tissue windows. Excessively bright contrast can create “bloom artifact” that obscures adjacent tissues including thrombus. Bone windows minimize this effect while allowing evaluation of contrast-filled vascular structures. Some PACS interfaces have preset optimized “vascular window” settings. Others allow the user to adjust and then save window settings.

Figure 7-28

Segmental pulmonary embolism, CT pulmonary angiography.

A, A filling defect representing a pulmonary embolus is visible in a segmental artery to the left lower lung segment. Contrast leaking around the thrombus is visible as a white halo around the thrombus, which appears as a dark circle in cross section. A pleural effusion is also present (dark gray “fluid density” on soft tissue windows). B, Close-up.

Several additional pieces of information may be helpful in the evaluation of the scan. First, pulmonary emboli are more common in vessels in lower lung segments (58% of cases), and these should be carefully inspected.

Second, many pulmonary emboli do not completely obstruct the vessel, and a characteristic appearance of contrast leaking around the embolus is often seen ( Figures 7-23 through 7-28 ). A possible pulmonary embolus seen on one axial image should be tracked through multiple adjacent images to confirm or refute the finding ( Figures 7-22 and 7-29 ; see also Figure 7-36 ). Coronal and sagittal plane images can also assist in this evaluation (see Figures 7-25 and 7-27 ).

Figure 7-29

Pulmonary embolism, multilobar, seen with CT pulmonary angiography.

This 54-year-old woman with recurrent ovarian cancer presented with progressive dyspnea over a 2-week period. The patient has pulmonary emboli involving more distal branches of the pulmonary arteries than those that we have considered previously. A single complete slice (A) is shown to illustrate one of the affected vessels in context. The series of coned-in images then tracks that vessel through the adjacent slices. The close-up corresponding to the full slice is number 9. Some vessels are seen in short-axis cross section and have a circular appearance with circular clot. Other vessels are seen in long-axis cross section and contain clot that appears linear. Arrows have been placed to assist you in following a vessel and thrombus through multiple slices.

Third, inspection of lung windows may aid in the detection of PE. As stated earlier, selecting lung windows simply refers to picking a default setting on a PACS that shifts the CT gray scale to accentuate the fine detail of low-density tissues such as lung. On lung

Box 7-2

  • 1.

    Choose soft tissue or vascular window setting. Some PACS systems have preset vascular windows. These alter the normal soft tissue window to decrease bloom artifact caused by the contrast bolus.

  • 2.

    Assess contrast bolus quality.

  • 3.

    Assess for motion artifact.

  • 4.

    Locate the main pulmonary artery, and inspect for saddle embolism.

  • 5.

    Moving cephalad or caudad, inspect each large-order vessel for emboli.

Pearls for Pulmonary Embolism

  • Look for more PEs in caudad vessels.

  • Look for contrast leak around embolism.

  • Use the patient’s pain location as an aid.

  • Check lung windows for evidence of pulmonary infarction.

Pitfalls for Pulmonary Embolism

  • Motion gives a false negative or positive.

  • Tachypnea gives a false negative or positive.

  • A slow scanner gives a false negative or positive.

  • An obese patient gives a false negative or positive.

  • Poor bolus gives a false negative or positive.

  • Lymph nodes give a false positive.

  • External compression gives a false positive.

Algorithm for Interpreting CT for Pulmonary Embolism
window settings, parenchymal abnormalities such as linear atelectasis and wedge-shaped peripheral opacities (representing infarcts) may be visible. Figures 7-30 through 7-42 demonstrate these CT lung window abnormalities, as well as the corresponding CT soft tissue window and chest x-ray findings. Once a parenchymal abnormality is noted on lung windows, the viewer should return to soft tissue window settings, where inspection of the vessels leading to the abnormal lung segment may reveal a PE. This step is necessary to differentiate pulmonary infarct, because a parenchymal density may also represent pneumonia or mass. Pleural effusions may be helpful in detection of a PE by pointing to a lung region of concern, but they are equally common in patients with and without PE, and their presence should not be interpreted as confirming PE.

Figure 7-30

Pulmonary infarction: Axial computed tomography (CT) image.

CT lung window in a patient with pulmonary embolism. A wedge-shaped, peripheral, pleural-based parenchymal density is visible in the right lung. This is the CT correlate of the classic x-ray finding, Hampton’s hump. An adjacent pleural effusion is present. The dome of the liver is visible, because this is a slice through the lower thorax. Although the lung window can suggest pulmonary infarct, the appearance is also consistent with pneumonia, so the soft tissue window must be inspected to identify thrombus in a vessel supplying that lung region. The clot causing a parenchymal infarct may not be visible on the same slice, so inspect all slices.

Figure 7-31

Pulmonary infarction, subacute: Axial computed tomography (CT) image.

A CT lung window demonstrates a peripheral, pleural-based density in the left lung—the CT analogue of Hampton’s hump. This patient presented nearly 1 month after an acute episode of pleuritic chest pain and dyspnea after an airplane trip. No filling defect was visible on any of the soft tissue window slices, presumably because of spontaneous lysis of a pulmonary embolus. In the right clinical context, this finding is compatible with pulmonary infarct from pulmonary embolus—but pneumonia or mass lesions can give a similar CT appearance, so inspection of the soft tissue window remains important.

Figure 7-32

Pulmonary embolism (PE): Hampton’s hump.

Computed tomography scan from the patient in Figure 7-3 . A lung window demonstrates the same wedge-shaped peripheral density seen on the patient’s chest x-ray. This pulmonary infarct is in the watershed of the pulmonary artery obstructed by thrombus, a PE. Soft-tissue windows showing the PE are reviewed in Figure 7-33 .

Figure 7-33

Pulmonary embolism (PE): Hampton’s hump.

Same CT pulmonary angiogram as Figure 7-32 . A, Soft-tissue window. B, Close-up. A PE is present in a branch pulmonary artery, seen in long-axis cross section. This thrombus is outlined in contrast, a common finding sometimes called railroad tracking in the radiology literature. Interpreting chest CT for PE requires some getting used to. This figure has two other regions that appear to be occlusions on this single image, but review of adjacent images proves that these densities lie outside of the pulmonary artery. Novice readers might be deceived by the manner in which the pulmonary artery moves in and out of the plane of this image. We review many more examples that clarify this.

Figure 7-34

Pulmonary embolism (PE) with visible infarct on chest x-ray.

This 48-year-old female presented with sudden onset of pleuritic pain along her left costal margin with dyspnea and hemoptysis. She had experienced some cough the prior 2 weeks. A left lower lobe opacity was noted on chest x-ray and is visible on both posterior–anterior (PA) (A) and lateral (B) views. The upper surface of the left diaphragm is obscured on the PA x-ray, and increased density overlies the heart on this view. On the lateral x-ray, the thoracic spine fails to become darker approaching the diaphragm (as is normal) because of the overlying lung density. This was interpreted as likely pneumonia by the radiologist. PE was suspected based on the sudden onset of symptoms, and CT pulmonary angiography was performed ( Figure 7-35 ). Remember that pneumonia and pulmonary infarct are indistinguishable on chest x-ray.

Figure 7-35

Pulmonary embolism (PE) with visible infarct on chest x-ray.

This computed tomography (CT) image (viewed on lung window settings) shows the same infiltrate as in the chest x-ray in Figure 7-34 . Compare the normal right lung with the left lung, which shows a patchy, ground-glass appearance. This appearance can be caused by pulmonary infarction and hemorrhage (as in this case), atypical infection, or aspiration. The right lung has a central density, but this is the dome of the diaphragm or uppermost liver, because this slice is taken low in the chest near the upper abdomen. The critical teaching point is that chest x-ray findings suggesting pneumonia may represent pulmonary infarction. When PE is strongly suspected, chest CT should be performed to further evaluate the patient. Ventilation–perfusion (VQ) scan may be less helpful in this scenario, because an infiltrate on chest x-ray would likely result in a ventilation defect with a matched perfusion defect on a VQ scan—by definition, an intermediate probability scan for PE. VQ could be diagnostic if additional unmatched perfusion defects are found. The soft-tissue windows are shown in Figure 7-36 and confirm PE. Interestingly, the patient was found to be hyperthyroid and thrombocytopenic, perhaps contributing to pulmonary hemorrhage.

Figure 7-36

CT pulmonary angiogram from patient with visible pulmonary infarct on chest x-ray.

Same patient as Figures 7-34 and 7-35 , soft-tissue windows. A single complete slice is shown for orientation (A), corresponding to image number 14. Coned-in views of the main pulmonary arteries are shown to allow these vessels to be tracked through multiple slices. A large thrombus is seen in short-axis cross section, giving it a circular appearance. A crescent of contrast is seen partially outlining this thrombus, which does not completely fill the vessel at this level. The thrombus is a tubular cast of the vessel from which it originated and is visible on several adjacent slices because of its length. This thrombus lies in the pulmonary artery supplying the left lower lobe, explaining the infarct in that location. The superior vena cava is filled with very dense contrast, creating beam-hardening (streak) artifact with a sunburst appearance overlying adjacent structures.

Figure 7-37

Pulmonary embolism (PE), massive: Visible infarct on noncontrast “renal protocol” computed tomography (CT).

This 42-year-old female presented with left flank pain and cough. She had recently been diagnosed with likely lung cancer but had not undergone biopsy or other workup or treatment. The initial evaluation by the emergency physician suggested renal colic, and a noncontrast abdominal CT was performed. A, Soft-tissue window. B, Lung window for the same slice. The cephaladmost slices from abdominal CT routinely include the lower lung, and on the lung window a left lower lobe density was noted—interpreted appropriately by the radiologist as “heterogeneous opacities in the left lower lung, which may be the result of infection, aspiration, or spread of malignancy.” However, another explanation for this appearance is pulmonary infarction from PE. The emergency physician obtained chest x-ray that also showed an appearance consistent with infiltrate ( Figure 7-38 ). With this apparent diagnosis in hand based on imaging, the patient was admitted to an observation unit and treated for pneumonia. The next morning, PE was considered and confirmed by contrasted chest CT. The take-home point is that the appearance of pulmonary infarction and pneumonia can be identical on chest x-ray and CT lung window. In both cases, the density of lung tissue increases because of the presence of fluid, cellular debris, inflammatory cells, and possibly alveolar hemorrhage. When the clinical history suggests PE, the presence of an infiltrate on chest x-ray or CT is not diagnostic of pneumonia and does not rule out PE. Compare with the chest x-ray in Figure 7-38 and the CT pulmonary angiogram in Figure 7-39 .

Figure 7-38

Pulmonary embolism (PE) chest x-ray.

Following the noncontrast abdominal CT in Figure 7-37 , the patient underwent chest x-ray, showing increased density in the left lower lobe. The diaphragm and left heart border are obscured on the posterior–anterior x-ray (A), and the retrocardiac space appears abnormally dense on the lateral view (B) (the “spine sign”—absence of the normal progressive lucency of the thoracic spine as it approaches the diaphragm). These abnormalities were interpreted as evidence of pneumonia by the emergency physician, though they were the result pulmonary infarction from PE (see Figure 7-39 ). The radiologist suggested infection, edema, or atelectasis but did not mention infarction. Pulmonary infarction and infectious infiltrate can have identical appearances on chest x-ray. The patient also has a known right hilar mass. Compare with the noncontrast CT in Figure 7-37 and the CT pulmonary angiogram in Figure 7-39 .

Figure 7-39

Pulmonary embolism with visible infarct.

Same patient as in Figures 7-37 and 7-38 . CT pulmonary angiography demonstrates a filling defect completely obstructing the left lower lobe pulmonary artery. On the right, a lung mass is seen, and hilar adenopathy adjacent to the right main pulmonary artery is seen. How can you distinguish a mass adjacent to the artery from a clot within? In some cases, they may be indistinguishable, but often inspection of several adjacent slices can allow the two to be discriminated. Thrombus and adenopathy or other soft-tissue masses share the same dark gray (soft-tissue density) on soft-tissue windows. Therefore it is not the color that should be relied upon. Instead, follow the vessel in question through several slices to determine whether the apparent cutoff is simply the result of the vessel turning and traveling outside of the plane of the single CT slice. If the contrast-filled vessel can be followed through several slices, the soft-tissue mass is likely extrinsic to the vessel. If the vessel does not appear to be filled with contrast in adjacent slices, the soft-tissue density is likely thrombus within the vessel—a pulmonary embolus. The next figure shows a series of coned-in views to allow you to see the distinction between thrombus and soft-tissue mass external to the vessel.

Figure 7-40

Pulmonary embolism (PE): Distinguishing adenopathy from thrombus.

Image number 6 corresponds to the full computed tomography image in Figure 7-39 —review that figure before proceeding with this one. Start with image 1 in the top left and track the normal right pulmonary artery (marked by a white arrow ) as it turns and is visible as a contrast-filled circular cross section in several slices. It then is visible in long-axis section and merges into the pulmonary trunk. In none of the slices shown is it obstructed with thrombus. However, a lymph node outside of the vessel is easily mistaken for a PE. Now follow the left pulmonary artery (marked by an open arrow ), and you will see that it remains obstructed in several adjacent slices. A branch to the right upper lobe diverges, but the branch to the left lower lobe (open arrow) remains obstructed in every slice and does not fill with contrast. Cases such as this are common and require careful attention by the radiologist to avoid misdiagnosis.

Figure 7-41

Pulmonary embolism (PE), massive.

This 63-year-old female underwent mastectomy for breast cancer 5 days prior and awoke with pleuritic right chest pain and dyspnea. Her chest x-ray shows a blunted right costophrenic angle on the right on the posterior–anterior view (A) and increased density on the lateral view (B). PE was suspected, and CT pulmonary angiography was performed ( Figure 7-42 ).

Figure 7-42

Pulmonary embolism (PE), massive.

These CT pulmonary angiography images show a filling defect in the right lower lobe pulmonary artery, a PE. The watershed region of lung supplied by this vessel is infarcted, resulting in increased density on chest computed tomography and in the chest x-ray in Figure 7-41 . A, Soft-tissue window. B, Lung window of the same slice. C, Close-up from A showing the thrombus in more detail.

False-positive and false-negative CT pulmonary angiography results may occur due a number of factors. A poor contrast bolus may not opacify the pulmonary arteries sufficiently to allow the filling defect of a pulmonary embolus to be recognized. Ironically, a very dense contrast bolus can also lead to misdiagnosis because of streak artifact that can obscure thrombus (see Figures 7-21, 7-36, and 7-47 ). A slow scanner or an extremely tachypneic patient may result in a false-negative or nondiagnostic scan because of excessive motion artifact. Lymph nodes immediately adjacent to blood vessels appear dark gray and may be mistaken for pulmonary emboli by inexperienced readers. A blood vessel compressed by an adjacent structure such as a lymph node, airway, or mass may have an irregular contour that may be mistaken for the filling defect of a PE. Extremely obese patients may have poor-quality scans resulting from underpenetration of radiation. Intentional inspiration and “breath hold” immediately before CT acquisition can introduce an artifact leading to false-positive interpretation by the following mechanism. With slower CT scanners, the patient is often instructed to take a deep breath and then to stop breathing during the scan to reduce motion artifact. Deep inspiration results in a sudden decrease in intrathoracic pressure, pulling noncontrasted blood into the right heart from the inferior vena cava. This can result in indeterminate or false-positive interpretation in a minority of cases, because the noncontrasted blood (which appears dark gray) may be mistaken for the filling defect of a PE. Ironically, faster scanners might worsen this artifact if deep inspiration is encouraged, because the entire CT acquisition occurs rapidly during the peak of the effect of inspiration.

Do CT Findings Predict Acute Morbidity and Mortality from Pulmonary Embolism?

A number of scoring systems have been proposed for severity of PE by CT. Surprisingly, saddle PE does not predict high mortality. CT can detect physiologic consequences of massive PE such as right ventricular dilatation, ventricular septal bowing, and decreased size of the left atrium and pulmonary veins from decreased pulmonary venous return. To date, studies are equivocal, with some suggesting that CT evidence of right ventricular dysfunction may predict morbidity and mortality and thus might be a criterion for aggressive therapy using interventional radiologic techniques, which are described in detail in Chapter 16 .

CT Pulmonary Angiography Sensitivity: When Is a Negative Scan Enough?

Although many measures of CT sensitivity can be considered, let’s start with two summary statements:

  • 1.

    A normal CT predicts a very low risk for PE in patients with low to moderate pretest probability.

  • 2.

    When very high clinical suspicion exists for PE, additional imaging is warranted following a negative CT pulmonary angiogram.

Later, we review the evidence for these statements.

CT as a diagnostic test for PE was attempted as early as 1978, but early attempts offered poor resolution, sensitivity, and specificity. This resulted from the use of single-slice, nonhelical technology. Because images were acquired at large distance intervals and with relatively thick slices, small pulmonary emboli were undetectable. Image acquisition speed was slow, resulting in motion artifact during respiration. By the late 1990s, studies of CT using single-slice helical scanning began to report CT sensitivity of 87% to 91% with specificity of 78% to 98%, which compared favorably with the alternative diagnostic tests, VQ scan and pulmonary angiography. By 2002 to 2005, reports emerged of modern helical multislice scans offering superior image resolution with visualization of subsegmental pulmonary arteries, limited gaps in data, and rapid scan acquisition, eliminating respiratory and cardiac motion artifact. For these reasons, when evaluating studies on the sensitivity and other test characteristics of CT for PE, it is important to determine whether modern CT equipment was used in the study. Although CT remains a limited test, it uses the same basic principles as traditional pulmonary angiography as described earlier, and the test characteristics of the two modalities have converged as CT technology has continued to improve. The most current studies of CT show high sensitivity and specificity when compared with pulmonary angiography. Questions have begun to arise about the proper criterion diagnostic standard when comparing the two techniques, because pulmonary angiography itself is subject to false positives and false negatives.

Before examining the evidence in detail, let’s reexamine our goal in performing diagnostic imaging for detection of PE. CT accuracy can be evaluated using two general strategies. The first is a “disease-oriented outcome” standard, meaning the presence or absence of PE, as detected by some reference test and compared with CT. The second is a “patient-oriented outcome” standard, based on the clinical outcome (morbidity or mortality) for a patient with a normal CT scan who is not treated with anticoagulation. The second may be the more important standard, because our primary goal as emergency physicians is to prevent morbidity and mortality.

Literally hundreds of published articles exist on the topic of CT for PE; a PubMed search using the terms “CT,” “pulmonary,” and “angiography” found 1679 matches with more studies published each day. (The author performed that first search on March 8, 2010, but by March 21, 2011 the number of PubMed matches had grown to 2025). Here, we consider a few of the key studies underlying our understanding of CT sensitivity and specificity. Early studies of single-detector CT were haunted by questions of undetected subsegmental pulmonary emboli with possible significant patient morbidity and mortality resulting from undiagnosed and untreated thrombus. However, new studies of multidetector CT demonstrate the ability to image subsegmental pulmonary arteries. Most importantly, patient outcomes after negative CT are similar to those after negative traditional pulmonary angiography. A 2005 review found that the incidence of PE 6 to 12 months after negative traditional pulmonary angiography was approximately 1.6%, whereas a negative CT pulmonary angiogram carried a 1.3% average incidence of VTE. Exceptions to this may include patients with symptoms of deep venous thrombosis (DVT), in whom further evaluation may be warranted if CT pulmonary angiography is negative. To be fair, these outcome numbers are influenced not only by the sensitivity of the two tests, but also by the risk profile of the patient populations being tested. Patients subjected to formal pulmonary angiography are typically at high risk (high pretest probability) of PE, warranting the use of an invasive test for evaluation. Thus a low rate of PE following a negative angiogram in this population is impressive, reflecting high test sensitivity. In contrast, patients undergoing CT pulmonary angiography have a low overall risk of PE, so good outcomes following normal CT pulmonary angiography are as much a measure of the low pretest probability of disease as of the test’s sensitivity. We will consider this issue in more detail in the discussion to come.

Outcome Studies Following Negative CT Pulmonary Angiography

A systematic review and meta-analysis (including both single and multidetector CT) published in JAMA in 2005 found that the likelihood ratio negative for PE following a negative chest CT was 0.07 (95% CI = 0.05-0.11). The likelihood ratio negative for mortality attributable to PE was 0.01 (95% CI = 0.01-0.02) at follow-up of 3 to 12 months. These values are similar to those reported for conventional pulmonary angiography. Other investigators have also reported good clinical outcomes (98% or greater survival without venous thromboembolic disease) in the 6 months after a negative chest CT, without additional DVT testing. The Christopher Study, a prospective multicenter study of 3306 patients published in JAMA in 2006, examined VTE outcomes in patients with negative chest CT who were not anticoagulated. The 3-month rate of VTE was only 1.3% (95% CI = 0.7%-2.0%), with a mortality rate of 0.5% (95% CI = 0.2%-1.0%). A 2009 meta-analysis found a similar 3-month incidence of VTE (1.2%, 95% CI = 0.8%-1.8%) following normal CT pulmonary angiography and conventional pulmonary angiography (1.7%, 95% CI = 1.0%-2.7%). Fatal pulmonary emboli were rare in the 3 months following a normal CT, occurring in 0.6%. The authors also evaluated the incremental safety provided by performing bilateral compression ultrasound to evaluate for DVT but found no statistically significant difference in 3-month risk for PE or fatal PE with this additional testing strategy.

In JAMA in 2007, Anderson et al. reported a randomized, controlled, single-blinded noninferiority trial comparing CT and VQ scan to assess the safety of CT as an initial test for acute PE. The study examined a high-risk population of 1417 patients, all with a Wells score of 4.5 or greater or positive D-dimer results. Patients were randomized to assessment with either VQ scan or CT scan. Initial diagnosis with PE was made for 19.2% of patients in the CT group and 14.2% of patients in the VQ scan group. Patients with negative imaging results did not receive anticoagulation and were followed for 3 months to determine the interval development of either PE or proximal DVT. Only 0.4% of patients with negative initial CT scan results and 1.0% of those with negative VQ scan results developed thromboembolism during the follow-up, with no statistical difference between the two groups. This study offers strong evidence that either CT scan or VQ scan is a safe initial approach to rule out PE in the emergency department, with a negative predictive value of 99%.

You may recall that negative predictive values are subject to variation depending on the rate of disease in the study population and are relatively discouraged as a reported measure of a test’s accuracy for this reason. Consider the extreme example of a test that is always negative for PE and therefore has a sensitivity of 0%. If used in a study population consisting of 99 patients without PE and 1 patient with PE, the test would have a 99% negative predictive value, because only a single patient has the disease. Then, why should we accept a negative predictive value in Anderson et al.’s study? This study examined a high-risk population, with an overall rate of PE of 16.5%. This is likely a higher rate of thromboembolic disease than would occur in most emergency department cohorts being evaluated, so the test likely will perform with a similarly high negative predictive value in our patients. Consider how our hypothetical 0% sensitivity test would perform in this population. It would fail to identify all patients with PE (16.5%), so the negative predictive value would be only 83.5%. Anderson et al.’s study suggests that both VQ and CT perform well in sorting from a high-risk population those patients who can safely avoid anticoagulation. The authors point out that CT diagnosed more patients with PE than did VQ scan, yet those with negative CT or VQ fared equally well without anticoagulation. This implies that some of those diagnosed with PE by CT scan either did not really have the disease or did not require anticoagulation therapy for it. Overdiagnosis of PE remains a potential concern with CT scan, as this may subject patients to unnecessary anticoagulation.

CT, VQ scan, and Likelihood Ratios: Altering Pretest Odds With a Negative Diagnostic Imaging Test

Another measure of test diagnostic accuracy is likelihood ratio. Two likelihood ratios can be calculated for every test, based on the test’s sensitivity and specificity. The likelihood ratio positive (LR+) is the probability of a person who has the disease in question testing positive divided by the probability of a person who does not have the disease testing positive. This is also mathematically represented as LR+ = sensitivity/ (1-specificity). The likelihood ratio negative (LR-) is the probability of a person who has the disease in question testing negative divided by the probability of a person who does not have the disease testing negative. It is mathematically represented by LR− = (1-sensitivity)/specificity. The pretest odds of the diagnosis multiplied by the appropriate likelihood ratio determines the post-test odds. Odds and probability can be mathematically interconverted. Although the pretest odds cannot be specifically determined for an individual patient, it can be estimated by the physician based on factors such as the overall prevalence of disease in a given emergency department and the given patient’s similarity to the overall population (e.g., more at risk or less at risk than an average patient). A likelihood ratio positive greater than 10 strongly increases disease probability, effectively ruling in disease for all but the lowest-risk patients. A likelihood ratio negative less than 0.1 strongly decreases disease probability, effectively ruling out disease in all but the highest-risk patients. Given this background, what are the LR+ and LR− values for CT pulmonary angiography and VQ scan (a test for pulmonary embolism discussed later in this chapter)?

Roy et al. performed a systematic review and meta-analysis of strategies for diagnosis of acute PE, published in BMJ in 2005. The authors provide likelihood ratios for CT and VQ scan, which are useful in our clinical decisions. Positive likelihood ratios were as follows: “high probability” VQ scan was 18.3 (95% CI = 10.3-32.5), CT was 24.1 (95% CI = 12.4-46.7), and lower extremity venous ultrasound was 16.2 (95% CI = 5.6-46.7). Because positive likelihood ratios greater than 10 are generally considered to be helpful in ruling in a disease process, all three diagnostic strategies could be considered confirmatory if positive in a patient with a moderate or high pretest probability of PE. Negative likelihood ratios were as follows: normal or near-normal VQ scan was 0.05 (95% CI = 0.03-0.10), and negative CT plus negative lower extremity ultrasound was 0.04 (95% CI = 0.03-0.06). Because a test with a likelihood ratio negative less than 0.1 is considered to provide strong evidence against a disease process, a normal VQ or CT plus ultrasound can be used to rule out PE in all but the highest-risk patients. The authors noted that the likelihood ratio negative of a negative CT alone (without ultrasound) was only 0.11 (95% CI = 0.06-0.15) and therefore concluded that CT alone should only be used to rule out PE in low-risk patients. Adding ultrasound evaluation may be prudent in patients with higher clinical risk. A low-probability VQ scan had a negative likelihood ratio of 0.36 (95% CI = 0.25-0.50), meaning that it reduces the likelihood of PE but only moderately. In very-low-risk patients, this may equate to an acceptably low risk for PE, but in high-risk patients, a “low probability” VQ scan does not rule out PE. Likelihood ratios are based on sensitivity and specificity values, so what do published studies say about CT sensitivity and specificity?

Studies of CT Pulmonary Angiography Sensitivity and Specificity

A 2002 meta-analysis of 12 studies from 1990 to 2000 comparing CT to standard pulmonary angiography or high-probability VQ scan found an overall sensitivity of 74.1% and specificity of 89.5%, with broad reported ranges for both sensitivity (57% to 100%) and specificity (68% to 100%). A systematic review and meta-analysis published in 2005 in Radiology (including single and multidetector CT) found the pooled sensitivity for CT to be 86% (95% CI = 80.2%-92.1%) with a specificity of 93.7% (95% CI = 91.1%-96.3%). In other words, a positive CT is likely to rule in PE correctly, but a negative CT might miss as many as one in five patients with PE. A 2006 review reached similar conclusions, finding that CT pulmonary angiography alone was relatively insensitive but, when combined with lower extremity DVT diagnostic testing, had a false-negative rate of only 1.6%.

In 2006, the results of the multicenter PIOPED II study were published in the New England Journal of Medicine. This National Institutes of Health–funded prospective study used a composite reference standard, including additional imaging results, to determine the accuracy of multidetector CT. The study included 4-, 8-, and 16-detector CT scanners. Overall, the study found CT pulmonary angiography to be 83% sensitive (95% CI = 76%-92%) with a specificity of 96% (95% CI = 93%-97%). The likelihood ratio positive was 19.6 (95% CI = 13.3-29.0), indicating that a positive CT scan strongly predicts the presence of PE. The likelihood ratio negative was 0.18 (95% CI = 0.13-0.24), indicating that a negative CT substantially reduces but does not exclude the possibility of PE. Remember that a test with a likelihood ratio positive greater than 10 is thought to suggest a disease process strongly, whereas a likelihood ratio negative less than 0.1 is necessary to exclude a diagnosis confidently. The investigators also reported the positive predictive values in patients with intermediate and high pretest probability and the negative predictive value of CT angiography in patients with low pretest probability. Positive predictive values of CT in intermediate- and high-risk patients were 92% and 96%, respectively. Negative predictive value was 97% in low-risk patients. As described earlier, positive and negative predictive values are influenced by the prevalence of disease in the subject groups and are generally discouraged as a means of describing test properties. However, in this case, reporting predictive values stratified by clinical pretest probability is appropriate, because validated tools (Wells score and others) are available to us as emergency physicians to allow us to identify patients with similar probability of disease. The authors concluded that a CT finding that is concordant with pretest probability is highly predictive, whereas discordant imaging and clinical risk assessment should be followed with additional testing. The relatively low sensitivity of CT pulmonary angiography in PIOPED II (83%) may come as a surprise, and deserves comment. The reference standard for the diagnosis of PE in PIOPED II was designed to be extremely conservative, and included the diagnosis of DVT by venous ultrasound in a patient whose other diagnostic tests for PE were negative. Thus a DVT was assumed to be a surrogate for the diagnosis of PE, and a negative CT pulmonary angiogram in this setting was considered to be a false negative. While from a clinical perspective, patients with DVT require anticoagulation, it is not actually true that all patients with DVT also have PE. Thus, this reference standard exaggerates the false negative rate (and thus decreases the apparent sensitivity) of CT for PE. 13.5% of PE diagnoses in PIOPED II were based on such ultrasound findings. If these patients in truth had isolated DVT without PE, the negative CTs that occurred in some of these patients would be true negatives, not false negatives, and the sensitivity of CT would be higher than that reported by the PIOPED II investigators.

In another publication, the PIOPED II investigators recommended several diagnostic pathways based on clinical pretest probability. They point out that a negative CT angiogram in a low-risk patient has an excellent negative predictive value (96%) and recommend against treatment in this group. They point out a slightly improved negative predictive value (97%) when CT venography (CTV) of the lower extremities is also performed, although controversy exists about this technique because the small additional diagnostic yield comes at the cost of considerable additional radiation exposure. Notably, they recommend additional diagnostic testing in low pretest probability patients with positive CT angiography results resulting from positive predictive values of only 68% for segmental PE and 25% for subsegmental PE. Segmental and subsegmental filling defects on CT are more prone to interobserver error and may result from poor contrast bolus or other artifacts, rather than PE. They are therefore less predictive of PE. If CT demonstrates main or lobar PE, for which positive predictive value is high (97%), the PIOPED investigators recommend treatment without further testing. Filling defects in main or lobar pulmonary arteries are usually readily recognized and easily distinguished from artifact; therefore, they are more predictive of PE.

For patients with moderate pretest probability assessment, the PIOPED II authors suggest treatment in accordance with CT results without further diagnostic testing because of good negative and positive predictive values in this group (89% and 92%, respectively). In patients with high-probability clinical assessment, they recommend treatment for positive CT findings (positive predictive value = 96%) but further workup if CT is negative because of a negative predictive value of only 60% for CT angiography and 82% for CT angiography plus lower extremity CTV.

These recommendations from PIOPED II may be unnecessarily conservative, because they reflect a disease-oriented outcome based on CT sensitivity, not based on patient outcome. PIOPED II did follow patients to 3 and 6 months by phone interview, but the clinical outcomes of patients with negative CT were not reported. It is not clear from the study that PEs missed by CT scan resulted in patient deaths or significant morbidity. Other studies have shown a very low yield of routine lower extremity imaging for DVT in asymptomatic patients with negative chest CT. Rates of additional DVT found using this technique are as low as 0.7% to 2.7%, with costs as high as $200,000 per additional isolated DVT diagnosed. An overall algorithm incorporating pretest probability and CT results in shown in Table 7-4 .


Pretest Probability and CT Results

Pretest Probability of Pulmonary Embolism CT SCAN RESULT
Segmental or Subsegmental Pulmonary Embolism Main or Lobar Pulmonary Embolism
Low probability Excludes PE Does not completely confirm PE; consider additional imaging to confirm diagnosis (repeat CT, VQ, pulmonary angiogram, or lower extremity imaging for DVT) Confirms PE
Moderate probability PE unlikely, but consider lower extremity imaging for DVT Confirms PE Confirms PE
High probability Does not completely exclude PE; consider additional imaging to confirm diagnosis (VQ, pulmonary angiography, or lower extremity imaging for DVT) Confirms PE Confirms PE

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Jul 4, 2019 | Posted by in GENERAL RADIOLOGY | Comments Off on Imaging of Pulmonary Embolism and Nontraumatic Aortic Pathology

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