Pneumonia

CXR and chest imaging are generally of limited value in upper respiratory infections. On CXR, pneumonia manifests as areas of increased density within the pulmonary parenchyma. The increased density is usually focal but may be multifocal or diffuse. Depending on the causative organism and the health and immune status of the patient, the density may manifest as confluent parenchymal consolidation (where vessels are obscured within the density), as hazy ground glass density (where vessel margins can be detected within the density), or as coarse reticular or reticulonodular opacities. These densities may be marginated by pleural or fissural boundaries. If available, the use of both posteroanterior (PA) and lateral projections is often helpful in detecting, confirming, or localizing areas of increased parenchymal density (Figs. 8-2 and 8-3).

Figure 8-2 Chest x-ray of a patient with pneumonia. A, Posteroanterior view reveals a patchy opacity overlying the left lung base (large arrow). Note that the left cardiac border is preserved, indicating that the pneumonia is more likely in the left lower lobe. If it were lingular and abutting the left cardiac border, the left cardiac border would be obscured (the “silhouette” sign). B, The lateral view confirms left lower lobe location of the pneumonia, as indicated by increased density of the lower thoracic vertebral bodies (arrow). Normally, on a lateral chest x-ray, the thoracic vertebral bodies become increasingly lucent from superior to inferior. Increased density of lower thoracic vertebral bodies indicates the presence of radiodense material (in this case, a left lower lobe pneumonia) attenuating the x-ray beam.

Figure 8-3 Chest x-ray of another patient with pneumonia. A, Posteroanterior view reveals a faint opacity overlying the right lung base (arrows). The density does not abut the right heart or diaphragm, and thus the “silhouette” sign is of no help in determining middle versus lower lobe location. B, The lateral view reveals increased density overlying the heart (longer arrow), confined by the major fissure (shorter arrows), indicating right middle lobe location of the pneumonia. Note the vertebral bodies become more lucent from superior to inferior, indicating the absence of lower lobe processes overlying the vertebrae.

Heart Failure

There were 5.2 million ED visits for congestive heart failure (CHF) in 2004. At age 40, the lifetime risk of developing CHF for both men and women is one in five. Progression or exacerbation of CHF can cause dyspnea due to pulmonary vascular congestion or its more advanced form, pulmonary edema. Pulmonary edema can be classified as of hydrostatic origin (increased intravascular pressure, as in left ventricular failure or volume overload) or of permeability origin (increased permeability of the pulmonary alveolar-capillary membrane, as in acute respiratory distress syndrome [ARDS]). Although there is likely some overlap in the pathophysiology, the etiology of pulmonary edema cannot routinely be distinguished by CXR.

The sequence by which CHF leads to pulmonary edema and may manifest on CXR is familiar. Left ventricular failure results in increased pressure within the pulmonary venous system leading to pulmonary venous distention. The increased size of pulmonary veins on CXR, particularly in the upper lobes, manifests as “cephalization,” for which the determination can be relatively subjective at imaging. As pulmonary venous capacitance is exceeded, pulmonary vessels begin to leak transudative fluid into the pulmonary interstitium, including the septal, peribronchial, and perivascular spaces, and into the pleural space. The CXR correlates include septal lines (or “Kerley B” lines), peribronchial cuffing, indistinctness of vessel margins, and pleural effusions, respectively. With further progression, fluid begins to accumulate in alveolar spaces resulting in more confluent density that obscures vessel margins but in contrast accentuates the appearance of bronchial airways resulting in air bronchograms (Fig. 8-4).

Figure 8-4 Patient with cardiomegaly and recurrent episodes of congestive heart failure. A, Posteroanterior view obtained when the patient was otherwise healthy reveals grossly clear lungs and cardiomegaly. There is a normal paucity of lung markings at the periphery of the lungs near the pleural margins. B, A posteroanterior view obtained when the patient was in congestive heart failure with pulmonary edema reveals diffusely increased lung markings and faint opacification at the bases. C, A magnified view of the right lung base reveals prominent septal markings in the subpleural lung periphery, or “Kerley B” lines (arrow), as well as more consolidated density overlying the right lung base (asterisk).

CT of the Pulmonary Parenchyma

Computed tomography allows for more refined analysis of the pulmonary parenchyma. Similar to CXR, pulmonary parenchymal pathology is detected by changes in parenchymal density and architecture. With section thicknesses of 2 mm or less, axial images allow for evaluation of pulmonary parenchymal architecture at the level of the secondary pulmonary lobule, the smallest unit of lung structure marginated by connective tissue septa. The secondary pulmonary lobule consists of small and terminal bronchioles (accompanied by terminal arterioles) along with their associated acini (usually 12 or fewer in number). This complex of terminal bronchovascular structures and their associated acini is confined by interlobular septae. The interlobular septae contain pulmonary veins and pulmonary lymphatics, the latter also found along the bronchovascular complex. Changes to the architecture of the secondary pulmonary lobule occur in a multitude of disease processes, and characterization of the architectural changes allows for refinement of differential diagnostic considerations. Of course, larger-order anatomy is clearly defined by CT as well.

Changes to the architecture and density of the secondary pulmonary lobule can be organized according to the structures involved, including peripherally located septal structures, centrally located bronchovascular structures, and more generalized abnormalities affecting both. A detailed instruction on CT of pulmonary parenchyma is beyond the scope of this chapter, but several excellent resources are available on this subject, including the Requisites text on thoracic radiology. However, a general overview of the differential considerations associated with architectural derangements described above is useful, and a brief synopsis is provided below.

Septal thickening may be smooth, nodular, or irregular. Differential considerations for smooth septal thickening include pulmonary edema (with septal thickening being the equivalent of “Kerley B” lines seen on CXR) or ARDS, and pneumonia or pulmonary hemorrhage (Fig. 8-5). Septal thickening seen with these entities may be associated with “ground glass” density, the so-called crazy paving pattern. The “crazy paving” pattern has also been described as characteristic of alveolar proteinosis. Nodular septal thickening may be seen in lymphangitic metastases as well as sarcoidosis and silicosis. Nodules seen in sarcoidosis are characterized as perilymphatic, and thus may be centrilobular or septal (lymphatics are associated with both the septae and bronchovascular structures). Pulmonary fibrosis may also result in septal thickening, which may be irregular in nature and may be associated with honeycombing or other common findings of fibrosis, such as traction bronchiectasis.

Figure 8-5 Patient with congestive heart failure and pulmonary edema. Thickened interlobular septae (arrows) define the borders of the intervening secondary pulmonary lobules. Additional findings that may be seen in congestive heart failure/pulmonary edema are shown, including centrilobular opacities (white oval), ground glass opacity (black oval), and pleural fluid seen posteriorly (single asterisk) and within the major fissure (double asterisks).

Centrilobular opacities or nodules generally imply abnormalities of the small airways or vascular diseases, and are usually related to bronchiolitis of varying etiologies. The combination of centrilobular opacities/nodules with dilated/opacified bronchioles has been termed the “tree-in-bud” sign (Fig. 8-6). In the ED, centrilobular opacities/nodules are usually seen in the setting of an infectious bronchiolitis that may be due to bacterial or atypical organisms. Pulmonary aspiration can give a similar appearance. Other differential considerations for centrilobular opacities/nodules include pulmonary edema and hemorrhage, vasculitis, bronchoalveolar cell carcinoma, acute or subacute hypersensitivity pneumonitis, noninfectious bronchiolitis (as can be seen in smoking-related interstitial lung disease/respiratory bronchiolitis), and panbronchiolitis.

Figure 8-6 Examples of centrilobular opacities (arrows) and the “tree-in-bud” sign (ovals) in a patient with a history of nonspecific interstitial lung disease who presented with an acute cough. Subsequent CT scan (images not provided) showed resolution of the centrilobular opacities, which were therefore presumed infectious (bronchiolitis or bronchopneumonia) in etiology.

More generalized (panlobular) processes may lead to either ground glass or more consolidated opacities. If ground glass opacities are detected, the differential diagnosis is assisted by identification of ancillary findings. Ground glass opacities in the presence of honeycombing or other findings of fibrosis should point toward differential considerations among fibrotic lung diseases. Ground glass opacities in the presence of septal thickening (“crazy paving” pattern) should raise differential considerations including pulmonary edema, pneumonias of varying etiologies, and pulmonary hemorrhage, as well as entities less commonly encountered in the ED, including hypersensitivity pneumonitis, ARDS, and alveolar proteinosis. If ground glass opacities are encountered in the absence of ancillary findings the differential considerations become even broader and include interstitial pneumonia, infection, and drug reaction, in addition to the entities listed above (Fig. 8-7). Differential considerations for more consolidated densities include entities such as pneumonias, pulmonary edema, ARDS, and pulmonary hemorrhage, as well as acute eosinophilic pneumonia, masses, and fibrotic processes. Familiarity with the concept of evaluating pulmonary parenchyma based on analysis of the structures of the secondary pulmonary lobule will serve emergency radiologists well in their approach to formulating differential diagnoses for parenchymal disease.

Figure 8-7 Example of ground glass opacities due to pulmonary edema in a postpartum patient with a history of preeclampsia, who presented with leg swelling and shortness of breath. Note the patchy hazy density that does not obscure the underlying vascular structures.

Chest CT Techniques and Protocols

This section outlines general principles guiding the selection of CT techniques and scan parameters. While there can be wide variability between scanner types and manufacturers in technological capabilities, nomenclature, and technical detail, the basic underlying considerations are applicable across these platforms. A working knowledge of these considerations can aid the radiologist in optimizing CT scan performance while remaining good stewards of radiation safety.

Indication-specific CT Protocol Techniques

Routine Chest CT

This is often performed without IVCM to further assess a radiographic parenchymal abnormality (e.g., pulmonary nodule). However, IVCM is helpful for assessment of empyema or mediastinal or hilar abnormalities.

Pulmonary Embolus CTA

A typical protocol includes bolus detection on the main pulmonary artery, followed by a breathhold delay and scanning in the caudal to cranial direction. Most other thoracic CT protocols utilize a cranial to caudal scan direction. This scan direction is often reversed in pulmonary embolus CTA (CTPA) in order to minimize respiratory motion artifact in the lower lobes, where the majority of pulmonary emboli occur.

If a lower extremity venogram is not included, a high-quality CTPA may be performed with approximately 80 mL of IV contrast injected at 4 mL per second. If a lower extremity venogram is performed following CTPA, 100 to 125 mL of IVCM are instead needed, and images are acquired at intervals from the pelvis to the knees after an approximately 3-minute delay.

Upper Extremity Deep Venous Thrombosis or Superior Vena Cava Syndrome

A delayed venous phase scan should be performed if there is high clinical suspicion for upper extremity or central vein thrombosis. The delayed phase produces more uniform venous opacification and eliminates the mixing artifacts typically observed from dense IVCM injected through one arm mixing in the SVC with the unopacified blood arriving from the other arm (Fig. 8-8). Coronal reformations can greatly aid diagnosis.

Figure 8-8 Superior vena cava (SVC) thrombus following recent central line removal. A, Early phase axial image. Dense contrast in the SVC (curved arrow) produces streak artifact that partially obscures the SVC thrombus (arrow) and makes it difficult to differentiate streak artifact from mixing artifact with unopacified blood from the left brachiocephalic vein. B, Delayed (90 seconds) phase axial image eliminates streak and mixing artifacts.

Aortic Dissection CTA

Currently, full dissection CTA protocols may include:

• A noncontrast scan of the chest only.

• An arterial phase scan through the chest (+/- abdomen and pelvis) performed either with or without cardiac gating.

• A delayed phase scan through the chest, abdomen, and pelvis.

The initial noncontrast scan is used to assess for a thrombosed false lumen or isolated intramural hematoma, both of which will appear denser than the unopacified blood in the aortic lumen. If a noncontrast scan was not initially obtained (such as a pulmonary embolus CTA study), a 20- to 30-minute postcontrast delayed scan can be obtained, as IVCM will have adequately cleared the intravascular space. This permits the radiologist to troubleshoot the rare case in which a contrast-enhanced scan may raise suspicion for isolated intramural hematoma but is not sufficiently diagnostic for the radiologist.

The arterial phase scan is often performed with cardiac gating in order to reduce the pulsation artifact, which can mimic focal aortic dissection at the aortic root. However, this artifact has a characteristic appearance on axial and MPR images, and can typically be readily differentiated from aortic dissection (Fig. 8-9). If the radiologist is readily familiar with this diagnostic pitfall, a nongated arterial phase scan can be used so as to reduce radiation exposure, which is significantly greater on cardiac-gated scans. If cardiac gating is utilized, a regular heart rate is required, preferably 65 or fewer beats per minute. For younger ED patients (generally younger than 50 years old) with a low pretest probability of aortic dissection and a low incidence of significant atherosclerotic disease, we screen with a physician-monitored, nongated, contrast-enhanced chest CT only in order to reduce the radiation exposure from multiple phase protocols. If needed, additional scanning can be readily undertaken if results of this scan show anything other than a normal aorta. Very rarely is this necessary.

Figure 8-9 Pulsation artifact: typical aortic root pulsation artifact from a non-gated study, not to be confused with aortic dissection. A, A sharply defined band of low-density artifact (longer arrow) extends across the left side of the proximal ascending aorta. The artifact extends beyond the aortic margin to the right atrial appendage (shorter arrow), helping to confirm its artifactual nature. B, Sagittal reformation showing motion artifacts (arrows) arising in each cardiac cycle. C, Repeat study performed the following day with cardiac gating, eliminating the cardiac motion artifact.

The CT scan through the abdomen and pelvis is performed to assess distal extension of the intimomedial flap, involvement of visceral or iliac arteries, and end organ ischemia. Therefore, it should be prescribed as routine in high-risk patients or those with known aortic dissection presenting with acute symptoms. But the abdomen and pelvis can be scanned selectively in patients with low pretest probability. For those in whom dissection was identified by active physician monitoring of the screening chest CT, the scan can readily be continued through the abdomen and pelvis during the arterial phase with delayed imaging acquired as needed. This is a viable option for institutions with radiologists who can actively monitor CT acquisitions while the patient is on the gantry table. Although the 24/7 operations of the ED can make this challenging to implement during nonbusiness hours, greater organization around the practice of emergency radiology is likely to make this more feasible in the future.

Pneumomediastinum and/or Evaluation of Esophageal Injury

In the ED, CT is often used rather than fluoroscopy to assess for possible esophageal injury. The scan protocol should include an initial scan with neither oral nor intravenous contrast. Subsequently, the patient should take a few swallows of Gastrografin, and a repeat scan (with or without intravenous contrast, depending on indication) should be performed. The “scout” noncontrast scan is included in order to readily differentiate Gastrografin extravasation from soft tissue calcification or a small foreign body (e.g., a fish bone). Because both gas and contrast material extravasation are intrinsically high-contrast evaluations, low-dose techniques can be used to reduce radiation exposure.

Coronary CTA

There can be significant variability in CT scan technique depending on local CT scanner technology and institutional decisions about whether to perform a focused coronary CTA only or a “triple rule-out” that simultaneously assesses the aorta and pulmonary and coronary arteries. The numerous variables and technical details are beyond the scope of this chapter. Briefly, however, the study may be prescribed from a topogram or a low-dose unenhanced chest CT performed for calcium scoring. The CTA is then either initiated by automated bolus detection or, following a scan delay, derived from a test bolus. Cardiac gating is required, preferably with a heart rate equal to or less than 65 beats per minute. Tube current dose modulation schemes, if available, are recommended to reduce the associated radiation exposure by limiting tube current during the systolic portion of the cardiac cycle. Images are reconstructed at multiple intervals of the cardiac cycle to permit identification of image sets free of cardiac motion artifact. Numerous efforts in CT scanner technology are aimed at optimizing coronary CTA evaluation. As these technological advances are exploited through innovative clinical applications, CT protocols and scanning requirements for coronary CTA are likely to evolve in the short term.

The Pleura

The pleura is a specialized tissue layer covering the lungs and the internal surface of the chest cavity. The visceral and parietal components form a continuous layer and create a potential cavity, the pleural space, which is generally visualized radiographically only when local or systemic pathology develops. Normally a small amount of fluid (15 to 20 mL) lies in each pleural cavity and lubricates the sliding lung surface during the respiratory cycle. Pleural fluid originates in the interstitium and is drawn away from the pleural space along a gradient toward the low-pressure pleural capillaries, ultimately draining into the pulmonary venous system. Pleural fluid is continuously secreted and absorbed; disruption of this equilibrium leads to effusion.

The pleural space is maintained below ambient pressure by chest wall recoil, the actions of gravity, and muscular contraction of the diaphragm. Loss of vacuum integrity leads to rapid collapse of the lung airspaces.

Pericardium

The pericardium is an investing connective tissue layer covering the heart and proximal great vessels, separating the cardiac structures from the remainder of the middle mediastinum.

Hemopericardium

Hemopericardium is most often the result of acute blunt or penetrating trauma, from direct pericardial damage, myocardial contusion, or proximal aortic injury. Hemorrhage into the pericardial sac can rapidly lead to tamponade and circulatory collapse. In the absence of a history of trauma, type A aortic dissection, coronary artery aneurysm rupture, or postinfarct cardiac rupture must be considered. However, a dense pericardial effusion is not a sine qua non of hemopericardium or incipient tamponade. Radiographic and CT findings must be interpreted in conjunction with history and physical exam findings. Echocardiography should be performed if there are features causing concern for hemodynamic compromise (Fig. 8-10).

Figure 8-10 Axial CT images showing hemopericardium (white arrows) secondary to type A aortic dissection (black arrows indicate type A dissection flap within the ascending aorta; apparent duplication of the flap may be due to motion). Dissection extending into the descending thoracic aorta, with a hyperdense true lumen (curved arrow) and hypodense false lumen (asterisk), is noted.

Mediastinum

Pneumomediastinum

Typical causes of pneumomediastinum include trauma, asthma, drug use (Valsalva-induced), infection, and spontaneous pneumomediastinum. Traumatic causes (other than typical blunt or penetrating external trauma) may be the result of scope, tube, or line insertion (i.e., iatrogenic), positive pressure ventilation, or internal barotrauma related to vomiting (Boerhaave syndrome) or coughing against a closed glottis (Fig. 8-11). Pneumomediastinum generally requires no treatment apart from addressing the underlying cause.

Figure 8-11 CT showing spontaneous pneumomediastinum (black and white arrows) in an asthmatic patient.

SVC Syndrome

SVC syndrome refers to the development of facial and upper extremity edema, swelling, and collateral venous engorgement secondary to superior vena cava obstruction. Associated findings include upper body erythema, confusion, chest pain, and hoarseness. In the developed world, most cases are related to malignant invasion of the SVC. Historically, tuberculous infection and syphilitic aneurysm were more common causes. Indwelling central catheters have come to play a larger role in recent years and can lead to SVC syndrome via stricture and thrombosis. Other causes of SVC syndrome include extrinsic compression by aneurysm or lymphadenopathy and fibrosing mediastinitis usually secondary to the inflammatory response elicited by infection with Histoplasmosis capsulatum. In younger patients, benign causes predominate. Malignancy is the most common cause over age 40.

Because SVC obstruction impairs venous drainage of the head and neck, cerebral and laryngeal edema may occur. For these reasons, the development of SVC syndrome is considered a medical emergency, although only a minority of patients are at risk of death from cerebral edema.

CXR may reveal a mediastinal abnormality in patients with clinically suspected SVC syndrome, such as a mediastinal mass or lymphadenopathy. Contrast-enhanced CT and MR angiography are the most reliable noninvasive methods of definitive diagnosis. CT is generally preferred as the initial study, owing to the prevalence of lung cancer and lymphoma as causative factors in the adult population and the ease and accuracy with which CT delineates these findings (Fig. 8-12).

Figure 8-12 SVC syndrome: axial and coronal contrast-enhanced CT. Multiple collaterals and dilatation of azygos and internal mammary veins (arrows) in a patient with severe SVC narrowing due to tumor mass encasement (oval).

Relevant CT Anatomy

On axial sections, the aorta is generally round and its diameter should gradually taper more distally as vessels branch from its lumen, although there are some notable exceptions that represent normal variants in its size and shape. It is important to be familiar with the appearance of these variants at imaging so that they are not mistaken for disease.

Normal variants of the aortic contour identified on CTA are best recognized on MPR or three-dimensional (3D) images; these include the aortic spindle, ductus diverticulum, branch vessel diverticula, and pseudocoarctation. The aortic spindle is a smooth circumferential bulge below the region of the isthmus, representing normal mild dilatation of the region of the posterior arch. The ductus diverticulum is a focal convex bulge along the anterior undersurface of the aortic isthmus. The obtuse angles it forms with the aorta can be used to help distinguish it from a post-traumatic pseudoaneurysm, which more characteristically forms acute angles with the aortic wall. Branch vessel diverticula show smooth obtuse margins with a branch vessel emanating from the apex of the infundibulum. These too can be mistaken for a post-traumatic pseudoaneurysm at a branch vessel origin. Recognition of these is aided by their tendency to occur in characteristic locations, such as the left subclavian artery and the third right intercostal artery. Pseudocoarctation results from elongation of the aortic arch, which characteristically results in kinking at the site where the aorta is tethered by the ligamentum arteriosum. Aortic wall thickness is best evaluated on axial CT images. Imaging of healthy adults has shown that the aortic wall thickness is less than 1 mm or imperceptible on axial CTA images.

Aneurysm

Thoracic aortic aneurysm is defined as an aortic size that is 50% greater than the expected aortic diameter. However, in practice, a 5-cm axial dimension is most often used since intervention is otherwise rarely considered in the asymptomatic patient. Distal aortic segments should generally be smaller in diameter than more proximal segments except for the previously noted anatomic variants. If this relationship is reversed, aortic monitoring for aneurysm development should be considered. CT can characterize thoracic aneurysms by their location and shape. Three fourths of aortic aneurysms are atherosclerotic in etiology, fusiform in shape, and located in the descending aorta. However, approximately 20% of atherosclerotic aneurysms are saccular, particularly in the arch and descending portions. Incidence of aortic rupture is related to aneurysm size. An important goal for imaging is to provide accurate measurements. Conventional catheter-based aortography underestimates true aortic diameter, as it reflects only the size of the patent lumen and does not include contributions from intraluminal thrombus or mural thickening. CT accurately evaluates aneurysm dimensions, the extent of intralumenal thrombus and mural thickening, the integrity of the aortic wall, and its relationship with contiguous structures. The chapter in this text on vascular emergencies contains a more detailed section on thoracic and abdominal aortic aneurysms and their complications. Thoracic aortic aneurysms carry a high incidence of concomitant abdominal aortic aneurysms such that screening of the abdomen should generally be undertaken with CT or US when thoracic aneurysm is detected.

Infectious Aortitis

An infected aorta, whether normal caliber or aneurysmal, can represent a diagnostic challenge, as patients may be asymptomatic until late stages or may present with nonspecific clinical symptoms. Nearly 50% of infected aneurysms occur in the thoracic or thoracoabdominal aorta, a significantly higher than expected rate given distribution of atherosclerotic aortic aneurysms. More than 90% show a saccular morphology, often lobulated. Early detection by CT can permit intervention before a rapidly progressive course with sepsis and/or rupture. CT reveals subtle periaortic edema, stranding, and fluid in the initial stages. Rim enhancement of periaortic soft tissues followed by disruption or loss of intimal calcifications often precedes aortic enlargement. Close follow-up CT is advised since development of large aneurysms and marked growth have been reported in short intervals. An infected aorta may also maintain a normal caliber. Periaortic gas and gas within the aortic wall are specific findings but are seen in less than 10% of cases. Lack of mural calcification within an aneurysm suggests a nonatherosclerotic etiology and therefore raises greater concern for infection. Nuclear scintigraphy with labeled leukocytes or gallium-67, when correlated with CT findings, can increase confidence in this diagnosis.

Syphilis, a now infrequent cause of infectious aortitis, has a typical course that can be assessed by CT. CT demonstrates enlargement of the aorta, which progresses to an aneurysm formation that most commonly involves the ascending portion or arch. Most syphilitic aneurysms are saccular, but about 25% are fusiform. The pattern of fine and pencil-line dystrophic calcification is characteristically seen. However, this finding is often obscured by thick, irregular, coarse calcifications of secondary atherosclerosis.

Aortic Dissection

Aortic dissection occurs when intravascular blood breaches the intima and dissects within the media of the aortic wall. Imaging is critical for establishing this diagnosis and for guiding medical or surgical intervention. Chest radiography continues to play a role in the initial assessment of patients with suspected aortic dissection, principally because it provides readily available diagnostic information that helps to exclude other differential considerations (e.g., pneumothorax). Its value is otherwise limited, since a normal CXR cannot exclude, nor can an abnormal CXR confirm, aortic dissection. Findings of aortic and/or mediastinal widening lack specificity and require further evaluation with cross-sectional imaging, while up to 25% of dissection cases will appear normal at radiography. Patients for whom radiography provides insufficient alternate explanation of their symptoms and for whom aortic dissection remains a diagnostic consideration must undergo cross-sectional imaging to exclude dissection.

CT, MRI, and transesophageal echo (TEE) have all been utilized for the diagnosis of acute dissection. CT compares well with MRI and TEE. Although all three modalities were reported to have 100% sensitivity, specificity was highest for CT at 100%. Aortography has a sensitivity of only 88% with false negative diagnoses often related to thrombosed or faint opacification of the false lumen, equal opacification of true and false lumen, unusual intimal tears, and intimal tears proximal to the catheter tip. When CT findings were directly compared with surgical findings, Yoshida found 100% accuracy, sensitivity, and specificity for CT. CT was also effective in identifying the entry site of the intimal tear, as well as determining whether there was pericardial effusion or aortic arch involvement, with 95% sensitivity and 100% specificity as confirmed with surgical results. The advantage of CT in aortic arch involvement has also been confirmed by Sommer, who found a sensitivity/specificity of 93%/97% for CT, compared with 60%/85% for TEE and 67%/88% for MRI.

The principal criterion for CT diagnosis of aortic dissection is the presence of an intimomedial flap separating the true lumen from the false lumen. After intravenous contrast administration, the false lumen may opacify completely, partially, or, if thrombosed, not at all. An intimal flap was identified in 70% of conventional CT studies but has been reported in 100% of volumetric CT studies. Secondary findings, which are less specific but may be helpful in equivocal cases, include displacement of intimal calcifications toward the lumen, aortic widening, and mediastinal and pleural hemorrhage. Calcification of neointimized mural thrombus can occasionally mimic displaced intimal calcifications and lead to false positive diagnosis if not recognized.