Nontraumatic Emergency Radiology of the Thorax

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CHAPTER 8 Nontraumatic Emergency Radiology of the Thorax

An emergency medicine physician once told a bright-eyed medical student on the first clinical shift:

While that is a rather spartan synopsis of nontraumatic thoracic pathology encountered in the emergency department (ED), the underlying tenet stands up well in the practical evaluation of ED patients presenting with chest pain and other symptoms. Accordingly, this chapter on nontraumatic emergency thoracic radiology is organized primarily around evaluation of these entities, beginning with a review of chest radiography technique, and followed by sections on the pleura/mediastinum, aortic diseases, pulmonary embolism, and acute coronary syndrome (ACS). Lung parenchymal findings are covered with less emphasis, but are readily available with greater detail in other texts, such as Thoracic Radiology: The Requisites.

Multidetector computed tomography (MDCT) technique deserves and receives special emphasis in this chapter because it has overtaken and continues to overtake other imaging modalities for chest evaluation in ED patients. Clinicians have become enamored with the rapid, highly accurate, and thereby efficient diagnostic capability CT provides. The CT industry and the radiology profession continue to further these advantages with faster, higher-resolution scanners allowing for greater clinical applications and increasingly refined diagnoses. Similarly, the pressure for greater diagnostic sensitivity and specificity in the ED is at odds with decreased imaging utilization. The volume of chest CT exams ordered by ED physicians will almost certainly continue to rise. Perhaps the only significant counterbalance to increased utilization is the concern for population radiation exposure and the associated risk of cancers induced by ionizing radiation. Radiologists should be familiar with and sensitive to these concerns, readily able to advise clinicians and protect patients by being good stewards of radiation safety.


In a clinical environment where radiologists and ED physicians frequently have available “high-tech” CT scanners with dozens, even hundreds of detector rows, multiple radiograph sources, and electrocardiographic (EKG) gating, it is tempting to neglect or dismiss the value of the “low-tech” chest x-ray (CXR). However, neglecting the CXR and failing to develop the knowledge and skills needed for expert CXR interpretation is a mistake. Despite the advances in CT technology, the CXR remains the mainstay of first-line imaging for ED patients with chest complaints. The 2004 National Hospital Ambulatory Medical Survey (NHAMES) recorded 110.2 million ED visits, which resulted in 20.19 million CXRs performed. Indeed, a CXR is the most often ordered imaging exam as part of an ED patient visit. This compares to totals of approximately 22 million for all other x-rays combined, and 10.3 million for CT or magnetic resonance imaging (MRI) (the CT and MRI data were combined in the NHAMES report). Therefore, the emergency radiologist needs to have highly developed interpretive skills for chest radiography. Detailed instruction on CXR interpretation is well beyond the scope of this chapter, but many excellent sources are available for this, including the Requisites text on thoracic radiology.

One principle that serves radiologists well is the establishment of a systematic pattern through which the interpreter progresses as he or she reads a CXR. While naturally drawn to look at the lungs, and while evaluation of pulmonary parenchyma is paramount, the interpreter must unerringly include assessment of extrapulmonary anatomy on every CXR. This includes evaluation of anatomy below the diaphragm, of lung parenchyma posterior to the diaphragm, of the bony thorax, spine, shoulders, and chest wall soft tissues, of the heart contours, mediastinum, and pulmonary hila, of pleural surfaces and interfaces, and of complex areas such as the pulmonary apices. Establishing a pattern of evaluation that systematically includes all of the anatomy encountered on a CXR will serve to avoid unfortunate errors of CXR interpretation (Fig. 8-1).

For evaluation of the lung parenchyma, CXR has been in use for nearly a century. Pulmonary pathology is detected primarily by changes in pulmonary parenchymal density, as either decreased parenchymal density (cystic lung diseases and pneumothorax) or increased parenchymal density (masses, fluid, infection, fibrosis, or atelectasis). Roughly 10.3% of ED visits fall within the category of respiratory diseases, with 3.1% due to upper respiratory infections, 1.7% due to asthma, and 1.4% due to pneumonia (3.4% in patients over 65 years old).


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).

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).


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.

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.

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.

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.

Patient Screening

Scan Protocol Considerations

Contrast Timing Principles and Techniques

Care must be taken to optimize the timing of the CT scan relative to the injection rate, injection profile, and duration of IVCM administration. The specific timing details vary greatly depending on the duration of the scan (which depends greatly on the CT technology in use), and on the flow rate and quantity of injected contrast material. As a general rule of thumb, IV contrast should be injected at a minimum rate of 3 mL per second for CT evaluation of pulmonary embolus, aortic dissection, or traumatic aortic injury. Higher flow rates of 4 or more mL per second are preferable, but they shorten the duration of the contrast bolus. As a result, scan timing must be scrutinized to ensure that contrast opacification remains adequate throughout all portions of the scan.

Three techniques are commonly used to determine the initial scan delay after the start of IVCM injection:

Radiation Exposure and Techniques for Dose Reduction

Emergent (and overall) CT utilization continues to rise rapidly as a result of further technological advances, additional clinical applications, and greater CT availability. The associated radiation risks due to individual exposures, as well as population exposure levels, are gaining attention. The momentum behind these concerns will almost certainly lead to greater scrutiny around CT use. Radiologists are compelled to heed these concerns and to show that they are doing their part to optimize techniques that will reduce radiation exposure while maintaining high-quality imaging. Likewise, medical vendors are eager to advance their imaging technologies with tools that allow for reduced exposure. A variety of techniques exist to control patient exposure during CT. Radiologists should have a working knowledge of these techniques.

Many current CT scanners (and virtually all new scanners) include the capacity for automatic exposure control and dose modulation. In general, these functions should be enabled when available. Automatic exposure control adjusts the overall x-ray tube current to a predetermined quality or noise standard, or reference milliAmpere per second (mAs). Dose modulation rapidly adjusts tube output during the scan, either along the axis of the patient (longitudinal modulation) or during the gantry rotation around the patient (angular modulation) as the patient’s thickness and density vary in these directions. Additionally, most scanners intended for cardiac CT offer the capability for ECG-dose modulation, in which x-ray tube output is greatly reduced during systole.

Imaging of structures with a high degree of intrinsic tissue contrast can tolerate a higher level of noise than imaging structures of near uniform CT density. Both routine chest CT and CTA often involve inherently high-contrast structures, allowing for lower-dose techniques to be used. Dose reduction during CTA has been successfully performed without detriment to image quality by reducing kilovoltage (kV) to match the low K-edge of iodine in contrast-enhanced vessels.

Bismuth breast and thyroid shields have been successfully used to reduce doses to these radiation-sensitive organs by preferentially attenuating the lower-energy x-rays that do not contribute significantly to image quality. These are expected to play a more widespread role during CT imaging, particularly of younger patients.

Indication-specific CT Protocol Techniques

Aortic Dissection CTA

Currently, full dissection CTA protocols may include:

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.

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.


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.


Pneumothorax is the presence of air within the pleural space. The etiologies of pneumothorax are multifactorial (Table 8-1). The most common imaging test performed to assess for pneumothorax is the chest radiograph, or CXR. Ideally, this is performed with upright patient positioning so that the air–pleural interface can be readily identified toward the apices. Expiratory imaging may accentuate the contrast between lung tissue and intrapleural gas. This method may be particularly helpful for smaller pneumothoraces, but is generally not required. The presence of pneumothorax is often more subtle on supine radiography, and small pneumothoraces can be easily overlooked.

Table 8-1 Etiologies of Pneumothorax

Etiology Types
Trauma Penetrating or blunt; barotrauma
Idiopathic Primary or secondary
Iatrogenic Following biopsy, surgery, central line placement, thoracentesis, mechanical ventilation, bronchoscopy
Infection Pneumocystis carinii, necrotizing pneumonia
Neoplastic Langerhans’ cell histiocytosis, sarcoma, lung cancer, various others
Congenital/Acquired Emphysema, congenital bullae, lymphangioleiomyomatosis

Spontaneous pneumothorax occurs more frequently in smokers, asthmatics, and thin young men. The relative risk for male smokers is up to 20 times higher than for nonsmoking males. Risk increases in a linear relationship to the amount of smoking. Blebs are often found at thoracoscopy of patients presenting with spontaneous pneumothorax, and can be visualized by CT in up to 89% of patients. For this reason, chest CT is often ordered as a follow-on study to a CXR showing an unexpected spontaneous pneumothorax.

Primary spontaneous pneumothorax is differentiated from secondary spontaneous pneumothorax by the absence of underlying lung disease. Secondary spontaneous pneumothorax is due to underlying pleural or parenchymal disease, usually in the form of blebs or cysts. These may result from disease entities such as emphysema, Pneumocystis carinii pneumonia infection, or lymphangioleiomyomatosis. Spontaneous pneumothorax is sufficiently common as a component of the differential diagnosis for chest pain and dyspnea that a high index of suspicion should be maintained when evaluating routine chest radiographs for these indications. The frequency of central line placement in the ED is another reason to maintain a high index of suspicion for pneumothorax when evaluating all ED chest radiographs.

A tension pneumothorax occurs when air enters but cannot exit the pleural space. This can occur when the pleural defect allowing air passage into the pleural cavity mechanically functions like a ball-valve resulting in unidirectional air transit. The increasing intrapleural gas creates mass effect, and eventually can displace the mediastinum and compromise venous blood return to the heart. Progressive accumulation of air in the pleural cavity can lead to cardiovascular impairment and, if left untreated, death. Tension pneumothorax should be suspected when the trachea, heart, and/or mediastinum have been displaced from the midline, when the ipsilateral rib spaces have widened, and/or when the contralateral lung appears relatively compressed.

Several estimation methods for pneumothorax size are based on CXR measurements, but these are subject to wide interobserver variations in practice. A pragmatic rule of thumb is that a large pneumothorax is one that completely dehisces from the chest wall, while a small one does so only partially. This simple criterion identifies the majority of pneumothoraces requiring evacuation. If there is ambiguity as to whether an apical lucency represents intrapleural air or a large bulla, CT is generally definitive. Chest CT also permits volumetric or percent measurements of pneumothorax size that are more precise, although intervention usually occurs prior to CT evaluation.

Small pneumothoraces are usually followed radiographically to resolution. Failure of resolution and interval enlargement are common indications for invasive management. The treatment for a large pneumothorax (generally 15% or more of the hemithorax) is air aspiration or evacuation by intercostal chest tube or catheter. The radiologist should be familiar with the normal locations for appropriately inserted chest tubes. Intraparenchymal, extrathoracic, and interlobar placements should be communicated to the treating physician to allow for repositioning. The multiple sideports of the chest tube should all lie within the thoracic cavity. Increasing subcutaneous emphysema on repeat chest radiographs is a clue to the potential presence of an extrathoracic sideport and the need for repositioning or downsizing of the chest tube.

Additional radiographic signs associated with pneumothorax include the deep costophrenic sulcus sign seen on the supine radiograph. The “double diaphragm” sign is caused by nondependent air outlining the anteriordiaphragmatic attachment. Mimics of pneumothorax are multiple and may be due to overlying sheets, clothing, medical equipment, or skin folds. Repeat chest radiography after rearranging or removing the external structures is often adequate to exclude pneumothorax.

Recently, ultrasound (US) has gained attention as a rapid assessment tool to evaluate for pneumothorax in the ED and after chest interventions. The performance of US has been shown to be as good if not better than radiography, although it generally underperforms as a follow-up study. Additionally, greater variation in results should be expected due to differences in sonographer skill and experience. Traumatic pneumothorax is discussed in this text in Chapter 2, so only a brief comment is made here. The seal of the pleural space is easily broken by penetrating injury, and it is vulnerable because it is spread over a large surface area. Significant blunt trauma is estimated to cause pneumothorax in up to 30% to 40% of cases. It can lead to pneumothorax when broken ribs or other sharp structures expose the pleural space to atmospheric pressure, or when a preexisting bleb is ruptured. Fractured ribs on imaging should invoke a secondary search for pneumothorax. With positive pressure ventilation, barotrauma can lead to pneumothorax, particularly in patients with relatively noncompliant lung tissue (e.g., those with ARDS or interstitial lung disease). Barotrauma may also occur during sport diving or from nonpenetrating blast injuries resulting from explosive devices.

Pleural Effusion

Pleural effusion, defined as abnormally increased fluid within the pleural space, may be transudative or exudative in etiology. Transudative fluid is generally low in protein and typically develops in the setting of left heart failure, decreased oncotic pressure, or other systemic abnormality. Exudative fluid is often a consequence of breakdown of the barrier function of the pleura, leading to leakage of macromolecules and proteins. Less commonly encountered complex exudative pleural effusions include hemorrhagic fluid related to tuberculous infection, chylothorax related to thoracic duct injury, and eosinophilic effusions related to hypersensitivity (Table 8-2).

Table 8-2 Etiologies of Pleural Collections

Etiology Types
Trauma Hemothorax, chylothorax
Infectious Empyema, tuberculous effusion
Gestational/Fertility Ovarian hyperstimulation
Inflammatory Postpericardiotomy, eosinophilic
Drug induced Multiple factors
Reactive Ascitic, pancreatitis

Pleural fluid volume as low as 5 mL can be visualized on decubitus imaging. Approximately 200 mL is required to blunt the costophrenic sulcus on upright radiography. Small fluid collections can routinely be characterized on CT, US, and MRI. The CT appearance of pleural fluid varies depending on the density. Transudative effusions are near water density (i.e., approximately 0 Hounsfield units [HU]); hemorrhage and pus typically demonstrate increased density, often with a hematocrit effect in the case of hemorrhage. Low density on CT does not, however, exclude exudate. Long-standing infections may show complex septations or gas. US may help to characterize effusions by showing areas of loculation and septation, and is also commonly used for drainage guidance.

Pleural effusions may also be seen in the setting of malignancy, and occasionally in the setting of benign lesions, as seen in Meigs syndrome. Classically, Meigs syndrome is the presence of ascites and pleural effusion caused by benign ovarian fibroma, although other ovarian neoplasms are now commonly invoked as well. Meigs syndrome is uncommon and the pathophysiology is unclear. Most sources accept the explanation that the fluid is generated by the tumor itself and is often, but not exclusively, a transudate.


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.


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).


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.


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.

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