Nontraumatic Emergency Radiology of the Thorax


An emergency medicine physician once told a bright-eyed medical student on the first clinical shift, “All kinds of problems bring people in to see us with chest complaints. But just remember this—your job is to make sure nobody leaves the emergency department with any of only four entities undiagnosed, and those four entities are pneumothorax, aortic dissection, pulmonary embolism, and myocardial infarction. Now repeat that list to me four times. [The medical student regurgitates the list four times.] Good. Beyond these four entities, anything that’s causing their problem won’t cause you much of a problem.”

Although that synopsis of nontraumatic thoracic disease encountered in the emergency department (ED) is rather spartan, 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 (PE), and acute coronary syndrome (ACS). Lung parenchymal findings are covered with less emphasis, but they 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. The ready availability of CT and its high sensitivity and specificity, matched with a rapid scan performance, have made it the test of choice for a broad range of thoracic diagnoses. Aside from issues of health care costs, 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 and be readily able to advise clinicians and protect patients by being good stewards of radiation safety.

Chest Radiography

Chest pain is one of the most common patient presentations in the ED. Despite widespread availability of “high-tech” CT scanners, it remains vital to develop the knowledge and skills needed for expert chest radiograph interpretation, because the chest radiograph remains the mainstay of first-line imaging for many ED patients with chest-related symptoms. The emergency radiologist needs to have highly developed interpretive skills for chest radiography. Detailed instruction on chest radiograph interpretation is beyond the scope of this chapter, but many excellent sources are available, 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 chest radiograph. Although one is naturally drawn to look at the lungs—and although evaluation of pulmonary parenchyma is paramount—the interpreter must unerringly include assessment of extrapulmonary anatomy on every chest radiograph. The evaluation should include anatomy below the diaphragm, lung parenchyma posterior to the diaphragm, the bony thorax, spine, shoulders, and chest wall soft tissues, the heart contours, mediastinum, and pulmonary hila, pleural surfaces and interfaces, and complex areas such as the pulmonary apices. Establishing a pattern of evaluation that systematically includes all of the anatomy encountered on a chest radiograph will help prevent unfortunate errors of chest radiograph interpretation ( Fig. 8-1 ).

FIGURE 8-1, Chest radiograph of a patient presenting with cough and fever. A faint area of opacification within the left midlung proved to be pneumonia (black arrow) . Additionally, a small left apical carcinoma was detected (white arrows) . Because of multiple overlying structures, including the first ribs and the clavicles, the pulmonary apices are a “danger” area in terms of risk of missed findings on chest radiographs. Close inspection of the apices is warranted on every chest radiograph.

Pulmonary disease is detected primarily by changes in pulmonary parenchymal density, with either a decrease (e.g., cystic lung diseases and pneumothorax) or an increase (e.g., masses, fluid, infection, fibrosis, or atelectasis) in density.

Pneumonia

On a chest radiograph, pneumonia manifests as areas of increased density within the pulmonary parenchyma as a result of alveolar consolidation. The increased density can be focal, multifocal, or diffuse. Depending on the causative organism and the immune status of the patient, the density may appear as confluent parenchymal consolidation (with vessels obscured within the density), hazy ground glass density (with vessel margins able to be detected within the density), or coarse reticular or reticulonodular opacities. Air bronchograms may be present when the alveolar opacities accentuate the airways. These densities may be marginated by pleural or fissural boundaries. The use of both frontal and lateral projections is helpful in detecting, confirming, and localizing the areas of pneumonia ( Figs. 8-2 and 8-3 ).

FIGURE 8-2, Chest radiograph of a patient with pneumonia. A, A posteroanterior view reveals a patchy opacity overlying the left lung base (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 the left lower lobe location of the pneumonia, as indicated by increased density of the lower thoracic vertebral bodies (arrow) . Normally, on a lateral chest radiograph, 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, A chest radiograph of another patient with pneumonia. A, 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 whether the pneumonia is located in the middle versus lower lobe. B, The lateral view reveals increased density overlying the heart (longer arrow) , confined by the major fissure (shorter arrows) , indicating that the pneumonia is located in the right middle lobe. Note that the vertebral bodies become more lucent from superior to inferior, indicating the absence of lower lobe processes overlying the vertebrae.

Heart Failure

Progression or exacerbation of congestive heart failure can cause dyspnea as a result of pulmonary vascular congestion or its more advanced form, pulmonary edema. Pulmonary edema can be classified as hydrostatic origin (with increased intravascular pressure, as in left ventricular failure or volume overload) due to altered permeability (with increased permeability of the pulmonary alveolar-capillary membrane, as in acute respiratory distress syndrome [ARDS]). Although some overlap in the pathophysiology likely exists, the cause of pulmonary edema cannot routinely be distinguished by chest radiographs.

The sequence by which congestive heart failure leads to pulmonary edema and may manifest on a chest radiograph 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 a chest radiograph, particularly in the upper lobes, manifests as “cephalization,” which 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 chest radiograph 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 the alveolar spaces, resulting in more confluent density that obscures vessel margins ( Fig. 8-4 ).

FIGURE 8-4, A patient with cardiomegaly and recurrent episodes of congestive heart failure. A, A posteroanterior view obtained when the patient was otherwise healthy reveals grossly clear lungs and mild 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) .

Computed Tomography

Computed Tomography of the Pulmonary Parenchyma

CT allows for more refined analysis of the pulmonary parenchyma. In a similar manner to a chest radiograph, pulmonary parenchymal disease is detected by changes in parenchymal density and architecture. Axial images with section thicknesses of 2 mm or less permit 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, with 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 anatomic features are 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 the previously described architectural derangements is useful, and a brief synopsis is provided in the following text.

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 a chest radiograph), ARDS, 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, which also has been described as characteristic of alveolar proteinosis. Nodular septal thickening may be seen in lymphangitic metastases, as well as in 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 can cause irregular septal thickening and may be associated with other common findings of fibrosis, such as traction bronchiectasis and honeycombing.

FIGURE 8-5, A 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 causes. 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 may indicate an infectious bronchiolitis. 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. A subsequent computed tomography 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 (the “crazy paving” pattern) should raise differential considerations including pulmonary edema, pneumonias of varying causes, 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 pneumonia and drug reaction, in addition to the entities previously listed ( Fig. 8-7 ). Differential considerations for more consolidated densities include entities such as pneumonia, 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 that the patchy hazy density that does not obscure the underlying vascular structures.

Chest Computed Tomography Techniques and Protocols

This section outlines general principles guiding the selection of CT techniques and scan parameters. Although wide variability can exist between scanner types and manufacturers with regard to 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

Intravenous Contrast Material

All patients must be screened for allergy to intravenous contrast material (IVCM). Although IVCM is a critical part of evaluation for pulmonary embolus and aortic dissection, it can be omitted if the clinical indication is primarily for abnormalities of the lungs. Although protocols vary by institution, all policies should include screening for a history of allergy to contrast material and risk factors for contrast-induced nephropathy.

Pregnancy

Women of child-bearing age should be screened, because concerns regarding the use of ionizing radiation during pregnancy must be weighed against medical necessity (e.g., pretest probability and urgency), examination performance characteristics (e.g., sensitivity and specificity), and alternative methods of imaging (e.g., magnetic resonance imaging [MRI] and ultrasound [US]). Alternative imaging methods with similar examination performance characteristics should be used when they are available. For properly shielded chest radiographs or CT scans of the chest collimated to avoid direct irradiation of the gravid uterus, fetal radiation exposures are extremely low, and as such, concerns about fetal radiation exposure, in general, should not affect decisions to perform medically warranted chest imaging. Although data quantifying increased risk to the maternal breast during pregnancy are lacking, theoretical concerns do prompt some practitioners to prefer nuclear scintigraphy rather than CT for evaluation of pulmonary embolus in pregnant women (the fetal doses relating to these methods have been similarly small for both modalities but have continued to decrease as CT technology advances). When CT is performed, the number of nondiagnostic scans should be minimized by taking proactive steps to optimize CT scan quality (e.g., patient coaching for breathing and motion and excellent IV line placement), thereby reducing the need for repeat scanning.

Patient Preparation

Intravenous Line Placement

Whenever possible, contrast-enhanced chest CT studies should be performed using a 20-gauge or larger peripheral IV line, preferably located in a right antecubital location. An 18- to 20-gauge size will easily allow for power-injected flow rates of 3 to 6 mL per second. Right-sided IV line placement reduces streak artifact over the anterior superior mediastinum compared with left-sided placement because of elimination of dense IV contrast material passing through the left brachiocephalic vein. Antecubital placement results in more reproducible contrast material inflow characteristics and a reduced rate of infiltration compared with more peripheral placement.

Heart Rate Control

Cardiac gated protocols (coronary CT angiography [CTA] for gated aortic dissection) generally require a regular cardiac rhythm. With current single-source 64-MDCT techniques, coronary CTA is best performed with heart rate controlled to 65 beats or less per minute. However, further advances such as quicker gantry rotation, greater numbers of detector rows, and/or dual x-ray source scanners are likely to lessen or obviate the current requirement for lower or regular heart rates.

Scan Protocol Considerations

Contrast Material 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 on the CT technology in use) and on the flow rate and quantity of injected contrast material. As a general rule of thumb, IVCM should be injected at a minimum rate of 4 mL per second for CT evaluation of pulmonary embolus, aortic dissection, or traumatic aortic injury. Higher flow rates shorten the duration of the contrast bolus. As a result, scan timing must be scrutinized to ensure that contrast material opacification remains adequate throughout all portions of the scan.

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

  • Fixed or empiric delay. The time delay is selected based on scanner speed, experienced best estimates of the time required to reach the vascular bed of interest, and, if applicable, patient factors such as cardiac output and IV line location.

  • Automated contrast bolus detection, or bolus tracking. A monitoring scan is repeated at a fixed scan position, and the acquisition scan is triggered when the contrast density exceeds a preset threshold in a vessel selected as the region of interest.

  • Timing bolus. The transit time from the injection site to the vascular bed of interest is directly observed by repeat scanning at a fixed position after administration of 10 to 20 mL of IVCM (followed by a saline solution flush). The time to peak enhancement is determined on the basis of the timing bolus plus a recirculation delay, and the corresponding timing delay is subsequently used for IVCM during the acquisition scan.

Radiation Exposure and Techniques for Dose Reduction

Emergent (and overall) CT utilization has risen rapidly as a result of technological advances, a broad range of clinical applications, and widespread availability of CT. This phenomenon has raised concerns about associated radiation risks both to individuals and to the population as a whole and has increased scrutiny regarding CT use. Radiologists must do their part to optimize techniques that will reduce radiation exposure while maintaining high-quality imaging. Likewise, medical vendors have continued to advance their imaging technologies with tools that reduce radiation exposure. A variety of techniques exist to control patient exposure to radiation during CT. Radiologists should have a working knowledge of these techniques.

Most current CT scanners (and virtually all new scanners) include the capacity for automatic tube current modulation, also called dose modulation . These functions should be configured when available. Tube current modulation adjusts the overall x-ray tube current to a predetermined image quality or noise index or adjusts it based on a reference tube current time product (ref mAs) that would be warranted for a patient of the defined reference size. These techniques adjust x-ray tube output during the scan, either along the long axis of the patient (longitudinal modulation) or during the gantry rotation around the patient (angular modulation) as the patient’s x-ray attenuation varies in these directions. Additionally, scanners intended for cardiac CT offer the capability for electrocardiographic (ECG) dose modulation or prospective scanning, in which x-ray tube output is greatly reduced or eliminated during systole.

Imaging of structures with a high degree of intrinsic tissue contrast material 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, permitting lower dose techniques to be used. Administration of lower doses may be accomplished by reducing mAs through appropriate configuration of scanner-specific tube current modulation techniques. Reducing the x-ray tube peak kilovoltage (kVp) further provides opportunities not only to reduce radiation dose but also to increase vascular enhancement for the same contrast bolus, or alternatively, to maintain contrast enhancement with reduced contrast volume.

Manufacturers of CT equipment have recently developed iterative reconstruction techniques. Although the underlying algorithms vary by manufacturer and continue to evolve, these techniques are all designed to reduce image noise (and certain imaging artifacts) that occur after a certain CT acquisition. If a reduced dose acquisition is performed, iterative reconstruction may then be used to maintain the desired level of image quality. Because the appearance of the resultant image may vary in subtle ways from traditional filtered back-projection, many manufacturer software versions permit configuration of the iterative reconstruction strength so that practices can find the right balance between noise reduction and image appearance. Resultant dose reductions on the order of 30% to 50% are frequently achieved with these techniques, and even greater dose reductions are becoming more widespread as the technology advances.

Bismuth breast and thyroid shields are used in some facilities to reduce radiation dose to these organs, but they are not currently recommended by the American Association of Physicists in Medicine because they introduce artifacts throughout the image, and comparable dose reductions can be achieved through use of other methods. If these shields are used, it is important to apply them after acquisition of the planning projection radiographs and to use them only on scanners that do not incorporate real-time mA adjustments that can paradoxically increase the dose to better penetrate through the shields.

Image Reconstruction

The following image reconstructions should be performed routinely:

  • 3- to 5-mm axial lung algorithm images

  • Axial soft tissue algorithm images:

    • Routine chest: 3 to 5 mm

    • Dissection CTA: 3 mm or thinner

    • Pulmonary embolus CTA: 2.5 mm or thinner—preferably 1 to 1.5 mm

Coronal and/or sagittal multiplanar reformations (MPRs) have become routine at many institutions. MPRs are particularly useful in the assessment of vascular anatomy and osseous structures, but they also can be helpful in localizing parenchymal lesions relative to the fissures and confirming motion artifacts or anatomic pitfalls on PE or dissection CTA. Routine sagittal oblique (“candy cane”) MPRs are often added to aorta evaluations. Thick maximum intensity projection (MIP) images may be added to aid in PE or lung nodule detection. Minimum intensity projection images are occasionally useful in evaluation of the airways.

Indication-Specific Computed Tomography Protocol Techniques

Routine Chest Computed Tomography

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

Pulmonary Embolus Computed Tomography Angiography

A typical PE CTA protocol includes bolus monitoring on the main pulmonary artery, followed after a breath hold delay by scanning from lung apices to bases. For scan durations less than approximately 10 seconds, high-quality PE CTA may be performed with 50 to 75 mL of IVCM injected at 4 to 5 mL per second, depending on the kVp used.

Upper Extremity Deep Venous Thrombosis or Superior Vena Cava Syndrome

Compression and Doppler US is the test of choice for both lower and upper extremity deep venous thrombosis. For high clinical suspicion of central venous thrombosis causing superior vena cava (SVC) syndrome, CT may be performed with a venous phase timing (typically 50 to 60 seconds) that achieves more uniform venous opacification and reduces the mixing artifacts that are typically observed when dense IVCM injected through one arm mixes in the SVC with the non-opacified blood arriving from the other arm ( Fig. 8-8 ). Coronal reformations greatly aid diagnosis.

FIGURE 8-8, Superior vena cava (SVC) thrombus after recent central line removal. A, An early phase axial image. Dense contrast material in the SVC (curved arrow) produces a streak artifact that partially obscures the SVC thrombus (arrow) and makes it difficult to differentiate the streak artifact from a mixing artifact with unopacified blood from the left brachiocephalic vein. B, A delayed (90 seconds) phase axial image eliminates streak and mixing artifacts better delineating thrombus in the SVC (arrow) .

Aortic Dissection Computed Tomography Angiography

Traditional dissection CTA protocols include the following elements:

  • A noncontrast scan of the chest

  • An arterial phase scan through the chest (± the 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 appear denser than the non-opacified blood in the aortic lumen.

The arterial phase scan is often performed with cardiac gating to reduce 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 typically can be 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 to reduce radiation exposure and to simplify scan acquisition because cardiac gating is more challenging in this frequently tachycardic patient population. Recently developed high-pitch scan modes allowing scan durations through the entire chest on the order of 1 second have also been used successfully to eliminate aortic root pulsation artifacts without the need for cardiac gating.

FIGURE 8-9, Pulsation artifact: a typical aortic root pulsation artifact from a nongated 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, A repeat study performed the following day with cardiac gating, eliminating the cardiac motion artifact.

A 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 routinely in high-risk patients or in those with known aortic dissection presenting with acute symptoms.

More streamlined examinations with reduced anatomic coverage, fewer scan phases, and a drastically reduced radiation dose can be successfully implemented in low-risk patients (including most of the ED patients who undergo imaging for possible aortic dissection). For patients with a low pretest probability of aortic dissection and a low incidence of significant atherosclerotic disease, screening is performed with a non-gated contrast enhanced chest CTA, with direct monitoring by a radiologist at the scanner. If aortic dissection is detected during this chest CTA, scanning is extended through the abdomen and pelvis to capture the full extent of the dissection in an arterial phase. (In practice, the extended scan region is prescribed up front, and a real-time decision is made to either stop at the chest or continue through the abdomen.) Although it is rarely needed, further scanning is then performed to problem solve; delayed imaging of the abdomen and pelvis may be performed as needed to clarify end-organ perfusion. If the CTA raises suspicion for an isolated intramural hematoma but is not sufficiently diagnostic for the radiologist, a 5- to 10-minute delayed postcontrast scan is added, because IVCM will have adequately cleared the intravascular space. Even more infrequently, a repeat chest CTA with cardiac gating may be performed if a pulsation artifact cannot be differentiated from subtle ascending aorta disease. This approach requires a practice model in which radiologists can actively monitor CT acquisitions while the patient is on the Gantry table. Although the 24-hours-a-day, 7-days-a-week operations of the ED can make this procedure particularly challenging to implement “after hours,” greater organization around the practice of emergency radiology is likely to make it 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 a possible esophageal injury. The scan protocol typically includes an initial low-dose scan without use of either oral contrast material or IVCM. Subsequently, the patient takes a few swallows of enteric contrast material, and a repeat scan (with or without IVCM, depending on the indication) is performed. The “scout” noncontrast scan is included to readily differentiate enteric contrast 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, reduced-dose techniques are used to reduce radiation exposure on this initial scan phase.

Coronary Computed Tomography Angiography

Significant variability can exist 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” procedure 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 monitoring or after 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 are recommended to reduce the associated radiation exposure using ECG dose modulation or prospective scanning, in which x-ray tube output is greatly reduced or eliminated during systole. Images are reconstructed at multiple intervals of the cardiac cycle to permit identification of image sets free of cardiac motion artifacts.

The Pleura, Pericardium, and Mediastinum

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 disease develops. A small amount of fluid (15 to 20 mL) normally 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

Pneumothorax is the presence of air within the pleural space. The causes of pneumothorax are multifactorial ( Table 8-1 ).

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, persons with asthma, 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 chest radiograph 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 blebs or cysts 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.

The most common imaging test performed to assess for pneumothorax is the chest radiograph. Ideally, the chest radiograph is performed with upright patient positioning so that the air–pleural interface can be readily identified toward the apices. It is seen as a thin white line where the outer margin of the visceral pleura and lung is separated from the parietal pleura and the chest wall, with lack of vessel markings beyond the pleural line. 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 radiography performed in the supine position, because small pneumothoraces can be easily overlooked from the air collecting anterior and medially.

Additional radiographic signs of pneumothorax seen on the supine radiograph include the deep costophrenic sulcus sign and the “double diaphragm” sign caused by nondependent air outlining the anterior diaphragmatic attachment.

A tension pneumothorax occurs when air enters but cannot exit the pleural space, which can occur when the pleural defect allowing air to pass into the pleural cavity functions mechanically 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. Imaging findings of tension pneumothorax include mediastinal shift away from the side of the pneumothorax, widening of the ipsilateral rib spaces, and/or relative compression of the contralateral lung.

Several estimation methods for pneumothorax size are based on chest radiograph measurements, but these methods are subject to wide interobserver variations in practice. If ambiguity exists about 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 monitored radiographically until they resolve. Failure to resolve 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 side ports 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 side port and the need for repositioning of the chest tube.

Many possible mimics of pneumothorax exist, including overlying sheets, clothing, medical equipment, or skin folds. Repeat chest radiography after rearranging or removing the external structures can be performed to exclude pneumothorax.

Bedside US in expert hands is a rapid assessment tool that can detect pneumothorax more accurately than a supine chest radiograph, making it especially useful in acutely ill patients after line placement or trauma. The four sonographic signs described in the literature to assess for pneumothorax include the lung sliding sign (regular rhythmic movement synchronized with respiration between the visceral and parietal pleura), the lung pulse (subtle rhythmic movement of the visceral pleura upon the parietal pleura with cardiac oscillations), presence of B lines (indicating that the visceral pleura is opposing the parietal), and the lung point (absence of any sliding or B lines, indicating the presence of pneumothorax). Traumatic pneumothorax is discussed in greater detail in Chapter 2 , but in brief, penetrating injury easily breaks the seal of the pleural space, which is vulnerable because of its large surface area. Significant blunt trauma is estimated to cause pneumothorax in up to 30% to 40% of cases. Pneumothorax can occur 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 prompt a secondary search for pneumothorax. Barotrauma related to positive pressure ventilation can lead to pneumothorax, particularly in patients with relatively noncompliant lung tissue (e.g., persons with ARDS or interstitial lung disease). Barotrauma also may 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 cause. Transudative fluid is generally low in protein and typically develops in the setting of left heart failure, decreased oncotic pressure, or another systemic abnormality. Exudative fluid is often a consequence of breakdown of the barrier function of the pleura, leading to leakage of macromolecules and proteins.

Pleural fluid volume as low as 5 mL can be visualized on decubitus chest radiograph 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 effusions can become loculated, with an irregular pleural contour. US is a very useful tool to further characterize the effusion by showing areas of loculation and septation, and it is also commonly used for drainage guidance.

Pleural effusions also may be seen in the setting of malignancy, often related to pleural metastatic deposits. Meigs syndrome is a rare benign condition that causes pleural effusion and ascites in the setting of a benign ovarian fibroma, although other ovarian neoplasms are now commonly invoked as well. Meigs syndrome is uncommon and the pathophysiology is unclear, although it is often believed that the fluid is generated by the tumor itself and is most commonly a transudate.

Hemothorax

Traumatic hemothorax can occur after blunt or penetrating trauma. Blunt trauma may cause direct venous or arterial rupture or may disrupt vessels as a result of rib fracture. Penetrating trauma can cause mediastinal, intercostal, substernal, or diaphragmatic vascular injury with resultant intrapleural hemorrhage.

Intrapleural blood may manifest on a chest radiograph as a localized collection or as diffuse relative opacification of one or both hemithoraces. Much smaller collections can be detected on CT with the added certainty of density characterization allowed by evaluation of HUs in a region of interest. CT, particularly when performed during IVCM administration, may identify active extravasation from an arterial injury. Progressive enlargement of hemothorax is likely due to arterial injury, whereas venous hemorrhage is more likely to stabilize. An unevacuated hemothorax, particularly if it is large, can lead to adhesions and fibrothorax, potentially restricting lung function.

Empyema

Empyema refers to abscess formation in the pleural space. Although usually a result of adjacent pneumonia, it is also known to develop after hematogenous seeding, trauma, or iatrogenesis. In the setting of suspected empyema, chest CT should be performed with administration of IVCM. The presence of a “split pleura” sign (i.e., enhancement of the visceral and parietal pleura) is strongly suggestive of empyema. Several studies have shown improved health outcomes with early evacuation of empyema, often in conjunction with fibrinolytic therapy.

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