Key Clinical Questions
What are the different types of plain chest radiographs and when would you order them?
What are the limitations of the anteroposterior (AP) film?
How does the chest radiography differentiate between different types of pneumonia from atelectasis?
What are the radiographic changes you should look for when considering acute, potentially life-threatening causes of chest pain?
What radiographic abnormalities require follow-up?
The majority of hospitalized patients routinely have chest radiographs on admission or prior to surgery. Chest radiographs provide a snapshot of the patient’s physiologic health and insights into a wide variety of systemic diseases. Chest radiographs have the highest yield when obtained to evaluate acute cardiopulmonary signs or symptoms, or to assess the possibility of a complication following a procedure. Chest x-rays are also used to monitor critical illness in the intensive care unit (ICU), response to therapy as in congestive heart failure or pneumonia, and stability of pulmonary nodules.
The clinician can minimize unnecessary test ordering and delays in diagnosis by recognizing the indications for different types of radiographs and their limitations. Table 114-1 summarizes the different types of chest projections, indications, and technical considerations. A posteroanterior (PA) radiograph provides more information than an anteroposterior (AP) projection. Due to magnification based on distance from the image data collector or film, the heart will appear larger on bedside AP chest radiographs and also in obese individuals. Hence, an AP image may suggest heart failure (upper lobe diversion, cardiomegaly, wide mediastinum, and high hemidiaphragms) in patients without fluid overload and significant pulmonary pathology may not be obscured. An AP film is also more likely to miss a small pneumothorax due to anterior collection of air, and diffuse shadowing may signify either poor inspiration or a posterior pleural effusion. Therefore, a PA radiograph may be required for more definitive diagnosis and is the preferred initial study. However, the patient must be able to cooperate and be clinically stable in order to be transported to another area in the hospital for acquisition of a posteroanterior radiograph. Although the standard chest radiograph may provide information about the overall health of the bones, special views should be obtained to properly assess the thoracic spine and shoulder joints in cases of trauma or infection. Rib fractures in particular may indicate more severe pulmonary injury than what is readily apparent from the plain film.
TABLE 114-1Types of Chest Radiographs ||Download (.pdf) TABLE 114-1 Types of Chest Radiographs
|Type of Film ||Indications ||Technical Considerations |
|Posteroanterior radiograph ||Preferred image unless patient unstable to evaluate acute signs and symptoms of the chest ||Patient stands with anterior chest against film cassette; exposure is full inspiration |
|Anteroposterior radiograph ||Alternative to PA chest for unstable patients || |
Film cassette placed behind patient, portable x-ray machine used
Rotation is more likely than with a PA film
|Lateral view ||To localize an abnormality seen in another view; to identify abnormalities obscured by the heart or costophrenic recess || |
|Lateral decubitus view ||To identify a small pleural effusion or to distinguish from pleural thickening; to determine if raised hemidiaphragm due to subpulmonary hemothorax; to confirm clinical impression that pectus excavatum with depressed sternum is cause of unusual cardiac contour or cardiomegaly ||Patient lying with his abnormal side down |
|PA inspiration- expiration views ||To identify pneumothorax; expiration to identify inhaled foreign body when gas trapping is evident || |
|Apical lordotic views ||To examine the lung apex usually obscured by clavicle and upper ribs || |
The interpretation of any radiographic test begins with assessing the adequacy and technical quality of the film(s) in view. Normal chest radiograph anatomic structures contribute to the radiographic appearance of the chest (Figures 114-1 and 114-2). The right hemidiaphragm should reach the anterior end of the right sixth or seventh rib or the posterior end of the ninth rib on full inspiration. The degree of inspiration affects the appearance of the lower zone vessels that seem more prominent with poor inspiration. The clinician may mistakenly diagnose basilar pneumonia or cardiomegaly if the radiograph has the domes of the diaphragms at the posterior end of seventh ribs or higher. Comparison with prior radiographs that look like the current examination can be most helpful when viewing radiographs without a radiologist. This is analogous to comparing a current electrocardiogram to a baseline electrocardiogram in a patient with possible cardiac ischemia. Then the examiner should carefully inspect the heart, lungs, mediastinum, and chest wall. The bones should be examined for fracture and metastatic disease. The examiner should also routinely check for the presence and position of any invasive medical equipment such as central lines, feeding tubes, or endotracheal tubes (Table 114-2 and Figure 114-3).
(A) Normal chest radiograph anatomic schematic drawing of fissures on PA radiograph. 1, minor fissure; 2 to 4, major fissure; 5, superior accessory fissure; 6, inferior accessory fissure. (B) Normal chest radiograph anatomy schematic drawing of structures on PA radiograph 1, normal apical opacity; 2, aortic nipple; 3, descending aortic interface; 4, air in esophagus; 5, aortic pulmonary stripe; 6, diaphragm.
Lobar and segmental anatomy of lungs. (Reproduced, with permission, from Doherty GM. Current Diagnosis & Treatment: Surgery. 13th ed. New York: McGraw-Hill; 2010. Fig. 18-7.)
ICU patient with dense consolidation and air bronchograms well seen in right lung base corresponding with pneumonia. Support lines include endotracheal tube, left subclavian central venous catheter and left chest tube placed for pneumothorax that may be due to line placement or barotrauma in setting of multiorgan system failure with injury pulmonary edema present.
TABLE 114-2Support Lines ||Download (.pdf) TABLE 114-2 Support Lines
|Support Device ||Optimum Placement ||Proximal Limit ||Distal Limit ||Common Malposition |
|Endotracheal tube ||Middle of intrathoracic trachea ||Tip even with top of clavicle ||Tip 2 cm from carina ||Tip in right mainstem bronchus |
|Central venous catheter ||Superior vena cava ||Brachiocephalic vein ||Cavoatrial junction ||Right atrium; inferior vena cava; azygous vein following arch posteriorly; internal mammary vein with slight lateral direction; persistent left superior vena cava can be acceptable depending on vessel size |
|Peripherally inserted central catheter ||Depends on use; localization will change with arm position ||Arm for long-term peripheral access ||Cavoatrial junction ||Visiting Nurse Association (VNA) service may require superior vena cava |
|Swan-Ganz catheter ||Right or left main pulmonary artery ||Right ventricle ||Interlobar descending pulmonary artery ||Distal placement only when wedged |
|Nasogastric tube ||Stomach || || ||Side vent marker needs to be distal to gastroesophageal junction |
Clinicians should always provide radiologists with sufficient information to interpret a radiograph in the clinical context of the patient. Otherwise, the radiologist may generate a wide differential diagnosis that may lead to unnecessary additional imaging or overlook subtle signs of infection in an immune-compromised host.
Consideration of chest radiographic findings that support a new diagnosis of a systemic disease almost always benefits from direct consultation with the radiologist; a study requisition does not allow an interchange of specific clinical information that can alert the radiologist to findings that might otherwise be ignored.
CHEST RADIOGRAPHIC TERMINOLOGY
The Fleischner Society Lexicon (Tuddenham 1984) is the standard reference resource for chest radiographic terminology (Table 114-3). The term opacity is used to describe the addition of substances to lungs that results in lighter gray to white appearance of normally dark-gray lungs. The term density is not used because density is a photographic term for increasing blackness in the image.
TABLE 114-3Glossary of Terms ||Download (.pdf) TABLE 114-3 Glossary of Terms
|Descriptive Term ||Differential Diagnosis |
|A relatively acute development of a diffuse process that includes little if any consolidation, corresponds with acute interstitial pneumonia (AIP), injury pulmonary edema, corresponding to clinical diagnosis of adult respiratory distress syndrome (ARDS) |
Solitary pulmonary nodule
Typically homogeneous parenchymal lesion with sharply defined margins, ≤3 cm
Usually standard chest radiograph will not detect nodules <1 cm
Nodules between 1 and 2 cm in size may be missed due to overlapping bones or vascular structures
Decreased lung volume, at any level of lung organization
May be associated with other signs of volume loss in the hemithorax (ipsilateral shift of the mediastinum, decreased spacing of ribs and elevation of the diaphragm)
Collapse refers to complete lung atelectasis
Subsegmental and segmental atelectasis refer to discoid or plate-like atelectasis based on projection
Pneumonia, pulmonary embolism, and abdominal fluid or pain that causes splinting
Mucoid impaction at the level of any bronchus, leading to collapse patterns that are specific for each lobe
In the case of the bronchus intermedius, atelectasis may involve both the right middle and right lower lobes
Low lung volumes and expiration (focal atelectasis)
Kerley A lines
|Distention of anastomotic channels between peripheral and central lymphatics of the lungs |
Kerley B lines
Short (<2 cm long), straight, horizontal parallel lines (<1 mm thick) at the lung periphery that end at right angles against the pleura
Generally absent along fissural surfaces in any zone but most frequently observed at the lung bases at the costophrenic angles on the PA radiograph, and in the substernal region on lateral radiographs
Fluid in interlobular septa, or dilated lymphatic channels visible with elevation of the pulmonary capillary wedge pressure (usually 25 mm Hg or higher)
Associated with congestive heart failure (CHF) and interstitial lung diseases (ILD)
Kerley C lines
Short, fine lines throughout the lungs, with a reticular appearance
Least common of Kerley lines
|Thickening of anastomotic lymphatics or superimposition of many Kerley B lines |
The simplest measurement of the cardiac silhouette, the transverse diameter of the heart, compares the measurements of the widest width of the heart with the widest width of the thorax on standard PA chest radiographs. Cardiomegaly is a nonspecific finding in fluid overload states. The heart may enlarge from baseline without meeting criteria for cardiomegaly, be normal in the setting of acute lung injury, or enlarged for other reasons. Viewing images with prior plain films provides a more reliable assessment of the presence of cardiomegaly due to a wide range of normal and abnormal heart sizes. An important sign of a possible pericardial effusion, separation of epicardial and pericardial fat, should prompt comparison with prior films to determine if there has been rapid enlargement and development of a globular configuration. A characteristic cardiac contour may suggest left ventricular enlargement, but right ventricular enlargement will, for the most part, be indistinguishable from right ventricular displacement in an enlarged heart. It takes at least 2 years of untreated hypertension to result in a hypertensive cardiovascular silhouette with ectasia of the aorta and more horizontal axis of the heart on PA chest radiograph. For patients with “labile” hypertension, the presence of target end organ damage would be an indication for treatment. Calcification and a change in contour may suggest left ventricular aneurysm, and bulging of the lower third of the left cardiac border may signify aortic valve disease. Prominence of left heart border or posterior enlargement of the left atrium may suggest the possibility of mitral stenosis.
Compare current chest radiograph with prior chest radiographs to determine if there is
A new separation of epicardial and pericardial fat
Oligemic appearance of lungs
Anatomic landmarks within the heart are only identified if they are calcified or associated with radiopaque markers, such as coronary stents, prosthetic valves, and closure devices for patent foramen ovale.
Forty percent of the lung area and 25% of the lung volume may be obscured by the heart and mediastinum on a PA or AP chest radiograph. Both lungs should be equal in size. Fissures should not be wider than hairline. The outline of the hemidiaphragms is usually smooth, arcuate, with the highest point medial to the midline of the hemithorax. Normally, airways are invisible unless they are abnormally thickened or pass through an area of consolidation. Consolidation is the hallmark of airspace disease. Air bronchograms are seen on projection radiographs as lucent tubular branching structures within a larger opacity produced by confluent filling of airspaces by fluid and other substances (Figure 114-3). Volume loss in the region may also contribute to the opacity.
Some terms suggest a broad differential diagnosis that may be considerably narrowed by the clinical context. Large irregular opacities may result from consolidation, lobar collapse, carcinoma, pleural abnormalities, or chest wall lesions. Single or multiple nodular opacities may reflect malignant causes (primary bronchogenic carcinoma, solitary or multiple metastasis) and benign causes (granulomas, arteriovenous malformations [AVMs], intrapulmonary bronchogenic cysts, bronchial atresia, and traumatic hematomas). Collapse is often reserved for lobar collapse but by definition, atelectasis is correct at all levels whether a subsegment, segment, lobe, or complete atelectasis of the entire lung. The differential diagnosis for collapse is most importantly an obstructing lesion; an endobronchial tumor may be primary lung cancer (including carcinoid that has recently been reclassified as a flavor of lung cancer); endobronchial metastasis (particularly breast, gastrointestinal tract, and renal cell carcinoma); foreign bodies (such as a peanut or bullet); and secretions as mucoid impaction (particularly important in an intubated patient). Pneumonia may occur with collapse related to secretions and in particular aspiration pneumonias may be more likely to be associated with atelectasis. Atelectasis commonly occurs in the postoperative setting due to low lung volumes. In babies, atelectasis may also reflect decreased surfactant—unusual in adults. Radiographic clues to the presence of atelectasis include: crowding of airways and vessels within the lobe, crowding of ribs, shift of mediastinum and other structures, raised hemidiaphragm, compensatory hyperexpansion of ipsilateral lobe and contralateral lung. Additional terms are presented in Table 114-3.
Acute airspace disease = water, pus, blood.
Bilateral symmetric disease favors water.
Focal air space disease favors pneumonia.
Bilateral asymmetric and sparing of periphery are associated with hemorrhage.
Normally, blood vessels should be much more apparent in the lower lung zones than in the upper lung zones. Lines seen within 2 cm of the chest wall probably represent interstitial abnormalities such as edema, fibrosis, or metastatic disease.
PRACTICE POINT Mediastinal contour abnormalities
Lymphoma: Typically, a lobulated anterior mediastinal mass that most likely represents matted lymph nodes with associated mediastinal lymph nodes. Lymphadenopathy can also occur in sarcoidosis and infection.
Thymoma: More focal and unilateral than lymphoma, not associated with paratracheal lymphadenopathy, seen in older patients.
Germ cell tumor: Characteristic fat and calcification particularly in young patient.
Metastatic disease: Middle mediastinum more likely to be involved by metastatic disease from testicular germ cell tumors, renal cell carcinoma, or melanoma.
Vascular congenital anomaly or in a patient who has had cardiac surgery pseudoaneurysm at bypass pump cannulation site.
The mediastinum is divided into radiographic compartments that differ somewhat from the anatomic divisions of the mediastinum.
The anterior mediastinum includes the retrosternal clear space seen on lateral chest radiograph. Radiologists may use either the anterior surface of the aorta or the anterior wall of the trachea as the posterior boundary of this compartment.
The middle mediastinum extends from this boundary to 1 cm behind the anterior surface of the vertebral bodies on the lateral view.
The posterior mediastinum extends posteriorly from the middle mediastinum to the posterior chest wall. The structures in this region all lie posterior to the mediastinum.
It is sometimes useful to apply the term superior mediastinum to the region above the aortic arch although not a compartment. The vascular pedicle is assessed on the frontal view with greater magnification expected on bedside anteroposterior radiographs than standard posteroanterior radiographs. Distention of the azygous vein to greater than 11 mm in diameter along right side of trachea just above bifurcation signifies pulmonary vascular engorgement.
The hila are often considered with the mediastinal structures. The border-forming structures are the pulmonary arteries. The left pulmonary artery is approximately 2 cm higher than the right pulmonary artery. This slope, sometimes referred to as the hilar angle, may be altered as in the case of right upper lobe volume loss elevating the right hilum. The direction of the right and left central pulmonary artery differs resulting in expected mild asymmetry. The upper limit of normal currently used on CT scans for the main pulmonary artery is 24 mm with borderline to 29 mm. The upper limit of the normal range in size of the right interlobar descending pulmonary artery most easily measured on chest radiographs is 16 mm for a man and 14 mm for a woman. Increased intravascular pressure may be temporary as in the case of pulmonary edema or long standing as in the case of pulmonary artery hypertension.
The differential diagnosis of a mass in the anterior mediastinum includes thyroid enlargement (continuous with the thyroid gland causing deviation of the trachea), a thymoma or thymic cyst (typically marginated and sometimes lobulated), lymphoma and small-cell lung cancer (which may involve multiple lymph node groups), or a germ cell tumor (sometimes evidenced by fat, hair, and teeth). The differential diagnosis of middle mediastinal masses includes tumors involving the esophagus, thyroid, and lymph nodes, duplication cysts including bronchogenic cysts (most frequently at the bifurcation of trachea and central airways, sometimes paraesophageal or intraparenchymal), lymphadenopathy, pericardial cysts (characteristically adjacent to the heart, especially in the cardiophrenic sulcus and smoothly marginated), intrathoracic goiter (with heterogeneous tissue), tracheal tumors, and vascular variants. Posterior mediastinal masses may represent neurogenic tumors, extramedullary hematopoiesis, and esophageal abnormalities.
In an otherwise healthy adult, bilateral, noncalcified hilar adenopathy suggests sarcoid. In a patient with a prior history of malignancy, the presumption has to be malignancy. Most common malignancies that cause hilar adenopathy include bronchogenic carcinoma, lymphoma, bronchial carcinoid, and extrathoracic primary tumors metastasizing to the chest. Nonmalignant causes include pulmonary arterial or venous dilation or tortuosity, cysts, granulomatous adenopathy, and benign tumors. Reactive and malignant adenopathy may be radiographically indistinguishable unless there is obvious calcification. Vascular abnormalities are often asymmetric and can simulate adenopathy. The first step is to compare with prior films. Consultation with a radiologist and serial review of images will facilitate differentiation of hilar lymphadenopathy from pulmonary artery enlargement.
Both whole lung atelectasis and pleural effusion may cause complete whiteout of a hemithorax. The direction of mediastinal shift may suggest the likely possibility. The shift will be toward the opaque hemithorax when the lung collapses. Pleural effusion on the other hand occupies space and can cause contralateral shift of the mediastinum. Since both can be present at the same time, it is possible for the mediastinum to be midline with balanced volume loss due to atelectasis and pleural effusion. A low diaphragm will cause a right shift of the mediastinum, and a high diaphragm will cause a left shift.
Fluid overload typically has characteristic radiographic signs that may be correlated with the severity of the process. Early changes include minimal cardiomegaly and equalization of flow to upper and lower zones corresponding to pulmonary capillary wedge pressure of 15 to 25 mm Hg. The diameter of the upper lobe vessels is less than or equal to the lower lobe vessels at the same distance from the hilum, and pulmonary vessels in the first intercostal space are greater than 3 cm. Kerley B lines are present at the basal aspects of the lung with progressive worsening of heart failure. These markings cannot represent blood vessels because vessels are not normally seen as lung markings in the peripheral quarter of the lungs. Frank pulmonary edema (fluid accumulation in the alveolar spaces) becomes evident radiographically when bilateral, predominantly basilar and perihilar alveolar infiltrates are seen, and vessels near the hila become indistinct due to interstitial fluid accumulation.
Pulmonary edema may occur under special circumstances. Up to one-third of opiate overdoses develop pulmonary edema. Pulmonary edema due to inhaled or intravenous opiate abuse or inhalation of solvents or “crack” cocaine may have permeability edema with normal cardiomediastinal silhouette. Rapid clearing of edema is typical and pneumomediastinum or pneumothorax is occasionally associated.
Pulmonary hemorrhage may produce similar acute radiographic signs to pulmonary edema but the patient should have risk factors for pulmonary hemorrhage, should not have signs of fluid overload on examination, and the changes would resolve over a few days into a coarse interstitial pattern. Iatrogenic acute fluid overload would be expected to resolve very quickly with appropriate treatment (Figure 114-4).
(A) Perihilar airspace opacities are consistent with noncardiogenic pulmonary edema. Note sparing of lung bases and normal size of heart. (B) Coronal chest CT in the same patient with pulmonary edema. (C) Axial chest CT.
Radiographic criteria of pulmonary edema
Cephalization in upright patient
Lateralization in dependent lung of patient lying primarily on one side
Equalization when neither upper or lower lobe vessels predominate
Perihilar “bat-wing” pulmonary edema
Kerley B lines in lower zones
Enlargement of hilar pulmonary vessels
Limitations of the chest plain film in the diagnosis of fluid overload
Poor inspiration (less than the seventh rib) makes the lower zone vessels appear more prominent.
Patients with severe parenchymal lung disease may have atypical radiographic changes for edema.
The AP chest film may be misleading regarding cephalization and heart size.
The chest radiograph is mandatory for patients suspected of pneumonia, for acutely ill patients with new respiratory complaints or hypoxia, for patients with an exacerbation of chronic obstructive pulmonary disease, for immunocompromised patients with fever, and for elderly patients with confusion. The diagnosis of pneumonia can only be made through radiographic imaging, but a chest film cannot definitively identify the causative pathogen or rule out noninfectious causes (Table 114-4). Clinical pneumonia in the immune-compromised host can present with a normal chest radiograph, as classically seen with Pneumocystis jiroveci (formerly PCP). Unlike a normal host, patients with neutropenic fever may have only subsegmental atelectasis or focal peribronchial thickening in the presence of a bacterial infection. Hence, with the knowledge of the patient’s immune status and exposure history, the radiologist will lower the threshold for detection of subtle abnormalities and compare with a baseline study whenever possible.
TABLE 114-4Typical Pneumonia Patterns ||Download (.pdf) TABLE 114-4 Typical Pneumonia Patterns
|Multilobar Pneumonia ||S. pneumoniae and L. pneumophilia More Common |
|Bilateral diffuse pulmonary infiltrates in an immunocompetent patient ||More likely due to congestive heart failure or inhalation of a toxin or allergen than to a pneumonia caused by an atypical pneumonia |
|Community-acquired pneumonia due to methicillin-resistant Staphylococcus aureus ||Often bilateral cavitary lesions |
|Aspiration pneumonia || |
In a supine patient: left lower lobe (LLL) due to more posteriorly directed left mainstem bronchus
Time course: More homogeneous consolidation within 2 days of aspiration
Necrotizing pneumonia (Gram-negative and anaerobic organisms)
Cavities sometimes becoming thick walled over a period of a few weeks, thereby mimicking tuberculosis (TB). Unlike TB, lymphadenopathy is uncommonly associated
|Cavitary lesions || |
S. aureus, Pseudomonas; TB; Aspergillus infections (pulmonary infarct picture)
Mixed flora including anaerobes, aspiration (along with empyema)
Klebsiella (may have a bulging fissure sign), E. coli
Thin-walled cavities: Coccidioides immitis
|Mass-like lesions || |
Acute histoplasmosis: Hilar adenopathy and focal alveolar infiltrates
Disseminating form: Multiple nodules and hilar adenopathy
Blastomycosis: Mass-like opacities
A patient who is dehydrated will have decreased pulmonary vessel sizes with resulting overall decrease in vascularity on chest radiography. After rehydration signs of pneumonia may “bloom.”
Inhaled food is usually translucent, but if the inhalation has occurred some time previously, there may be segmental or lobar collapse. It is also possible for as little as 25 mm of sterile gastric contents to be aspirated more widely, resulting in Mendelson syndrome with visual appearance on chest radiograph that may be indistinguishable from pulmonary edema, although pulmonary vasculature is unlikely to be engorged by this process. Gravity directs the location, and underlying bronchiectasis may increase the likelihood of developing active infection. Patient position at the time of aspiration may lead to logical patterns besides the classically described pattern, involving the superior segments of the lower lobes and posterior basilar segments of the lower lobes.
Fungal infections in healthy individuals are most frequently due to endemic species in particular locations. Travel history can be vital to the radiologist in identifying the likely organism and decreasing the number of serologic tests required to confirm the specific diagnosis. The size, number of nodules, and associated findings, including more chronic calcification from reactivation of prior infection, may help distinguish histoplasmosis from coccidiomycosis. Small, numerous nodules associated with mediastinitis (evidenced by linear calcifications), large calcified lymph nodes, and tiny calcifications in the spleen suggest an infection with histoplasmosis. The largest calcified lymph nodes, often referred to as histoplasmomas, may, for technical radiologic reasons, not appear calcified on standard chest radiographs with the high kilovolt techniques that decrease conspicuity of bones. Fewer large nodules with associated adjacent pleural thickening suggest coccidiomycosis.
PRACTICE POINT Radiographic signs of pneumonia
Consolidation from pneumonia may maintain, increase, or decrease the volume of the affected lung with air bronchograms present.
Atelectasis, irregular aeration, peribronchial thickening and interstitial prominence may characterize more subtle pulmonary infections.
Reactive lymphadenopathy is most common in ipsilateral hilum.
Infection and infarction can have identical appearances on imaging studies.
Actinomycosis is the most frequent pneumonia to extend through the chest wall, characterized by suppurative and granulomatous inflammation that can lead to abscess formation and even sinus tracts through the skin that may be found on physical examination.
Varicella pneumonia occurs most frequently in pregnant women. Varicella pneumonia presents as diffuse, 5 to 10 mm nodular opacities that are poorly defined and may coalesce as the nodules increase in size. Although hilar lymph nodes may enlarge, they do not usually calcify. Healing can result in small calcific opacities throughout the lungs that are smaller in size and less uniform than that observed with prior histoplasmosis (Table 114-5).
TABLE 114-5Classic Presentations of Pneumonia ||Download (.pdf) TABLE 114-5 Classic Presentations of Pneumonia
|Organism ||Primary Finding ||Secondary Findings ||Evolution |
|Streptococcus pneumoniae ||Consolidation with air bronchograms that begins at the periphery and spreads to involve the entire segment or lobe; less likely with early appropriate treatment || |
Small pleural effusion (50%)
Possible hilar adenopathy; air bronchograms
Cavitation unusual for most serotypes but lymphadenopathy rare
|Transient round pneumonia 24-48 h, progresses to lobar consolidation, resolves by fading slowly |
|Mycoplasma pneumoniae ||Bronchial wall thickening || |
May have focal opacities
|Subtle persistent symptoms more prominent than radiographic findings |
|Legionella pneumophila ||A focal homogeneous opacity that may mimic a tumor followed by rapid progression to bilateral parenchymal involvement with associated pleural effusions without evidence of lympadenopathy || |
Sharply demarcated peribronchovascular opacity
Cavity formation may occur in immunocompromised patients but is uncommon in normal hosts
|Bilateral asymmetric opacities may range from ground-glass to dense consolidation |
|Consolidation with cavitation || |
May have sympathetic effusion
Staphylococcus may develop thin-walled cyst called a pneumatocele
Klebsiella may appear as enlarged, consolidated lobe
|Pneumocystis (carinii) jiroveci || |
Diffuse bilateral, fine to medium reticulonodular subtle opacities that could easily be overlooked
Chest radiograph may be normal (10%)
No pleural effusion
|Insidious can lead to consolidation |
|Aspergillus ||Nodular opacities with ground-glass halo || |
May be solitary or multiple
May also have consolidation
|Solid opacity that cavitates |
|Mucormycosis (Zygomycetes) ||Nodular opacity with ground-glass center ||May be solitary or multiple ||Evolves as infarction |
|Mycobacterium avium-intracellulare (MAI) and mycobacterium avium-complex (MAC) ||Bronchiectasis with tree-in-bud opacities ||Lymphadenopathy may be present ||Chronic colonization may not progress without treatment |
|M. tuberculosis || || || |
|Primary Infection ||Unilateral hilar lymphadenopathy and ipsilateral pleural effusion || |
Ipsilateral mediastinal lymphadenopathy
Consolidation may be radiographically absent
|Develop Ghon complex with granulomas that calcify within 2 y |
| ||Miliary opacities of hematogenous TB become visible ||Lymphadenopathy and pleural effusion may be present or absent ||Primary progressive TB |
|Reactivation TB ||Bronchiectasis and cavity particularly in upper lobe ||Upper lobe volume loss ||Development of new opacities |
The hematogenous spread of primary TB infection is radiographically inapparent in normal hosts. Miliary TB can be associated with primary progressive and reactivation of TB, particularly in immune-compromised patients. The visualization of micronodules on radiographs represents superimposition of multiple such shadows most likely seen at lung bases. Late presentation of miliary TB may result in greater visibility of nodules in lung apices due to the oxygen-rich environment favored by TB. Postprimary TB initially images as heterogeneous, poorly marginated opacities in the apical or posterior segments of the upper lobes or in the superior segments of the lower lobes, and later forms reticular and nodular opacities. Cavitation typically occurs within an area of consolidation and may result in endobronchial spread. Scarring, atelectasis, traction bronchiectasis, nodules, and calcification characterize healing. The presence of back or neck pain should be communicated to the radiologist to insure maximal study of the spine for osteomyelitis. The most frequently visible sign of Pott’s Disease is vertebra plana representing complete collapse of the affected vertebral body.
Usual interstitial pneumonia (UIP), rheumatoid lung, scleroderma lung, chronic hypersensitivity pneumonitis, asbestosis, and pulmonary drug toxicity may all produce similar radiographic abnormalities. Typically, UIP shows a pattern of bibasilar irregular linear opacities, which on high-resolution CT appear as ground-glass opacities, traction bronchiectasis, and honeycomb cysts in the periphery without associated adenopathy or pleural effusions. The presence of rheumatoid nodules and pleural effusion may help to radiographically distinguish rheumatoid lung from UIP. Small nodules or an upper lobe predominance may suggest chronic hypersensitivity pneumonitis. Pleural effusion or pleural plaques are a clue to the diagnosis of asbestosis. Pulmonary drug toxicity (amiodarone, bleomycin, methotrexate, nitrofurantoin) may also produce fibrosis (honeycomb cysts, architectural distortion, traction bronchiectasis).
Bronchiolitis obliterans typically appears as scattered air space consolidations (or as ground-glass opacities and consolidations without evidence of fibrosis on CT) in a peripheral and subpleural distribution with slightly reduced lung volumes. Bronchial wall thickening or bronchiectasis is commonly present. Bronchiolitis obliterans may have associated pleural effusions, nodules, or irregular linear opacities in a smaller number of patients. When parenchymal opacities are present, it is considered part of cryptogenic organizing pneumonia (COP, formerly BOOP). Pulmonary lymphoma and multifocal adenocarcinoma may have a similar radiologic appearance to COP on plain film imaging. Subtle ground-glass opacities seen on CT are often inapparent on chest radiographs.
Eosinophilic pneumonia from alveolar and interstitial infiltration by eosinophils and other inflammatory cells classically has peripheral and upper lobe opacities. The classic “reverse pulmonary edema” occurs in less than 50% of cases. Etiologies include pulmonary vasculitis (Churg-Strauss syndrome), allergic bronchopulmonary aspergillosis, and drug reactions.
Panlobular emphysema typically has regional or generalized decreased lung attenuation preferentially affecting the lung bases. Initially, centrilobular emphysema preferentially affects the apices as 2 to 10 mm lucencies without walls that later form large regions of decreased lung attenuation.
Parallel lines (tram tracks), ring shadows, and mucus plugs are characteristic images of bronchiectasis. Basilar bronchiectasis may result from viral pneumonia (such as adenovirus or measles in childhood), repeated aspiration, or prior bronchiectasis. Cystic fibrosis typically involves the upper lobes more than the lower lobes. Allergic bronchopulmonary aspergillosis may show cylindrical or saccular central, but not peripheral, bronchiectasis and preferentially involves the upper lobes.
Up to 90% of patients will have abnormality on chest radiographs at some time over the course of their illness. Tissue diagnosis showing microscopic noncaseating granulomas present in lungs, even when the radiographic appearance of the chest is normal, establishes the diagnosis. The most classic radiographic presentation includes bilateral symmetric hilar and mediastinal lymphadenopathy, particularly in subcarinal and right paratracheal regions. Differential diagnosis includes lymphoma. Less common, asymmetric hilar lymphadenopathy may result from sarcoid. Metastatic disease, TB, and other infections are unlikely to produce symmetric hilar lymphadenopathy. Irreversible end-stage lung disease seen in stage IV sarcoid has the greatest correlation between imaging findings and symptoms (Table 114-6).
TABLE 114-6Staging of Sarcoidosis ||Download (.pdf) TABLE 114-6 Staging of Sarcoidosis
|Stage ||Findings ||Location |
|0 ||Normal chest radiograph || |
|I ||Lymphadenopathy ||Bilateral hilar, subcarinal, right paratracheal regions |
|II ||Lymphadenopathy and pulmonary parenchymal opacities || |
Opacities along bronchovascular bundles, particularly in upper lobes
Small nodules that may also be seen peripherally
|III ||Pulmonary parenchymal opacities without lymphadenopathy ||Peribronchial thickening, small nodules |
|IV ||Honeycombing and traction bronchiectasis || |
Subpleural fibrosis accompanied by bronchiectasis
Lung opacities seen in stages II and III may also be present
| ||Alveolar sarcoid (stages II to IV) ||Consolidation due to interstitial granulomas filling alveoli |
INTERSTITIAL LUNG DISEASE OR DIFFUSE PARENCHYMAL LUNG DISEASE
The interstitium is the potential space between the alveoli and capillaries. Collagen deposition in the interstitium produces a radiographic appearance of diffuse interstitial opacification.
It is difficult and usually unnecessary to work up chronic interstitial lung disease during hospitalization for an unrelated acute illness. Fluid overload states cause pulmonary vascular engorgement from interstitial pulmonary edema producing thickening of interlobular septae on plain imaging. Repeated episodes of interstitial edema may lead to hemosiderin deposition, creating permanent visualization of interlobular septae even without pulmonary vascular engorgement or intrinsic interstitial lung disease. A nodular form of interstitial pulmonary edema may be reported as tiny nodular opacities or micronodules due to superimposed shadows. The clinical context is critical because micronodules may also represent hematogenous dissemination of infection (miliary TB or other fungal infections) or tumor. Visualization over time may help to avoid unnecessary evaluations for potential cancer. Unless directly related to the reason for admission, postdischarge follow-up after recovery of the acute illness would be advisable. See Table 114-7 for examples of common radiographic findings that may suggest an underlying chronic disease process or exposure.
TABLE 114-7Interstitial Lung Disease ||Download (.pdf) TABLE 114-7 Interstitial Lung Disease
|Cause ||Radiographic Finding |
|Asbestosis (prolonged exposure to asbestos) ||Lower-lung field predominance of infiltrates, pleural calcification, plaques |
|Silicosis ||Hilar egg-shell calcifications |
|Sarcoidosis ||Bilateral symmetrical hilar and paratracheal lymphadenopathy |
|Lymphangioleiomyomatosis (LAM) ||Pneumothorax in a premenopausal woman, chylous effusions |
Admission chest radiographs frequently identify incidental pulmonary nodules. By definition, a lung nodule measures up to 3 cm in diameter while a lung mass measures more than 3 cm in diameter. In clinical practice, these terms are not always used correctly. Doubling in less than 30 days generally indicates benign disease even when a lesion is large. Features of a nodular lesion and accompanying findings help to create a patient-specific differential diagnosis. Miliary TB, for example, may show diffuse 1 to 3 mm nodules that represent superimposition of micronodules not individually resolved by radiography. The larger volume of lung in the lung bases usually makes it more apparent in the bases than the apices, although a patient with a late presentation of miliary TB can have larger, and therefore more easily seen, tiny nodules in the lung apices due to the affinity of TB for the oxygen-enriched apical regions of the lungs.
When one solid pulmonary nodule is noted, the answer may be “in the jacket” (ie, 2 years of radiographic stability ensures that a solid nodule is benign). When multiple pulmonary nodules are present, necessary workup may be limited to explaining a prior infection. Nodules measuring less than 5 mm in diameter that are very well seen on chest radiographs, are likely calcified, and represent sequela of prior infection and require no further workup. Serial radiographs 6 months apart establish baseline when the patient has a positive PPD associated with scarring.
New nodules, nodules that increase in size, or nodules that have worrisome features should be evaluated by CT but not necessarily during the current hospitalization. Acute findings, such as atelectasis, pneumonia, pulmonary edema, and pleural effusions, often obscure important parenchymal findings. It may take 2 months or more for the appearance of the lung parenchyma following acute pneumonia to reach a new baseline. A plain film at that time may be sufficient to document complete clearing and the absence of an underlying nodule or central lesion causing a postobstructive pneumonia. The probability of cancer increases with the size of the nodule, although the size required for detection on chest radiographs varies with location. The best-quality chest CT scan requires the patient to be able to perform the breath-hold maneuvers. Figure 114-5 provides an algorithm for further evaluation of solitary pulmonary nodules. CT-based evaluation strategy is presented in Chapter 115.
Workup of solitary pulmonary nodule.
Typically, arteriovenous malformations appear as round, lobulated, well-defined masses ranging in size from less than one to several centimeters in diameter in the medial third of the lung. A chest radiograph may identify the enlarged feeding artery and draining vein, and a change in size may be apparent when erect versus supine radiographs are compared. Feeding vessels leading to the pulmonary nodule are prominent, enlarging rather than tapering along their often tortuous course. Small AVMs may require echocardiographic bubble study for detection. Radiographs may underdiagnose the number of AVMs present. It is therefore important to look for telangiectasias. Osler-Weber-Rendu syndrome is also known as hereditary hemorrhagic telangiectasia.
Hamartomas are solitary nodules usually less than 4 cm in diameter located peripherally in 90% of cases and may have a “popcorn-like” appearance due to calcification.
Granulomas form in response to inflammatory processes including TB and sarcoidosis. Radiographic confirmation of calcification, often possible for nodules measuring less than 5 mm in diameter, confirms the benign nature of the nodule.
Bronchial carcinoid tumors occur 85% of the time within the central bronchi as hilar masses with or without associated atelectasis or obstructive pneumonia. The other 15% of tumors arise peripherally as solitary, well-circumscribed pulmonary nodules.
Bronchogenic carcinoma may present as a smoothly marginated or spiculated nodule or mass. Adenocarcinoma has become the most frequent type of lung cancer. Early adenocarcinoma of lung can mimic an inflammatory process that might only be seen on CT scan. Even a very well-defined ground-glass opacity may be too subtle to see on chest radiographs because it does not obscure vessels.
Malignant pleural mesothelioma may image as a unilateral pleural mass, either focal or diffuse, is often associated with pleural effusion, and may locally invade the chest wall, mediastinum, or diaphragm. Pleural plaques from asbestos may be seen on the contralateral side, and are usually larger and more numerous in the mid to lower lung. More commonly encountered pleural tumors include solitary fibrous tumor and metastases.
Septic or bland infarcts, typically wedge-shaped and peripheral, are more numerous in the lung bases. Septic infarcts, usually 1 to 2 cm in diameter, cavitate in about 50% of nodules with moderately thick and irregular walls that decrease in size and eventually resolve, leaving in some cases a peripheral linear scar. Pleural effusions may be associated with septic or bland infarcts.
When the lesion has a central cavity, the description of the wall is most valuable. The course over time is also helpful. One-third to one-half of Wegener granulomatosis lesions progress from solid nodules to thick-walled cavities, to thin-walled cavities, and finally resolve without necessarily leaving a scar. Ten percent of patients may also develop diffuse pulmonary hemorrhage. An individual patient may have a mixture of these findings at the same time or over time. The presence of a fluid level in a cavity indicates communication with the tracheobronchial tree. It does not necessarily mean the cavity is infected. Cavitation is not always obvious on chest radiographs and superimposition of small and coalescing opacities may simulate a cavity without one being present. CT scanning is most reliable for identification and description of a cavitary lesion. Large cavitary lesions will also be apparent on magnetic resonance imaging (Table 114-8 and Figure 114-6).
TABLE 114-8Cavitary Lesions ||Download (.pdf) TABLE 114-8 Cavitary Lesions
|Wall Thickness ||Inner Surface ||Outer Surface ||Significance |
|Thin wall ||Smooth ||Smooth ||Cyst, bulla, pneumatocele |
|Thick wall ||Smooth ||Irregular ||Abscess with or without adjacent pneumonia |
|Thick wall ||Irregular ||Smooth, may be lobulated ||Malignant lesion particularly squamous cell carcinoma |
|Air-crescent ||Smooth ||Well-defined, may have ground-glass halo ||Invasive aspergillosis (occurs in immune-compromised host) |
Right upper lobe opacity with volume loss elevating the lateral aspect of the minor fissure contains a large central cavity due to necrosis. Gram-negative bacteria, such as Pseudomonas aeruginosa or anaerobic bacteria from oral flora is likely cause of this necrotizing pneumonia that has resulted from aspiration.
To identify a pneumothorax, first look at the boundary of a pneumothorax, which remains a thin white line parallel to the chest wall, in locations where it will be oblique to the ribs. Extensive lung opacities may obscure the thin white line, thereby creating a smooth boundary. Large bullae may be distinguished radiographically from a pneumothorax by their ring shadow or capsule. The sizing of a pneumothorax is often more reliable on chest radiographs than CT scans. Although symptoms dictate treatment of a pneumothorax rather than size, a reference for size ranges predicts the likelihood that intervention will not be required in an asymptomatic patient. In the absence of a continuing air leak, a small pneumothorax that is only visible above the lung apex will resolve in 5 days or less, at the rate of 1% of total volume of the hemithorax per day. In the erect patient, gas collection will only be seen above the lung apex, and pleural apposition will be maintained down the lateral chest wall. The apposition of lateral pleura is lost in a moderate pleural effusion, resulting in decreased resorption of pleural fluid and greater chance of requiring intervention. Large pneumothoraces allow separate visualization of lobes of the lung and may be associated with tension physiology including hypotension due to a potentially catastrophic decrease in venous return to the heart (Figure 114-7).
Tension pneumothorax. Expiratory radiograph of right tension pneumothorax increases the apparent shift of midline structures including the azygoesophageal line, seen here behind the heart, to the left of the spine. The three lobes of the right lung are seen separating from each other centrally with complete absence of lung markings peripherally. Increased space between ribs and depression of the right hemidiaphragm also indicate expansion of the space occupied by the pneumothorax.
PRACTICE POINT Pneumothorax
On the supine AP chest radiograph in the adult, one of the most reliable signs of pneumothorax is the deep sulcus sign. If air is in the pleural space, it can easily track down making the costophrenic angle deeper and more acute.
Quantitative measurements, whether percentage pneumothorax or centimeters of displacement from the chest wall, are less useful than expert radiologic consultation, particularly when chest radiographs are obtained at the bedside.
The sizing of pneumothoraces and pleural effusions is often more reliable on chest radiographs than CT scans.
When a patient also has significant pleural effusion providing opacity outside the lung, it may become nearly impossible to detect the pneumothorax on a supine bedside chest radiograph.
Normally, a thin white line represents the apposition of the parietal and visceral surfaces. Pleural disease, however, may cause expansion of the pleural space along with lobar collapse. Plain chest radiographs, rather than chest CT scans, may provide more reliable sizing of pleural effusions. An average of 300 cc of fluid is required to completely blunt a posterior costophrenic sulcus on a lateral chest radiograph. A small pleural effusion may not be visible on PA chest radiograph. A moderate pleural effusion is well seen on both PA and lateral views, and the distance between the stomach bubble and lung base may be increased. Subpulmonic collections may laterally displace the hemidiaphragmatic peak on the PA view. This does not in itself mean that the collection is trapped or loculated. Loculation may be associated with empyema, especially when it occurs in a patient who becomes increasingly ill despite improvement in treated pneumonia. A large pleural effusion severely restricts lung expansion, but retains visible lung on chest radiographs. A very large pleural effusion may result in complete whiteout of the hemithorax (Figure 114-8).
A very large pleural effusion can also cause tension physiology. Note contralateral shift of the mediastinum.
When a patient has a significant pleural effusion providing opacity outside the lung, it may become nearly impossible to detect the pneumothorax on a supine bedside chest radiograph. In this case, usually from barotraumas or line placement, the abnormal gas collection may take up to 5 days to become apparent, at which time the patient will have developed a pneumoperitoneum from a pneumomediastinum that communicated through the tight retroperitoneal cavity and dissected through the mesentery. Pneumoperitoneum has to be attributed to rupture of a hollow viscus until proven otherwise. For intubated patients who cannot be examined for an acute abdomen, this requires consultation with radiologists and other specialists and correlating with instrumentation.
EVALUATION OF CHEST PAIN AND/OR DYSPNEA
Commonly, chest radiographs are urgently ordered to evaluate causes of chest pain and to look for complications such as asymptomatic pulmonary edema in the setting of myocardial ischemia. Although the chest radiograph may be normal despite a life-threatening condition, such as an aortic dissection or pulmonary embolism (PE), plain chest radiographs may facilitate immediate identification if abnormal signs are present in addition to expediting management and further investigation.
Thoracic dissection: radiographic clues that should prompt advanced imaging
Widening of superior mediastinum >8 cm
Blurring of the aortic contour
Opacification of the angle between the aorta and the left pulmonary artery
Tracheal shift to the right
Depression of the left main bronchus to an angle <40° with the trachea
Note: Aneurysms of the aorta are defined by the following measurements:
Nonspecific radiographic findings associated with pulmonary embolism
A normal chest radiograph
Atelectasis the most common nonspecific finding associated with PE
Small pleural effusions
Abnormally increased lung lucency due to reduced pulmonary vessels distal to embolism (asymmetry of vessels)
Abrupt cutoff or rat-tail appearance of pulmonary vessels
More common than early features, later findings of pleural effusion, linear or wedge-shaped opacities due to infarction, cavitation of infarction
PRACTICE POINT Flail chest
Look for rib fractures that may indicate more serious thoracic injuries.
Two or more rib fractures in two or more places or when the clavicle and first rib are fractured indicates a flail segment, which is associated with pulmonary contusion and respiratory failure.
Patchy consolidation, although an early finding, may underestimate the severity of the injury.
PRACTICE POINT Ruptured esophagus
In the patient with severe central chest pain after vomiting, look for
Typical life-threatening disorders that can alter the contour of the cardiomediastinal silhouette are acute vascular emergencies (ie, leaking thoracic aortic aneurysm or aortic dissection). If prior films are available for comparison, changes in aortic vessel diameter between two films are likely to be significant. For a stable patient, differentiating great vessel pathology from mediastinal disease requires advanced imaging unless there are prior images for comparison. If the plain chest imaging shows an abnormality of the mediastinum (eg, widening or distorted contour) or a displacement or narrowing of the trachea, the following potentially life-threatening diagnoses should be considered: primary and metastatic malignancy (bronchogenic and esophageal carcinoma, germ cell tumors, lymphoma, and thymoma), aortic disease (aneurysm, coarctation, dissection), congenital cysts, and vascular abnormalities. Benign diagnoses include asymmetric fat deposition, intrathoracic goiter, esophageal hernia, and vascular tortuosity.
Although a chest radiograph lacks specificity in the diagnosis of PE, it provides valuable data to use in the selection of further imaging to evaluate for PE, especially when pretest probability of PE is low. A chest film may identify abnormalities that explain the patient’s symptoms or make interpretation of a ventilation scan indeterminate. If the chest radiograph is normal, a normal nuclear medicine perfusion study provides the best possible exclusion of PE. The patient with normal radiography will have an unambiguous ventilation/perfusion scan, and the normal CT will only add radiation and contrast without benefit as well as potentially lead to additional CT scans to prove stability of incidentally identified small lung nodules.
THE EVOLUTION OF RADIOGRAPHIC FINDINGS
The evolution of radiographic findings over time can correctly single out the likely diagnosis to explain a chief complaint. While acute consolidation of lung can be due to hemorrhage, pneumonia, or pulmonary edema, each of these processes undergoes a different evolution over time. The clinical presentation provides supporting data, including suggestive symptoms in the setting of known risk factors such as anticoagulation or heart disease, abnormal vital signs, or confirmatory physical signs. Hemorrhage occurs suddenly and resolves over several days with a coarse interstitial pattern as it resolves. The radiographic features of pulmonary edema depend upon the rapidity of onset; an interstitial pattern that may be accompanied by small pleural effusions may be seen when symptoms have a gradual onset, whereas perihilar consolidation is more commonly seen with symptoms that arise suddenly. Both forms can clear quite quickly, often within 24 hours, especially in patients on dialysis who can have wide fluctuations in fluid status. Pneumonia will cause increasing opacity; as it resolves, it will fade slowly, often over a prolonged period of time, well beyond the hospitalization.
The rate of radiographic improvement of pneumonia
The rate of radiographic improvement is directly related to age and, to a lesser degree, to the extent of radiographic involvement and to underlying chronic disease and alcoholism.
Eighty percent of patients less than or equal to 40 years of age with pneumonia will have complete resolution within 6 weeks after the initial diagnosis.
Only 20% of patients 80 years of age will have complete resolution during this time period.
Only about 67% of patients with community acquired pneumonia (CAP) will have clearing of pneumonia on chest imaging by the fourth week following initiation of treatment.
The evolution of these processes suggests the optimum time for follow-up imaging. For example, an elderly patient with pneumonia would not be expected to have radiographic resolution of a significant pneumonia at the time of his first follow-up appointment with his primary care physician in a week’s time. The timing of follow-up films should depend on the need to confirm a diagnosis or to assess response to treatment. One film obtained after the acute illness has likely resolved may be all that is necessary as a new baseline for future patient care. The timing of a chest radiograph to check for resolution of pneumonia depends on the age of the patient, the severity of the pulmonic process, and whether there is a high likelihood of postobstructive pneumonia (lobar collapse).
FINDINGS THAT REQUIRE FURTHER FOLLOW-UP IMAGING
It may be useful to divide such findings into two broad categories: (1) follow-up is needed to ensure the chest has returned to normal and (2) follow-up is needed to evaluate a previously unknown finding of potential significance, such as a lung nodule. The further workup of incidental nodules that require CT scanning is best deferred until the patient has recovered and the appearance of the chest has otherwise returned to normal. This is also true of investigations for interstitial lung disease. The central question regarding pulmonary nodules is whether the nodule is likely to be benign or malignant. Solitary pulmonary nodules may be an early manifestation of lung cancer. In one study, 40% of lung cancers were originally detected as a solitary pulmonary nodule. Opacification and consolidation with radiodense bone lesions in multiple ribs would suggest that disease has already become metastatic. It is also important to examine the hilum and mediastinum, especially in patients with a prior history of cancer. Variations of appearance based on visual features about margins, calcification, cavitation, and wall thickness may evolve over time. The presence of a mixture of solid, thick-walled cavities, thin-walled cavities, and resolution of prior nodules without scarring is far more specific for Wegener granulomatosis when these features are all seen in the same patient over time (Figure 114-8).
Chest radiographs are the most frequently obtained medical imaging during acute illness. The radiographs can provide physiologic as well as anatomic data. A baseline follow-up examination following resolution of the acute abnormality is mandatory for the care of patients with pneumonia and extremely helpful for the care of patients who have episodes of congestive heart failure, exacerbations of chronic obstructive pulmonary disease, or a tendency to develop acute abnormalities superimposed on chronic changes. As more data are accumulated during the workup of the acute illness, reconsideration of prior chest radiographs may rapidly provide additional information without additional radiography or more advanced imaging. Increasing the clinical information provided to the interpreting radiologist will result in more specific answers to clinical questions. The radiologic differential diagnosis will also be reduced through consideration of the evolution of the radiographic findings over time.
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