Urgent Findings on Portable Chest Radiography - AJR

AJR Integrative Imaging LIFELONG LEARNING FOR RADIOLOGY

Urgent Findings on Portable Chest Radiography: What the Radiologist Should Know—Review Ashwin Asrani1, Rathachai Kaewlai2, Subba Digumarthy2, Matthew Gilman2, Jo-Anne O. Shepard2

Objective Portable chest radiographs account for the majority of inpatient radiographs. Portable studies are usually obtained of acutely ill patients who may have urgent findings necessitating prompt detection and treatment. Urgent findings are defined as significant and unexpected findings requiring immediate corrective action. The purpose of this article is to illustrate common examples of urgent findings on portable chest radiographs and to provide useful tips for the radiologist. Clinical scenarios are included to orient the learner to the evaluation of urgent findings on portable chest radiography. The examples in this article are selected from various ICUs including medical, cardiac, neurology, cardiothoracic surgery, general surgery, orthopedic, and burn services.

Conclusion Portable chest radiographs are obtained of acutely ill patients who cannot stand up for a standard two-view chest radiographic study. Although portable radiographs may be technically limited, they still provide valuable information. Acutely ill patients often have multiple support devices and rapidly evolving findings. Knowledge of the clinical setting provides a clue to the urgent findings that might be expected.

Scenario 1 Clinical History A 71-year-old man presented with low cardiac output and elevated central venous pressure 2 weeks after cardiac surgery. He had undergone coronary artery bypass grafting with the left internal mammary artery to the left anterior descending coronary artery and the saphenous vein from the ascending aorta to the posterior descending branch of the right coronary artery. Aortic valve replacement with an ascending aortic tube graft and hemiarch replacement were also performed. Chest tube drainage showed a small amount of blood. Of note, he had undergone mediastinal explora-

tion for evacuation of a hematoma on postoperative day 1 because of leakage from the ascending aortic graft. Serial chest radiographs were obtained daily after cardiac surgery. Figures 1A and 1B are supine chest radiographs obtained on the second and third postoperative days, respectively. The patient underwent subsequent contrast-enhanced chest CT (Fig. 1C).

Description of Images The initial chest radiograph showed slight widening of the mediastinum (arrows, Fig. 1A). A subsequent chest radiograph (Fig. 1B) showed progressive widening of the mediastinum, worsening interstitial edema, and increased pleural effusions. Chest CT (Fig. 1C) revealed a high-attenuation collection in the mediastinum located to the right of the ascending aortic graft.

Conclusion Magnification on anteroposterior supine radiographs, lowvolume respiration, and lordotic positioning can produce an apparent widening of the mediastinum that is difficult to confidently distinguish from true abnormalities. This is especially true in critically ill or postoperative chest patients who cannot voluntarily take a deep breath. Additionally, crowding of normal vascular structures can be caused by the splinting effect of the chest. In this setting, serial chest radiographs are often helpful in identifying a change in cardiothoracic status in addition to repeated clinical and laboratory testing. Because the second radiograph was obtained using a similar technique and there were equal lung volumes compared with the baseline radiograph, an interval increase in mediastinal widening is likely to be a true finding. An aortic aneurysm is often a result of atherosclerotic disease and occurs frequently in elderly patients. Aortic root dilatation can occur in patients with severe hypertension and aortic valve stenosis. Dissection may complicate a

Keywords: chest imaging, emergency radiology, hemothorax, lobar collapse, mediastinal hematoma, pneumomediastinum, pneumothorax, pulmonary edema, pulmonary embolism, pulmonary hemorrhage, pulmonary infarct DOI:10.2214/AJR.09.7170 Received March 31, 2009; accepted after revision December 13, 2009. Department of Radiology, Weill Cornell Medical College, 525 E 68th St, New York, NY 10065. Address correspondence to A. Asrani ([email protected]).

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Department of Thoracic Radiology, Massachusetts General Hospital, Boston, MA.

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B Fig. 1—71-year-old man with low cardiac output and elevated central venous pressure 2 weeks after cardiac surgery. A, Initial chest radiograph shows slight widening of mediastinum (arrows). B, Subsequent chest radiograph shows progressive widening of mediastinum (arrows), worsening interstitial edema, and increased pleural effusions. C, Chest CT image reveals high-attenuation collection in mediastinum (arrow) located to right of ascending aortic graft.

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preexisting aortic aneurysm. Aortic dissection is a result of an intimal tear of the aortic wall, subsequent intramural hemorrhage, and creation of a false lumen. On conventional radiography, it may appear as widening of the mediastinum, blurring of the aortic arch, displaced aortic calcification, or deviation of a nasogastric or endotracheal tube. The risk of aortic dissection may be increased after recent cardiac surgery, especially surgery with bypass grafting. Although aortic dissection is a possible explanation of widening of the mediastinum in this patient, it is not common. Neoplasm that involves multiple lymph node groups, such as lymphoma or metastasis, can produce apparent mediastinal widening instead of a discrete mass. Hodgkin lymphoma has a peak incidence in the second and third decades, with a

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secondary peak in the fifth and sixth decades of life. It commonly involves two or more mediastinal nodal stations. Anterior mediastinal and paratracheal lymph nodes are the most frequently involved sites [1]. Extensive adenopathy due to metastatic disease from lung and distant primaries is prevalent with poorly differentiated tumors such as small cell tumors, retroperitoneal tumors, seminoma, thyroid carcinoma, and renal cell carcinoma. Changes in the size and appearance of these tumors (i.e., progression, recurrence, or improvement) typically take months after treatment. Mediastinitis and mediastinal abscess are serious, but uncommon, complications after cardiothoracic surgery. A deep sternal wound infection (i.e., bone and retrosternal infection) affects 0.4–5% of all patients after cardiac surgery,

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Urgent Findings on Portable Chest Radiography

with Staphylococcus aureus and Streptococcus epidermidis being the most common organisms. Obesity, diabetes, preoperative hemodynamic instability, preoperative renal failure on dialysis, and transfusions of more than 4 U of packed RBCs after surgery appear to be risk factors for the development of an infection [2]. Mediastinal infection can present on radiography as mediastinal widening. However, this finding often appears late in the postoperative period. Mediastinal widening in patients after cardiothoracic surgery due to hematoma is common. However, only small percentages (7–14%) of patients require reoperation for hemorrhage or tamponade. The wider the mediastinum is on the postoperative radiograph, the greater the chance of reoperation. Patients with an increase in mediastinal width after sternotomy of more than 70% usually require reoperation. On the other hand, some patients with minor mediastinal widening may require another operation if blood loss is clinically apparent [3]. Therefore, the decision to perform a second operation is based on the overall clinical picture rather than on the radiographic changes alone. The next diagnostic test to confirm postoperative hematoma is unenhanced and contrast-enhanced CT of the chest. On unenhanced CT, an acute mediastinal hematoma appears as a hyperattenuating collection of 50–90 HU that is usually

in the retrosternal space or adjacent to the site of surgery. After IV contrast administration, hematoma does not enhance. The advantages of contrast-enhanced CT include its superior ability to show thoracic vascular structures and active extravasation and to exclude other causes of mediastinal widening on conventional radiography such as aortic dissection or mediastinal abscess. Serial chest radiography may be used to follow hematoma after the diagnosis is confirmed with CT. MRI of the chest can detect hematoma; however, its main limitations are incompatibility with various ICU monitoring devices the patient may have and long acquisition time. PET has no role in the diagnosis of a hematoma. Anticoagulation therapy is mandatory in patients after cardiac valve surgery with the use of a mechanical valve prosthesis to prevent thromboembolism. Warfarin or other anticoagulants are used to sustain a desirable level of international normalized ratio (INR), which differs among patients according to their risk factors for thromboembolic episodes. Aspirin is added to a warfarin regimen to lower the incidence of thromboembolism. However, these approaches come with an increased risk of bleeding: the higher the INR level, the higher the risk of bleeding. Most commonly, bleeding occurs during the first 6 months of anticoagulation. Diabetes mellitus is not associated with an increased risk of postoperative hematoma [2].

Scenario 2 Clinical History

latures through the opacity coupled with the presence of a thickened minor fissure and blunting of the right costophrenic angle. Given the rapidity of the development of a pleural effusion in a patient who had recently undergone thoracic biopsy, hemothorax is the most likely diagnosis. Empyema can have an appearance similar to hemothorax but usually develops in days or weeks—not hours as in this patient. Empyema usually occurs in association with pneumonia but also may be caused by extension of infection from adjacent structures including the mediastinum, neck, or abdomen. Penetrating thoracic trauma, chest tube placement, thoracic surgery, and malignant pleural effusion may also be complicated by empyema. Lobar collapse appears as an opacity confined to the pulmonary lobe involved with evidence of volume loss. Lung volume loss can be shown as crowding and reorientation of pulmonary vessels, displacement of fissures, elevation of the diaphragm, displacement of the hilum, mediastinal shift, and crowding of the ribs. There is no sign of lung volume loss in this patient. Aspiration and aspiration-related pneumonia can be a cause of a rapidly appearing opacity. The distribution of the opacity is a key feature differentiating aspiration pneumonia from other causes of pulmonary consolidation. The characteristic location of aspiration is in the dependent portions of the lungs. Aspiration pneumonia should be suspected in patients who have known predisposing conditions such as seizure disorder, disturbances in esophageal motility, recent anesthesia, alcoholism, mental retardation, and head and neck tumors.

A 55-year-old man with a known history of amyloidosis presented after cardiac and hepatic transplantation with a right pleural mass. He underwent video-assisted thoracoscopic biopsy of the right pleural mass. Chest radiographs were obtained immediately (Fig. 2A) and 5 hours (Fig. 2B) after the procedure. The chest radiograph obtained after treatment is shown in Figure 2C.

Description of Images The initial postprocedural chest radiograph showed a right chest tube in position (white arrow, Fig. 2A). There was no pneumothorax. A pleural-based opacity was noted in the inferolateral aspect of the right hemithorax. The subsequent chest radiograph showed a hazy opacity involving the upper and mid right hemithorax (black arrow, Fig. 2B) that had developed during the interval. Note visible lung markings through the opacity. There was no evidence of right lung volume loss. The right chest tube was unchanged in position and appearance. The chest radiograph obtained after treatment with placement of additional right chest tubes (black arrows, Fig. 2C) showed a marked decrease of this opacity.

Conclusion The opacity in the right hemithorax of this patient has a characteristic appearance of pleural effusion, which includes homogeneous opacity and visible pulmonary vascu-

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B Fig. 2—55-year-old man with history of amyloidosis and cardiac and hepatic transplantation who underwent video-assisted thoracoscopic biopsy of right pleural mass. A, Initial postprocedural chest radiograph shows right chest tube in position (white arrow). There is no pneumothorax. Pleural-based opacity (black arrow) is noted in inferolateral aspect of right hemithorax. B, Subsequent chest radiograph shows interval development of hazy opacity (black arrow) involving upper and mid right hemithorax. Note visible lung markings through opacity. There was no evidence of right lung volume loss. Right chest tube (white arrow) is unchanged in position and appearance. C, Chest radiograph obtained after treatment with placement of additional right chest tubes (arrows) shows marked decrease of this opacity.

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Pulmonary edema appears as an airspace opacity that has a perihilar distribution. Septal lines may be present in the costophrenic angles. Prominence of the upper lobe pulmonary vasculature, indistinctness of the vessels, peribronchial cuffing, and a widened vascular pedicle are other signs of pulmonary edema. Occasionally, the distribution of pulmonary edema is not uniform. This lack of uniformity could result from the effect of gravity in patients who lie on one side: Fluid in the lungs tends to gravitate to the dependent side. The distribution of pulmonary edema can also be nonuniform in patients with severe pulmonary emphysema, concomitant pneumonia, or pulmonary embolism. In this patient, the opacity is most likely pleural in origin. The presence of pleural effusion (in this case, hemothorax) on imaging can be confirmed with chest radiography, ultrasound, or CT. A radiograph obtained with the patient

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in a lateral decubitus position shows shifting of the opacity to the dependent portion of the pleural cavity. A cross-table lateral radiograph can be used if the patient’s condition does not permit decubitus positioning. The finding of a pleural effusion on a cross-table lateral radiograph is a layering opacity in the posterior part of the pleural cavity. Ultrasound is a valuable tool for the assessment of several chest diseases with high accuracy, particularly when the pleural space is involved. Its advantages are low cost, absence of radiation exposure, bedside availability, and short examination time. Ultrasound can help detect pleural effusion, determine the possible nature of pleural fluid, and guide thoracentesis and drainage. On ultrasound, pleural effusion appears as a space between the visceral and parietal pleura with variable echogenicity depending on the type of effusion. Hemorrhagic effusion or hemothorax has a homogeneously echogenic pattern on ultrasound images [4].

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CT is the current modality of choice for the evaluation of chest diseases because of its ability to assess the lungs, mediastinum, pleura, and chest wall structures with high accuracy. Hemothorax appears on CT as high-attenuation pleural fluid or a collection that does not enhance. Expiratory chest radiography is used for the detection of small pneumothorax, not pleural effusion. During the expiratory phase of respiration, there is less air within the alveoli; therefore, the contrast between the pneumothorax and lung parenchyma becomes more apparent and easier to detect than on an inspiratory radiograph.

According to a survey of complication rates of 9783 CTguided transthoracic biopsy procedures (this patient had undergone video-assisted thoracoscopic biopsy, not transthoracic biopsy) performed in 124 medical centers in Japan [5], hemothorax occurred in nine cases (0.09%). Other severe complications included severe pulmonary hemorrhage (0.26%), shock and cardiopulmonary arrest (0.26%), tension pneumothorax (0.1%), air embolism (0.06%), and tumor seeding at the biopsy site (0.06%). Most patients with severe complications recovered without disability [5].


sualized. Subsequent chest CT revealed a large left pneumothorax (white arrow, Fig. 3B) and subcutaneous emphysema (black arrow, Fig. 3B) in the left chest wall.

A 35-year-old man presented after a fall from a 50-ft (15m) scaffold. He lost consciousness and was intubated at the site of trauma and transported to the emergency department. A supine chest radiograph (Fig. 3A) was obtained followed by a chest CT scan (Fig. 3B). An accompanying head CT scan (not shown) showed a depressed skull fracture with a large acute subdural hematoma and an intraparenchymal hematoma causing midline shift.

Description of Images A supine chest radiograph showed an endotracheal tube and a left subclavian venous catheter in optimal position. There was relative hyperlucency of the left hemithorax with a deep left costophrenic sulcus (white arrow, Fig. 3A), mediastinal shift to the right, and splaying of the left ribs. Air in the left chest wall (black arrow, Fig. 3A) was also vi-

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Conclusion Loss of pulmonary vascularity is a cause of increased lucency of the hemithorax commonly due to bullous emphysema and pulmonary embolism. Severe bullous emphysema may cause apparent decreased attenuation of the lung parenchyma and alteration of pulmonary vascularity, which results in hyperlucent lungs on chest radiography. Although the changes may be subtle on conventional radiography, they can be readily shown on CT. Emphysema typically involves both lungs and appears as an alteration of pulmonary vascularity, excessive lung inflation, widening of the retrosternal clear space, and increased anteroposterior diameter of the chest. In this patient, an increased lucency was unilateral and there were no other signs of emphysema.

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Fig. 3—35-year-old man who fell from 50-ft (15-m) scaffold. A, Supine chest radiograph shows endotracheal tube and left subclavian venous catheter in optimal position. There is relative hyperlucency of left hemithorax with deep left costophrenic sulcus (white arrow), mediastinal shift to right, and splaying of left ribs. Air (black arrow) in left chest wall is also visualized. B, Subsequent chest CT image reveals large left pneumothorax (white arrow) and subcutaneous emphysema in left chest wall (black arrow).

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Pulmonary embolism may obstruct and reduce blood flow in the affected pulmonary artery, resulting in hyperlucency of the affected portion of the lung. These areas may be segmental or lobar or may involve the entire lung. On CT, a hypoattenuating area of reduced pulmonary perfusion is shown distal to the occlusion of a segmental, lobar, or main pulmonary artery [6]. In this patient, lucency of the left hemithorax was accompanied by increased volume of the left hemithorax, which is unusual for pulmonary embolism [7]. A unilateral hyperlucent lung may be a result of air trapping due to bronchial obstruction from a neoplastic or nonneoplastic cause. An endobronchial mass may cause atelectasis or air trapping. In the latter circumstance, collateral air drift contributes to trapping of air beyond the site of bronchial obstruction. There is stretching of alveoli due to air trapping, which results in compression of pulmonary vessels and a hyperlucent lung best seen on expiratory images. In children, most bronchial obstructions result in air trapping, whereas an obstruction in adults often causes atelectasis. In this case, the acuity of the patient’s symptoms makes a left endobronchial mass unlikely. Pneumothorax produces hyperlucency of the hemithorax and is usually recognized by its typical location and configuration. Air rises to the nondependent portion of the pleural space and separates visceral from parietal pleural layers, resulting in

a visible visceral pleural line. An area beyond this line contains neither lung tissues nor vascular structures. Although pneumothorax is relatively easy to distinguish from hyperlucent lungs because of its aforementioned characteristic features on upright chest radiography, it may be difficult to diagnose when the radiograph is obtained of a supine patient. Because the highest portion of the pleural space lies in the anterior and anteromedial aspect at the base near the diaphragm in a supine patient, pneumothorax rises to that region. If pneumothorax is small or moderate, air may not separate lung tissue from the lateral chest wall or apex. Such pneumothoraces may be difficult to appreciate. Pneumothorax is the most common complication after placement of a central venous catheter, particularly if placed using a subclavian venous approach [8]. Signs of pneumothorax on supine radiographs include basilar hyperlucency, depression of the diaphragm, sharp mediastinal or diaphragmatic contour, distinct cardiac apex, and presence of the inferior edge of the collapsed lung [9]. A left pneumothorax would result in either no mediastinal shift or mediastinal shift away from the involved hemithorax. A small or moderate pneumothorax may not result in contralateral mediastinal displacement in some patients or if the patient is on positive pressure ventilation. In this situation, other signs of pneumothorax on supine radiography need to be sought.


Pneumoprecardium refers to substernal air anterior to the heart. It requires a lateral view chest radiograph for detection. Pneumoprecardium may be the only radiographic finding in patients with pneumomediastinum; therefore, obtaining both anteroposterior and lateral chest radiographic views is important [12]. The air outlining the superior surface of the diaphragm separates it from the heart and can result in a continuous diaphragm sign. Subcutaneous emphysema is common, but not specific, in patients with pneumomediastinum. Although a continuous diaphragm sign is not specific for pneumomediastinum given that it can be seen in pneumopericardium [13], subcutaneous emphysema is least specific for this condition. Possible causes of subcutaneous emphysema include blunt and penetrating trauma, pneumothorax, rib fracture, perforated esophagus, tracheobronchial injury, and gas gangrene. Multiple thin lucent streaks of air in the mediastinum may be confused with pneumothorax when air streaks extend over the lung apex, between the mediastinal border and the lungs, along the diaphragm, or behind the sternum. In these locations, air may be in the pleural space (pneumothorax) or in the mediastinum (pneumomediastinum). Air outlining the mediastinal extrapericardial portion of the pulmonary artery is definitive of pneumomediastinum. Pneumomediastinum is distinguishable from pneumothorax by the location and distribution of air in most cases. The configuration of air and change in distribution with a change

A 28-year-old man presented with acute onset of leftsided chest pain. There was no recent trauma, fever, cough, sputum production, or palpitation. His vital signs were stable. Chest radiography (Fig. 4A) was performed followed by chest CT (Fig. 4B).

Description of Images The supine chest radiograph showed streaky lucencies outlining the mediastinal structures (black arrows, Fig. 4A) and the neck and chest wall (white arrows, Fig. 4A). There was no pneumothorax. Chest CT showed extensive pneumomediastinum (black arrows, Fig. 4B) with extension to the neck soft tissues (white arrows, Fig. 4B).

Conclusion The radiographic signs of pneumomediastinum rely on the presence and amount of air outlining the normal mediastinal structures. The thymic sail sign is described as an elevated thymus in neonates or children with pneumomediastinum. Mediastinal air outlines the normal thymus, resulting in visibility of a normal thymus on radiography and producing a “sail” appearance [10]. The “ring-around-the-artery” sign refers to air outlining the major vascular structures in the mediastinum, particularly when air surrounds the mediastinal extrapericardial right pulmonary artery [11].

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Fig. 4—28-year-old man with acute onset of left-sided chest pain. A, Supine chest radiograph shows streaky lucencies outlining mediastinal structures (black arrows) and neck and chest wall (white arrows). There is no pneumothorax. B, Chest CT image shows extensive pneumomediastinum (black arrows) with extension to neck soft tissues (white arrows).

in patient position are also helpful to distinguish between the two entities. Pneumomediastinum appears as multiple thin lucent streaks that do not change with different positioning of the patient in contrast to pneumothorax [14]. Pneumomediastinum results from a variety of sources that may be intrathoracic or extrathoracic [15]. Intrathoracic structures that could give rise to pneumomediastinum include the trachea, major bronchi, esophagus, lung, and pleural space. In the neck, air may dissect through the soft tissues from fractured paranasal sinuses into the mediastinum. Pneumomediastinum may also result from peripheral alveolar rupture with dissection of air centrally along the interstitium and into the mediastinum

(Macklin effect) or from dissection of air into the mediastinum from perforation of hollow abdominal viscera. Intrathoracic causes of pneumomediastinum include airway obstruction (e.g., foreign body aspiration, asthmatic attack); straining against a closed glottis (e.g., severe and protracted vomiting, repeated Valsalva maneuvers); mechanical ventilation; and blunt chest trauma with transmural perforation of the trachea, proximal bronchi, or esophagus. Pneumothorax can occur secondary to pneumomediastinum. When there is an abrupt increase in mediastinal pressure, the mediastinal parietal pleura may rupture and cause a pneumothorax. In contrast, pneumothorax is unlikely to cause a pneumomediastinum.

Scenario 5 Clinical Scenario

region of the right upper lung zone with a sharply demarcated margin and elevation of the minor fissure (white arrow, Fig. 5B). There is also elevation of the right hemidiaphragm. Prompt flexible fiberoptic bronchoscopy revealed the cause of respiratory distress, which improved after aggressive suctioning. Follow-up portable chest radiography revealed near complete reexpansion of the right upper lobe with residual platelike atelectasis (white arrow, Fig. 5C).

A 36-year-old man with multiple gunshot wounds to the abdomen was admitted to the surgical ICU after exploratory laparotomy. Since admission to the surgical ICU, he developed tachypnea with decreased oxygen saturation and decline in mental status. Oxygen saturation failed to improve with a tent face mask, and a portable chest radiograph was then obtained.

Description of Images An initial portable frontal chest radiograph (Fig. 5A) provided for comparison shows low lung volumes but is otherwise unremarkable for any lung abnormality. A subsequent portable frontal radiograph of the chest obtained at the time of hypoxemia shows low lung volumes with opacity in the

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Conclusion Lobar pneumonia is unlikely to result in rapid volume loss of the right upper lobe and to improve rapidly after bronchoscopy and suctioning, as shown by the serial portable chest radiographs of this patient. Also, lobar pneumonia is more commonly encountered in the setting of community-acquired pneumonia rather than in the postoperative clinical setting [16].

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B Fig. 5—36-year-old man with multiple abdominal gunshot wounds in surgical ICU with acute hypoxia. A, Initial portable frontal chest radiograph provided for comparison shows low lung volumes but is otherwise unremarkable for any lung pathology. B, Subsequent portable frontal radiograph of chest obtained at time of hypoxemia shows low lung volumes, opacity in region of right upper lung zone with sharply demarcated margin, and elevation of minor fissure (arrow). There is also elevation of right hemidiaphragm. C, Follow-up portable chest radiograph reveals near complete reexpansion of right upper lobe with residual platelike atelectasis (arrow).

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Pulmonary embolism can present as sudden onset of hypoxemia in a postoperative ill patient in the ICU. The most common findings on a portable chest radiograph in a patient with pulmonary embolism are normal findings, nonspecific linear atelectasis, or a small pleural effusion [16]. Mediastinal hematoma may present clinically with hypoxemia, but it also is usually associated with hypotension and a drop in hematocrit. Findings on chest radiography include mediastinal widening, which is absent in this patient as evidenced by the serial radiographs. The size of the mediastinum remained unchanged on all radiographs. Lobar collapse after surgery is a common postoperative occurrence. Direct signs of lobar collapse on radiography include displacement of fissures and opacification of the collapsed lobe. Indirect signs include displacement of the hilum, a mediastinal shift toward the side of collapse, loss of volume in the ipsilateral hemithorax, crowding of the ribs, and com-

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pensatory hyperinflation of the remaining lobes. All the direct signs of right upper lobe collapse are present in the patient with the indirect signs being present to a much lesser degree. Rapid improvement of hypoxia mirrored by radiographic improvement of right upper lobe collapse after bronchoscopy and suctioning confirms the diagnosis. Hemothorax may occur in a postoperative patient, especially those with trauma. However, patients with hemothorax are more likely to have hypotension, hematocrit drop, and increasing sanguinous output through a chest tube along with sudden hypoxia. Also, a rapidly accumulating hemothorax is more likely to produce a dense whiteout of a hemithorax rather than a focal opacity in the right upper lung zone as seen in this patient. Bronchial obstruction resulting in lobar collapse may be caused by lesions outside the bronchial wall, within the wall of the bronchus, or within the lumen of the bronchus. Extrinsic

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compression by mediastinal lymph nodes, tracheobronchial stenosis, and endobronchial malignant mass are all causes of subacute to chronic obstruction. Complete bronchial obstruction usually causes collapse of the affected segment or lobe owing to gradual resorption of air. Collateral ventilation from adjacent segments may cause the affected segment or lobe to remain partially aerated. Also, tracheobronchial stenosis manifests over a subacute to chronic time period after surgery and not acutely as in this case. Foreign body aspiration may result in acute lobar collapse, but it commonly occurs in the lower lobes given the dependent bronchial anatomy and may also frequently result in hyperinflation of the affected

segment or lobe. Mucoid impaction is the most common cause of acute bronchial obstruction. Mucoid impaction may result in hypoxemia in the postoperative setting and improves rapidly after aggressive bronchoscopy and suctioning as evidenced by this case. Depressed cough reflex, splinting effects from pain, and thick tracheobronchial secretions are all known postoperative effects of anesthesia and surgery and contribute to the formation of mucus plugs that may result in atelectasis or lobar collapse. Rapid mobilization and ambulation after surgery actually prevent postoperative atelectasis and counter mucus plug formation.


secondary to peripheral embolization or by distention of the vessel by a large clot [18]. The reported sensitivity of this sign is 20% with a specificity of 80%. The low sensitivity of the Fleischner sign probably relates to the minimal dilatation of the pulmonary arteries that occurs after pulmonary embolism, and serial radiographs are needed to detect subtle changes in the size of the pulmonary arteries [7]. This sign is not present on this patient’s chest radiograph. The Westermark sign is an area of pulmonary oligemia distal to a large vessel that is occluded by emboli [19]. Although the reported sensitivity of this sign is very low (8– 14%), the very high specificity (92–96%) makes it an important one to keep in mind [7]. The Hampton hump, which pathologically represents a pulmonary infarct, appears as a well-defined pleural-based area of increased opacity with a convex medial border [20]. The convex medial border aids in the differentiation of pulmonary infarction from pleural thickening or free pleural fluid. The reported sensitivity of the sign is between 22% and 24% with a specificity of 82% [7]. The most common reported findings in patients with pulmonary embolism are atelectasis or parenchymal areas of increased opacity in the lower lung zones and pleural effusions [7]. The abnormality on our patient’s chest radiograph is much more than atelectasis. Ventilation-perfusion (V/Q) scintigraphy is a noninvasive method for diagnosing pulmonary emboli. V/Q scanning is more likely to be diagnostic in the absence of pulmonary opacities. A normal perfusion lung scan effectively rules out acute pulmonary embolism. A scan suggesting a high probability of acute pulmonary embolism should be considered diagnostic unless clinical suspicion is low. This test is highly sensitive but has a very low specificity [16, 21]. V/Q scanning is an appropriate choice for chest imaging when pulmonary embolism is suspected and CT is not appropriate [22]. CT angiography has become the mainstay for diagnosing pulmonary emboli. The sensitivity and specificity of CT angiography to detect pulmonary emboli on newer CT scanners approach 100%. A high-quality pulmonary CT angiogram should allow the clinician to exclude pulmonary embolism if

A 56-year-old man with a history of chronic low back pain managed with an epidural steroid injection presented with dyspnea and pleuritic chest pain. He was in his usual state of health until 2 days before admission when he began to experience right-sided chest and flank pleuritic pain with dyspnea after walking only a few steps. About 6 weeks earlier he had received an injection of steroids in his left hip to relieve his pain. After the injection, the patient experienced left leg swelling that resolved over weeks and before this current presentation. Physical examination revealed a normotensive, tachycardic, thin man with mild swelling in the left calf. Portable chest radiography and pulmonary CT angiography were then performed.

Description of Images A frontal portable radiograph of the chest revealed a peripheral, roughly wedge-shaped opacity in the right lower lung, likely in the right lower lobe (white arrow, Fig. 6A). An axial soft-tissue CT image of the chest showed filling defects in the right and left pulmonary arteries (white arrow, Fig. 6B) and a small right pleural effusion (black arrow, Fig. 6B). An axial lung window CT image revealed a large peripheral consolidation in the right lower lobe (black arrow, Fig. 6C) suggestive of a pulmonary infarct. An oblique coronal maximum-intensity-projection image showed a filling defect in the right pulmonary artery at the hilum (white arrow, Fig. 6D) with a branch extending up to the pulmonary infarct (black arrow, Fig. 6D).

Conclusion Atelectasis is reduced inflation of all or part of the lung. Reduced volume is seen accompanied by increased opacity on a chest radiograph of the affected part of the lung. Atelectasis is often associated with the abnormal displacement of fissures, bronchi, vessels, diaphragm, heart, or mediastinum [17]. None of these findings is present on this patient’s chest radiograph. The Fleischner sign is a prominent central artery that can be caused either by pulmonary hypertension that develops

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Fig. 6—56-year-old man who had received epidural steroid injection 6 weeks earlier for chronic low back pain presented with dyspnea and pleuritic chest pain. A, Frontal portable radiograph of chest reveals peripheral, roughly wedge-shaped opacity (arrow) in right lower lung peripherally, likely in right lower lobe. B, Axial soft-tissue CT image of chest reveals filling defects in right and left pulmonary arteries (white arrows) and small right pleural effusion (black arrow). C, Axial lung window CT image reveals large peripheral consolidation (arrow) in right lower lobe suggestive of pulmonary infarct. D, Oblique coronal maximum-intensity-projection image reveals filling defect (white arrow) in right pulmonary artery at hilum with branch extending up to pulmonary infarct (black arrow).

no clot is seen. Another major advantage of CT compared with other diagnostic tests for pulmonary embolism is its ability to reveal other potential causes of the patient’s symptoms [16]. Digital subtraction angiography has been the traditional reference standard for the diagnosis of pulmonary embolism. However, pulmonary angiography is an invasive test and is not readily available at all centers.

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Fibrin d-dimer testing is useful particularly in the outpatient population referred to the emergency department because of suspected pulmonary embolism. This usefulness is based on the high sensitivity of the test to the presence of venous thromboembolic disease. Because of the low specificity of d-dimer levels for diagnosing venous thromboembolism, d-dimer testing must be integrated in comprehen-

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sive, sequential diagnostic strategies that include clinical probability assessment and imaging techniques [23]. MR angiography of the pulmonary arteries is still a rapidly evolving technique. Contrast-enhanced and unenhanced angiographic techniques are widely available for high-spatial-resolution or real-time imaging of the pulmonary arteries. CT is, however, much faster, is relatively cheaper, and is more widely available than MRI. MRI may be considered a second-line technique to avoid contraindications to CT [24, 25]. The diagnostic criteria for acute pulmonary embolism include the following: • Arterial occlusion with failure to enhance the entire lumen because of a large filling defect; the artery may be enlarged compared with adjacent patent vessels. • A partial filling defect surrounded by contrast material, producing the “polo mint” sign on images acquired perpendicular to the long axis of a vessel and the “railway

track” sign on longitudinal images of the vessel. • A peripheral intraluminal filling defect that forms acute angles with the arterial wall [26]. The CT features of chronic thromboembolism are similar to those described with conventional angiography. A recanalized thrombus perpendicular to the artery wall appears as a web or band. Parallel to the arterial lumen, the incomplete recanalization thickens the artery walls with irregular contours of the intimal surface. CT angiography allows identification of additional features not detectable on angiograms, such as peripheral clots lining the arterial walls. A peripheral crescent-shaped intraluminal defect that forms obtuse angles with the vessel wall is an imaging finding diagnostic of chronic pulmonary embolism [26, 27]. Peripheral wedge-shaped areas of consolidation that may represent infarcts, along with linear bands, have been shown to be statistically significant ancillary findings associated with acute pulmonary embolism [28].


low lung volumes and portable technique, the heart appeared to be near the upper limit of normal in size or to be mildly enlarged. There were no pleural effusions or evidence of basilar atelectasis. An axial chest CT image obtained in lung windows showed bilateral central ground-glass opacities (black arrows, Fig. 7B) without evidence of focal consolidation. Mild enlargement of the heart confirming mild cardiomegaly was again noted. There was no evidence of pulmonary embolism on the CT study (not shown). A follow-up chest radiograph (Fig. 7C) obtained 48 hours later showed significant interval improvement in the bilateral perihilar opacities with residual opacities being present.

A 33-year-old morbidly obese woman (gravida 3, para 2) presented with worsening shortness of breath on day 6 after an emergent cesarean section. During the third trimester, 1 week before delivery, the patient developed hypertension and bed rest was prescribed. Her blood pressure continued to rise, so she was brought to the hospital for induction of labor. Labor failed to progress despite induction, and the decision was made to proceed with a cesarean section because of preeclampsia and failure to progress. She tolerated the cesarean section well and was able to ambulate soon after surgery. A day or two after hospital discharge, the patient began experiencing worsening progressive shortness of breath and found that she was not able to ambulate and began experiencing pleuritic chest pain. She was also concerned that her lower extremity edema had not improved much, so she presented to the emergency department for evaluation. A chest radiograph was obtained. On arrival, her blood pressure was markedly elevated, and ECG revealed a first-degree heart block. The elevated blood pressure was controlled using hydralazine. Also, d-dimer level was elevated, so a pulmonary embolism CT study was performed. After CT, the patient was given IV furosemide (Lasix, Sanofi-Aventis), which resulted in improvement in shortness of breath, pulmonary edema, tachypnea, and chest pain. She required no further diuresis or therapy to control hypertension.

Description of Images The initial frontal radiograph of the chest revealed bilateral perihilar opacities that appeared to involve the interstitium and airspaces and were most marked in the lower lungs bilaterally (black arrows, Fig. 7A). Even allowing for the

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Conclusion Predisposing factors for aspiration include debilitation, general anesthesia, altered mental status, neuromuscular disorders, and abnormalities affecting the pharynx and esophagus. Aspiration occurs most commonly on the right because of the straighter orientation of the right mainstem bronchus with respect to the trachea. When the patient is supine, the most frequently involved sites are the posterior segments of the upper lobes and superior segments of the lower lobes. The different clinical syndromes caused by aspiration include chemical pneumonitis, pneumonia, and airway obstruction. Aspiration of gastric acid with a pH of less than 2.5 can be fatal if massive, resulting in severe chemical pneumonitis within minutes (Mendelson syndrome). The chest radiograph typically shows focal consolidation that appears rapidly (i.e., within hours after the event) followed by the development of diffuse bilateral airspace opacities. The opacities generally can clear as rapidly as they develop [16]. Although these features are present in this case, the associated uncontrolled hypertension and its

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A

B Fig. 7—33-year-old morbidly obese multigravid woman who presented with worsening shortness of breath on day 6 after emergent cesarean section. A, Initial frontal radiograph of chest reveals bilateral perihilar patchy opacities (arrows) most marked in lower lungs bilaterally. Even allowing for low lung volumes and portable technique, heart appears to be near upper limit of normal in size or to be mildly enlarged. There are no pleural effusions or evidence of basilar atelectasis. B, Axial chest CT image in lung windows shows bilateral central ground-glass opacities (arrows) without evidence of focal consolidation. Again, note mild enlargement of heart confirming mild cardiomegaly. There was no evidence of pulmonary embolism on another CT study (not shown). C, Follow-up chest radiograph obtained 48 hours after A and B shows significant interval improvement in bilateral perihilar opacities with residual opacities.

C

disappearance with diuretic therapy cannot be explained only by aspiration. Acute respiratory distress syndrome (ARDS) refers to the severe end of the spectrum of acute lung injury (ALI). ALI is defined as a syndrome of acute and persistent lung inflammation with increased vascular permeability. ARDS can be defined as severe ALI resulting in worse hypoxemia and bilateral pulmonary opacities that may resemble pulmonary edema without an elevated left atrial pressure. ARDS represents the most severe form of permeability edema associated with diffuse alveolar damage, occurs without any increase in pulmonary capillary pressure, and is not caused or influenced by concurrent cardiac insufficiency. Primary or direct injuries to the alveolar and vascular endothelium result from exposure to chemical agents or infectious pathogens; secondary damage occurs because of a systemic biochemical cascade during sepsis, pancreatitis, severe trauma, or blood transfusion. Initially, most patients present with few, if any, clinical symptoms. Soon, however,

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they develop rapidly progressive dyspnea, tachypnea, and cyanosis. The early exudative stage shows few radiologic findings. Initially, interstitial edema is observed, followed rapidly by perihilar areas of increased opacity. The progression from interstitial edema to the filling of alveolar spaces corresponds to the appearance of widespread alveolar consolidation on air bronchograms. Compared with cardiogenic edema, the alveolar edema in ARDS usually has a more peripheral or cortical distribution. Radiologic signs that are typically seen in cardiogenic edema (e.g., cardiomegaly, apical vascular redistribution, Kerley lines) are absent [29]. “Flash pulmonary edema” is a general term that is sometimes used to describe a particularly dramatic form of acute decompensated congestive cardiac failure. In flash pulmonary edema, the underlying pathophysiologic principles and etiologic triggers are similar to those of less severe acute decompensated congestive cardiac failure. Acute decompensated congestive cardiac failure is most commonly caused by left ventricular systolic or diastolic dysfunction with or without

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additional cardiac pathology, such as coronary artery disease or valve abnormalities. However, a variety of conditions or events can cause cardiogenic pulmonary edema in the absence of heart disease, including primary fluid overload (e.g., due to blood transfusion), severe hypertension, renal artery stenosis, and severe renal disease. Flash pulmonary edema usually produces a radiographic appearance of batwing edema, which refers to a central, nongravitational distribution of alveolar edema and is seen in less than 10% of all pulmonary edema. In batwing edema, the periphery of the lung is free of alveolar or interstitial fluid. This pathologic condition develops so rapidly that it is initially observed as an alveolar consolidation, and the preceding interstitial phase that is typically seen in pulmonary edema goes undetected radiologically [29]. The signs and symptoms of Pneumocystis jiroveci pneumonia, formerly known as Pneumocystis carinii pneumonia (PCP), are nonspecific and show considerable variation in severity, including differences in manifestation in patients with AIDS and non-AIDS patients. The onset of the infection is heralded by nonproductive cough, increasing shortness of breath, and variable fever. In the HIV-positive patient, the infection is often insidious with a subacute onset of symptoms that develop over weeks to months, although more fulminant infection does occur. Other immunocompromised patients, such as transplant recipients and those receiving corticosteroids or cytotoxic agents, usually present with acute symptoms of fever, nonproductive cough, and marked shortness of breath that develop over 3–5 days. The radiographic manifestations of PCP are varied, but 80% of the time the infection initially appears as diffuse hazy opacities and may progress to diffuse patchy opacities. The pattern of distribution may vary from primarily perihilar and lower lobe disease to predominantly upper lobe disease, a pattern often, although not exclusively, seen in patients undergoing prophylaxis with aerosolized pentamidine. Typically, pleural effusions and lymphadenopathy are not present. If left untreated, the infection can progress to diffuse airspace consolidation and ARDS. With the increase in pentamidine, trimethoprim sulfamethoxazole, and dapsone prophylaxis, the classic radiographic pattern is being encountered less frequently and several features of PCP that were once considered unusual are now considered typical manifestations of this infection. Features of subacute untreated PCP include cystic lung disease, spontaneous pneumothorax, and an upper lobe distribution of parenchymal opacities [30, 31]. Because there is no history of immunocompromise in this patient, Pneumocystis jiroveci pneumonia is an unlikely diagnosis. Diffuse pulmonary hemorrhage is a syndrome characterized by widespread hemorrhage from the pulmonary microvasculature leading to hemoptysis and iron deficiency anemia; chest radiography shows bilateral airspace consolidation with apical sparing. Another radiologic feature of diffuse

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pulmonary hemorrhage is rapid clearing of the pulmonary opacities with treatment of the underlying cause. The cause of pulmonary hemorrhage depends on the patient’s immune status. The most common causes in the immunocompetent patient are antiglomerular basement membrane disease, also known as Goodpasture syndrome; collagen-vascular disease, most commonly including systemic lupus erythematosus and Wegener granulomatosis; and idiopathic pulmonary hemosiderosis. In immunocompromised patients, diffuse pulmonary hemorrhage is almost always associated with an underlying infection or lung injury [32]. Pulmonary edema can be either cardiogenic or noncardiogenic. Cardiogenic pulmonary edema is also termed “hydrostatic pulmonary edema” and “hemodynamic pulmonary edema.” Noncardiogenic pulmonary edema is also known as “increased permeability pulmonary edema.” Knowledge of the cause of pulmonary edema has important implications for treatment. Patients with cardiogenic pulmonary edema are typically treated with diuretics and afterload reduction. Patients with noncardiogenic pulmonary edema may require mechanical ventilation and steroids in addition to other specific treatment. The distinct mechanisms of cardiogenic and noncardiogenic pulmonary edema allow differentiation between the two on chest radiographs. Chest radiographs allow identification of up to 87% of patients with cardiogenic pulmonary edema and up to 60% of patients with noncardiogenic pulmonary edema [33]. There are several explanations for the limited diagnostic accuracy of chest radiography for pulmonary edema. Edema may not be visible until the amount of lung water increases by 30%. Any condition producing airspace opacification, such as alveolar hemorrhage or bronchoalveolar carcinoma, may mimic pulmonary edema radiographically. Also, substantial interobserver and technical variability may affect interpretation of radiographs [34]. Thus, chest radiography is not the definitive method by which to differentiate cardiogenic from noncardiogenic pulmonary edema. Plasma levels of brain natriuretic peptide (BNP) are often used in the evaluation of pulmonary edema because BNP is secreted by the heart in response to wall stretch or increased intracardiac pressures. In patients with congestive heart failure, plasma BNP level correlates with left ventricular end-diastolic pressure and pulmonary artery occlusion pressure. A BNP level of less than 100 pg/mL indicates that heart failure is unlikely, whereas a BNP level of greater than 500 pg/mL indicates that heart failure is likely. However, a BNP level of between 100 and 500 pg/mL provides inadequate diagnostic discrimination. In addition, BNP level can be elevated in critically ill patients even in the absence of heart failure [34]. BNP can also be secreted by the right ventricle, and moderate elevations have been reported in patients with acute pulmonary embolism, cor pulmonale, and pulmonary hypertension.

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Bedside transthoracic echocardiography can be used to evaluate myocardial and valvular function and can help identify the cause of pulmonary edema. In patients in whom medical history, physical examination, laboratory results, and chest radiography do not establish the diagnosis, transthoracic echocardiography should be used to assess left ventricular and valvular function. Although echocardiography is effective in identifying left ventricular systolic dysfunction and valvular dysfunction, it is less sensitive in identifying diastolic dysfunction, which may be a cause of pulmonary edema. Thus, a normal echocardiogram does not rule out cardiogenic pulmonary edema [34]. Pulmonary artery catheterization with a catheter such as a Swan-Ganz catheter is used to assess pulmonary artery occlusion pressure and is considered the reference standard for determining the cause of acute pulmonary edema. When catheterization is correctly performed, this pressure reflects the left atrial pressure based on the assumption that a static column is created between the pulmonary artery branch and the left atrium in the absence of any intervening vascular obstruction or stenosis. To confirm proper location of the catheter, obtaining a supine chest radiograph showing the tip within the main pulmonary trunks is sufficient. A pulmonary artery occlusion pressure of greater than 18 mm Hg indicates cardiogenic pulmonary edema or pulmonary edema due to volume overload [34]. Central venous pressure and right atrial pressure are nearly equal to diastolic right ventricular pressure in the absence of heart or lung disease. The mean central venous pressure and right atrial pressure normally range from 0 to 5 mm Hg and vary as intrathoracic pressure changes with respiration. Elevated central venous pressure may reflect

acute or chronic pulmonary arterial hypertension and right ventricular overload in the absence of any increase in left atrial pressure. Measurement of central venous pressure should not be considered a valid substitute for pulmonary artery catheterization because there may be poor correlation between the two. Cardiogenic edema can be graded as mild, moderate, or severe. The upright chest radiograph is more accurate than the supine portable chest radiograph in depicting the findings of pulmonary edema. The radiographic findings of pulmonary edema have been correlated with pulmonary capillary wedge pressure (PCWP). A normal PCWP is approximately 5 mm Hg. When PCWP is between 5 and 12 mm Hg, the chest radiograph appears normal. With the PCWP between 12 and 17 mm Hg, cephalization of the pulmonary vessels occurs on the upright chest radiograph and is the earliest radiographic sign. This finding is often termed “pulmonary venous hypertension.” With a PCWP of 17–20 mm Hg or moderate (or interstitial) pulmonary edema, corresponding signs on chest radiographs include perihilar or vascular haziness, Kerley lines, and peribronchial cuffing with or without pleural effusions. As intravascular hydrostatic pressures continue to rise with a PCWP of more than 25 mm Hg, fluid begins to fill the airspaces, resulting in alveolar or severe edema. It is important to remember that, in acute heart failure, a time lag is often observed between increased PCWP and radiologic manifestation of pulmonary edema because of the relatively slow movement of water through the widened capillary endothelial cell junctions. Similarly, as pulmonary edema resolves, the radiologic findings will persist and PCWP will decrease or even return to normal.


led to a preliminary diagnosis of polymyalgia rheumatica, and the patient was treated with prednisone. The patient initially noted some modest improvement in his constitutional symptoms, but after about 1 week his symptoms again worsened. His prednisone dose was then increased. A month later, his fatigue and exertional dyspnea had worsened, and he noted coughing with intermittent blood-tinged phlegm and lightheadedness. At presentation to our institution, he was hypertensive, tachycardic, and hypoxic and in acute renal failure. His perinuclear antineutrophil cytoplasmic antibody (pANCA) titer at presentation was in excess of 65,000.

An 84-year-old man with hypertension, gout, and hypothyroidism presented with hemoptysis, dyspnea, and lethargy. Approximately 6 months earlier when he was otherwise in his usual state of good health and highly functional, he developed vague and general symptoms of waxing and waning malaise and fatigue. He was evaluated by his primary care doctor and tested for antibodies to Lyme disease, which yielded negative findings. His symptoms persisted and included dyspnea and anorexia, and he developed myalgias and began to lose weight. He was hospitalized at an outside hospital for evaluation; that stay was notable for an abnormal chest radiograph, which was not available for review. The patient was treated with antibiotics for presumed pneumonia with symptomatic improvement. During the same admission, iron deficiency anemia was diagnosed (normal upper gastrointestinal tract and normal colonoscopy findings), erythrocyte sedimentation rate was > 100 mm/h, and antinuclear antibody titer was 1:12,000. These findings

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Description of Images The initial chest radiograph (Fig. 8A) showed bilateral patchy opacities on the right more than the left and most dense in the right lower lung. Note the lack of any lines or tubes on this radiograph. A radiograph (Fig. 8B) obtained 6 hours later showed the intubated status of the patient and revealed marked progression of the bilateral patchy opaci-

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A

B

Fig. 8—84-year-old man with hypertension, gout, and hypothyroidism who presented with hemoptysis, dyspnea, and lethargy. A, Initial chest radiograph shows bilateral patchy opacities, right more than left and most dense in right lower lung. Note lack of any lines or tubes on this radiograph. B, Subsequent radiograph obtained 6 hours after A shows marked progression of bilateral patchy opacities and intubated status of patient. These findings prompted chest CT. C, CT image reveals bilateral, right more than left, interlobular septal thickening and areas of ground-glass opacity producing crazy paving appearance (white arrow). Also marked is area of consolidation (black arrow) suggesting dense airspace opacification.

C

ties, which prompted chest CT (Fig. 8C). CT revealed bilateral, on the right more than the left, interlobular septal thickening and areas of ground-glass opacity producing a crazy paving appearance (white arrow, Fig. 8C). Also marked is an area of consolidation (black arrow, Fig. 8C) suggesting dense airspace opacification.

Conclusion Infectious pneumonia could certainly produce these radiographic and CT appearances with rapidly progressing airspace opacities. Also, infection with Serratia marcescens, a gram-negative organism, results in production of a pigment prodigiosin that is dark red to pale pink and is easily mistaken for blood—in this case, for hemoptysis [35]. However, this patient had already been treated with antibiotics and infection would not easily explain the elevated pANCA titer. Cryptogenic organizing pneumonia (COP) is a clinicopathologic syndrome that presents with an initial influenzalike illness and peripheral airspace consolidation that

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does not respond to antibiotics but responds favorably to steroids. The radiographic opacities in this case were predominantly central; progressed rapidly, which would be unusual for COP; and did not respond to steroid therapy. Also, the hemoptysis and pANCA titer elevation would not be explained by COP. Diffuse alveolar hemorrhage is an acute life-threatening event, and most patients present with dyspnea, hemoptysis, and radiographic airspace opacities. Diffuse pulmonary hemorrhage can occur in a wide variety of conditions, and one of the common causes is pulmonary renal syndromes in which vasculitis or capillaritis occurs. This would certainly explain the elevated pANCA titer. Acute interstitial pneumonia (AIP) is a rapidly progressive interstitial fibrosis. It usually presents with progressive dyspnea that progresses to respiratory failure over several weeks or months and occasionally presents with an antecedent virallike prodrome. Chest CT may show alveolar consolidation, ground-glass opacities, or both, often associ-

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ated with traction bronchiectasis. Although the clinical scenario and the radiographic opacities in this case could certainly represent AIP, the hemoptysis and elevated pANCA titer would not be explained by AIP. Hypersensitivity pneumonitis (HP) is a diffuse granulomatous interstitial lung disease caused by inhalation of various antigenic organic particles. HP traditionally has been classified as acute, subacute, or chronic. Acute HP is characterized by abrupt onset of symptoms within a few hours after heavy antigen exposure in a previously sensitized patient. The radiologic manifestations of acute HP are those of acute pulmonary edema. Because of the characteristic clinical manifestations and rapid resolution of symptoms, high-resolution CT is seldom performed in the evaluation of these patients. Subacute HP is caused by intermittent or continuous exposure to low doses of antigen. Chronic HP results from very low–level persistent or recurrent exposure to antigen. Patients often present with both subacute and chronic findings. The characteristic high-resolution CT manifestations of subacute HP consist of patchy or diffuse bilateral ground-glass opacities, poorly defined small centrilobular nodules, and lobular areas of decreased attenuation and vascularity on inspiratory images and of air trapping on expiratory images. Chronic HP is differentiated from subacute HP by the presence of fibrosis, which is characterized on high-resolution CT by the presence of reticulation and traction bronchiectasis and bronchiolectasis. Although the radiographic opacities in this case may closely resemble subacute HP, the absence of centrilobular nodules makes subacute HP less likely. Also, subacute HP would not explain the elevated pANCA level. A number of diseases can cause diffuse alveolar hemorrhage. Pulmonary capillaritis is the most frequent underlying histologic lesion described in diffuse alveolar hemorrhage. Although Wegener granulomatosis has been reported to be the most common cause of alveolar hemorrhage, it is usually marked by an elevation of the circulating antineutrophil cytoplasmic antibody (cANCA) titers. Churg-Strauss vasculitis does have elevated pANCA titers, but patients usually have asthma and peripheral eosinophilia and diffuse alveolar hemorrhage is very rare. More than half of the patients with pulmonary involvement in microscopic polyangiitis have diffuse alveolar hemorrhage and they frequently have glomerulonephritis, fevers, and myalgias, as in this case. Patients with Goodpasture syndrome have positive findings for antiglomerular basement membrane antibody (absent in this patient), and alveolar hemorrhage is more common in smokers. Although patients with systemic lupus erythematosus may have fevers, arthralgias, and pulmonary hemorrhage at onset in up to 11% of cases, serology is usually positive for anti–double-stranded DNA antibodies. Thus, there may be significant clinical and serologic overlaps among pulmonary renal syndromes. The crazy paving pattern is a common finding at thinsection CT of the lungs. It consists of scattered or diffuse

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ground-glass attenuation with superimposed interlobular and intralobular septal thickening. Initially described in cases of alveolar proteinosis, this pattern has subsequently been reported in a variety of infectious, neoplastic, idiopathic, inhalational, and sanguineous disorders of the lung [36, 37]. The crazy-paving pattern on thin-section CT scans is a nonspecific finding and has been reported to occur in mucinous bronchioloalveolar carcinoma, lipoid pneumonia, and nonspecific interstitial pneumonia. Endobronchial tuberculosis, on the other hand, usually produces the tree-inbud sign on thin-section CT. The features of the tree-in-bud sign are usually small peripheral centrilobular and well-defined nodules of soft-tissue attenuation that are connected to linear branching opacities that have more than one contiguous branching site. Tree-in-bud opacities represent bronchiolar thickening or bronchiolar luminal impaction with mucus, pus, or fluid, which demarcates the normally invisible branching course of the peripheral airways [38]. References 1. Bae YA, Lee KS. Cross-sectional evaluation of thoracic lymphoma. Radiol Clin North Am 2008; 46:253–264, viii 2. Cohn LH, ed. Cardiac surgery in the adult, 3rd ed. New York, NY: McGrawHill, 2008 3. Goodman LR. Postoperative chest radiograph. II. Alterations after major intrathoracic surgery. AJR 1980; 134:803–813 4. Tsai TH, Yang PC. Ultrasound in the diagnosis and management of pleural disease. Curr Opin Pulm Med 2003; 9:282–290 5. Tomiyama N, Yasuhara Y, Nakajima Y, et al. CT-guided needle biopsy of lung lesions: a survey of severe complication based on 9783 biopsies in Japan. Eur J Radiol 2006; 59:60–64 6. Marshall GB, Farnquist BA, MacGregor JH, Burrowes PW. Signs in thoracic imaging. J Thorac Imaging 2006; 21:76–90 7. Worsley DF, Alavi A, Aronchick JM, Chen JT, Greenspan RH, Ravin CE. Chest radiographic findings in patients with acute pulmonary embolism: observations from the PIOPED study. Radiology 1993; 189:133–136 8. Plewa MC, Ledrick D, Sferra JJ. Delayed tension pneumothorax complicating central venous catheterization and positive pressure ventilation. Am J Emerg Med 1995; 13:532–535 9. Ziter FM Jr, Westcott JL. Supine subpulmonary pneumothorax. AJR 1981; 137:699–701 10. Moseley JE. Loculated pneumomediastinum in the newborn: a thymic “spinnaker sail” sign. Radiology 1960; 75:788–790 11. Hammond DI. The “ring-around-the-artery” sign in pneumomediastinum. J Can Assoc Radiol 1984; 35:88–89 12. Rogers LF, Puig AW, Dooley BN, Cuello L. Diagnostic considerations in mediastinal emphysema: a pathophysiologic-roentgenologic approach to Boerhaave’s syndrome and spontaneous pneumomediastinum. Am J Roentgenol Radium Ther Nucl Med 1972; 115:495–511 13. Levin B. The continuous diaphragm sign: a newly-recognized sign of pneumomediastinum. Clin Radiol 1973; 24:337–338 14. Bejvan SM, Godwin JD. Pneumomediastinum: old signs and new signs. AJR 1996; 166:1041–1048 15. Zylak CM, Standen JR, Barnes GR, Zylak CJ. Pneumomediastinum revisited. RadioGraphics 2000; 20:1043–1057 16. Rubinowitz AN, Siegel MD, Tocino I. Thoracic imaging in the ICU. Crit Care Clin 2007; 23:539–573 17. Hansell DM, Bankier AA, MacMahon H, McLoud TC, Müller NL, Remy J. Fleischner Society: glossary of terms for thoracic imaging. Radiology 2008; 246:697–722 18. Fleischner FG. Unilateral pulmonary embolism with increased compensatory

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Urgent Findings on Portable Chest Radiography circulation through the unoccluded lung: Roentgen observations. Radiology 1959; 73:591–597 19. Westermark N. On the roentgen diagnosis of lung embolism. Acta Radiol 1938; 19:357–372 20. Hampton AO, Castlman B. Correlation of postmortem teleroentgenograms with autopsy findings: with special reference to pulmonary embolism and infarction. AJR 1940; 43:305–326 21. Tapson VF. Acute pulmonary embolism. N Engl J Med 2008; 358:1037–1052 22. Sostman HD, Stein PD, Gottschalk A, Matta F, Hull R, Goodman L. Acute pulmonary embolism: sensitivity and specificity of ventilation-perfusion scintigraphy in PIOPED II study. Radiology 2008; 246:941–946 23. Righini M, Perrier A, De Moerloose P, Bounameaux H. D-dimer for venous thromboembolism diagnosis: 20 years later. J Thromb Haemost 2008; 6:1059– 1071 24. Kluge A, Mueller C, Strunk J, Lange U, Bachmann G. Experience in 207 combined MRI examinations for acute pulmonary embolism and deep vein thrombosis. AJR 2006; 186:1686–1696 25. Ley S, Kauczor HU. MR imaging/magnetic resonance angiography of the pulmonary arteries and pulmonary thromboembolic disease. Magn Reson Imaging Clin N Am 2008; 16:263–273, ix 26. Wittram C, Maher MM, Yoo AJ, Kalra MK, Shepard JA, McLoud TC. CT angiography of pulmonary embolism: diagnostic criteria and causes of misdiagnosis. RadioGraphics 2004; 24:1219–1238 27. Remy-Jardin M, Mastora I, Remy J. Pulmonary embolus imaging with multislice CT. Radiol Clin North Am 2003; 41:507–519

28. Coche EE, Müller NL, Kim KI, Wiggs BR, Mayo JR. Acute pulmonary embolism: ancillary findings at spiral CT. Radiology 1998; 207:753–758 29. Gluecker T, Capasso P, Schnyder P, et al. Clinical and radiologic features of pulmonary edema. RadioGraphics 1999; 19:1507–1531; discussion, 1532– 1533 30. Kuhlman JE. Pneumocystic infections: the radiologist’s perspective. Radiology 1996; 198:623–635 31. Boiselle PM, Crans CA Jr, Kaplan MA. The changing face of Pneumocystis carinii pneumonia in AIDS patients. AJR 1999; 172:1301–1309 32. Primack SL, Miller RR, Müller NL. Diffuse pulmonary hemorrhage: clinical, pathologic, and imaging features. AJR 1995; 164:295–300 33. Aberle DR, Wiener-Kronish JP, Webb WR, Matthay MA. Hydrostatic versus increased permeability pulmonary edema: diagnosis based on radiographic criteria in critically ill patients. Radiology 1988; 168:73–79 34. Ware LB, Matthay MA. Clinical practice: acute pulmonary edema. N Engl J Med 2005; 353:2788–2796 35. Ioachimescu OC, Stoller JK. Diffuse alveolar hemorrhage: diagnosing it and finding the cause. Cleve Clin J Med 2008; 75:258, 260, 264–265, passim 36. Rossi SE, Erasmus JJ, Volpacchio M, Franquet T, Castiglioni T, McAdams HP. “Crazy-paving” pattern at thin-section CT of the lungs: radiologic-pathologic overview. RadioGraphics 2003; 23:1509–1519 37. Johkoh T, Itoh H, Müller NL, et al. Crazy-paving appearance at thin-section CT: spectrum of disease and pathologic findings. Radiology 1999; 211:155– 160 38. Eisenhuber E. The tree-in-bud sign. Radiology 2002; 222:771–772

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