Clinical and Radiologic Features of Pulmonary Edema
Thomas Gluecker, MD ,
Patrizio Capasso, MD ,
Pierre Schnyder, MD ,
François Gudinchet, MD ,
Marie-Denise Schaller, MD ,
Jean-Pierre Revelly, MD ,
René Chiolero, MD ,
Peter Vock, MD and
Stéphan Wicky, MD
1 From the Departments of Diagnostic and Interventional Radiology (T.G., P.C., P.S., F.G., S.W.) and Anesthesiology (J.P.R., R.C.) and the Division of Intensive Care Medicine (M.D.S.), University Hospital Center, CHUV, Lausanne 1011, Switzerland; and the Institute of Diagnostic Radiology, Inselspital, Bern, Switzerland (P.V.). Recipient of a Certificate of Merit award for a scientific exhibit at the 1998 RSNA scientific assembly. Received February 17, 1999; revision requested March 16 and received June 1; accepted June 14. Address reprint requests to P.C.

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Figure 1a. Increased hydrostatic pressure edema in a 33-year-old man with acute myelocytic leukemia who was admitted for fluid overload with renal and cardiac failure. Successive chest radiographs demonstrate progressive lobar vessel enlargement, peribronchial cuffing (arrows in b), bilateral Kerley lines (arrowheads in c), and late alveolar edema with nodular areas of increased opacity. The fluid overload is confirmed by the increasing size of the azygos vein.
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Figure 1b. Increased hydrostatic pressure edema in a 33-year-old man with acute myelocytic leukemia who was admitted for fluid overload with renal and cardiac failure. Successive chest radiographs demonstrate progressive lobar vessel enlargement, peribronchial cuffing (arrows in b), bilateral Kerley lines (arrowheads in c), and late alveolar edema with nodular areas of increased opacity. The fluid overload is confirmed by the increasing size of the azygos vein.
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Figure 1c. Increased hydrostatic pressure edema in a 33-year-old man with acute myelocytic leukemia who was admitted for fluid overload with renal and cardiac failure. Successive chest radiographs demonstrate progressive lobar vessel enlargement, peribronchial cuffing (arrows in b), bilateral Kerley lines (arrowheads in c), and late alveolar edema with nodular areas of increased opacity. The fluid overload is confirmed by the increasing size of the azygos vein.
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Figure 2. Increased hydrostatic pressure edema in a 53-year-old man with postoperative fluid overload. Pulmonary capillary wedge pressure was 20 mm Hg. High-resolution computed tomographic (CT) scan demonstrates inter- and intralobar septal lines predominating in the anterior portion of the left lung field with some peribronchial cuffing (arrow). Both lungs display diffuse ground-glass areas of increased attenuation with a gravitational anteroposterior gradient.
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Figure 3a. Bat wing edema in a 71-year-old woman with fluid overload and cardiac failure. Chest radiograph (a) and high-resolution CT scan (b) demonstrate bat wing alveolar edema with a central distribution and sparing of the lung cortex. The infiltrates resolved within 32 hours.
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Figure 3b. Bat wing edema in a 71-year-old woman with fluid overload and cardiac failure. Chest radiograph (a) and high-resolution CT scan (b) demonstrate bat wing alveolar edema with a central distribution and sparing of the lung cortex. The infiltrates resolved within 32 hours.
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Figure 4. Bat wing edema in a 66-year-old woman with fluid overload of renal origin who was undergoing hemodialysis for hypertensive nephroangiosclerosis. The patient was found unconscious after lying on her right side for several hours. Chest radiograph shows unusual recumbent bat wing pulmonary edema with associated right-sided pleural effusion.
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Figure 5a. Asymmetric pulmonary edema in a male patient with marked chronic obstructive pulmonary disease. Unenhanced CT scans obtained with lung parenchymal (a) and mediastinal (b) windows depict the edema as areas of diffuse ground-glass attenuation with an anteroposterior gradient. Fluid-filled subpleural bullae are best seen in b (lower left). (Courtesy of Prof J. Remy, Department of Radiology, Hopital Calmette, Lille, France.)
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Figure 5b. Asymmetric pulmonary edema in a male patient with marked chronic obstructive pulmonary disease. Unenhanced CT scans obtained with lung parenchymal (a) and mediastinal (b) windows depict the edema as areas of diffuse ground-glass attenuation with an anteroposterior gradient. Fluid-filled subpleural bullae are best seen in b (lower left). (Courtesy of Prof J. Remy, Department of Radiology, Hopital Calmette, Lille, France.)
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Figure 6. Asymmetric pulmonary edema in a 70-year-old man with end-stage fibrosis and bullous emphysema due to asbestosis who was admitted for cardiac failure. On a chest radiograph, the pulmonary edema infiltrates predominate at the lung bases because pulmonary blood flow is diverted to these regions by the upper lobe bullae. The fibrotic interstitial changes from asbestosis facilitate the entry of edema into the alveolar spaces.
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Figure 7. Asymmetric pulmonary edema in a 64-year-old woman with grade 3 mitral insufficiency. High-resolution CT scan shows pulmonary edema predominantly within the right upper lobe.
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Figure 8. Asymmetric pulmonary edema in a 37-year-old woman who had undergone orthopedic intervention of the femur in the right lateral decubitus position. The patient received 12 liters of blood during surgery. Chest radiograph demonstrates right-sided predominance of the pulmonary edema.
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Figure 9. Pulmonary edema with acute asthma in a 3-year-old child. Chest radiograph demonstrates heterogeneous pulmonary edema associated with peribronchial cuffing, ill-defined vessels, enlarged and ill-defined hila, and alveolar areas of increased opacity.
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Figure 10. Postobstructive pulmonary edema in a 31-year-old man with postextubation laryngospasm. High-resolution CT scan demonstrates marked pulmonary edema with peribronchial cuffing predominantly involving the central lung parenchyma. The lung cortex is remarkably free of alveolar edema and Kerley lines.
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Figure 11a. Pulmonary edema in a 56-year-old man with chronic thromboembolic disease. (a) High-resolution CT scan demonstrates hyperperfused right upper and left lower lobes with ground-glass areas of increased attenuation and enlarged arteries. The hypoperfusion of the left upper lobe is associated with a locally decreased vessel size. (b) Right pulmonary angiogram obtained at the same time demonstrates numerous segmental webs (arrows) and vascular occlusions that correlate well with the CT findings (cf a).
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Figure 11b. Pulmonary edema in a 56-year-old man with chronic thromboembolic disease. (a) High-resolution CT scan demonstrates hyperperfused right upper and left lower lobes with ground-glass areas of increased attenuation and enlarged arteries. The hypoperfusion of the left upper lobe is associated with a locally decreased vessel size. (b) Right pulmonary angiogram obtained at the same time demonstrates numerous segmental webs (arrows) and vascular occlusions that correlate well with the CT findings (cf a).
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Figure 12a. Pulmonary edema associated with veno-occlusive disease in a 28-year-old woman who was admitted for acute dyspnea. (a) Chest radiograph demonstrates pulmonary edema. (b) On a pulmonary angiogram obtained to exclude embolism, the peripheral pulmonary arteries are patent but have a thin, elongated appearance. Pulmonary capillary wedge pressure was normal, but mean pulmonary arterial pressure was 54 mm Hg. (c, d) High-resolution CT scans (d obtained caudad to c) obtained 2 days after admission demonstrate numerous inter- and intralobular thickened septa, peribronchial cuffing, small pleural effusions, and residual diffuse ground-glass attenuation. Pulmonary veno-occlusive disease was diagnosed at lung biopsy.
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Figure 12b. Pulmonary edema associated with veno-occlusive disease in a 28-year-old woman who was admitted for acute dyspnea. (a) Chest radiograph demonstrates pulmonary edema. (b) On a pulmonary angiogram obtained to exclude embolism, the peripheral pulmonary arteries are patent but have a thin, elongated appearance. Pulmonary capillary wedge pressure was normal, but mean pulmonary arterial pressure was 54 mm Hg. (c, d) High-resolution CT scans (d obtained caudad to c) obtained 2 days after admission demonstrate numerous inter- and intralobular thickened septa, peribronchial cuffing, small pleural effusions, and residual diffuse ground-glass attenuation. Pulmonary veno-occlusive disease was diagnosed at lung biopsy.
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Figure 12c. Pulmonary edema associated with veno-occlusive disease in a 28-year-old woman who was admitted for acute dyspnea. (a) Chest radiograph demonstrates pulmonary edema. (b) On a pulmonary angiogram obtained to exclude embolism, the peripheral pulmonary arteries are patent but have a thin, elongated appearance. Pulmonary capillary wedge pressure was normal, but mean pulmonary arterial pressure was 54 mm Hg. (c, d) High-resolution CT scans (d obtained caudad to c) obtained 2 days after admission demonstrate numerous inter- and intralobular thickened septa, peribronchial cuffing, small pleural effusions, and residual diffuse ground-glass attenuation. Pulmonary veno-occlusive disease was diagnosed at lung biopsy.
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Figure 12d. Pulmonary edema associated with veno-occlusive disease in a 28-year-old woman who was admitted for acute dyspnea. (a) Chest radiograph demonstrates pulmonary edema. (b) On a pulmonary angiogram obtained to exclude embolism, the peripheral pulmonary arteries are patent but have a thin, elongated appearance. Pulmonary capillary wedge pressure was normal, but mean pulmonary arterial pressure was 54 mm Hg. (c, d) High-resolution CT scans (d obtained caudad to c) obtained 2 days after admission demonstrate numerous inter- and intralobular thickened septa, peribronchial cuffing, small pleural effusions, and residual diffuse ground-glass attenuation. Pulmonary veno-occlusive disease was diagnosed at lung biopsy.
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Figure 13a. Pulmonary edema in a 5-year-old boy who was admitted 1 hour after nearly drowning in chlorinated water. (a) Chest radiograph obtained at the time of admission reveals cardiac enlargement, diffuse confluent alveolar patterns of pulmonary edema, and peribronchial cuffing. (b, c) Chest radiograph (b) and high-resolution CT scan (c) obtained 3 hours later demonstrate a marked decrease in pulmonary edema, although it still predominates in the dependent portions of the lungs. The cortical lung is remarkably free of interstitial edema, a finding that may suggest either direct alveolar damage from the inhaled water or edema following laryngospasm rather than secondary damage from the associated hypoxia. The laryngospasm was probably the major component given the rapid clearing of the areas of increased opacity.
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Figure 13b. Pulmonary edema in a 5-year-old boy who was admitted 1 hour after nearly drowning in chlorinated water. (a) Chest radiograph obtained at the time of admission reveals cardiac enlargement, diffuse confluent alveolar patterns of pulmonary edema, and peribronchial cuffing. (b, c) Chest radiograph (b) and high-resolution CT scan (c) obtained 3 hours later demonstrate a marked decrease in pulmonary edema, although it still predominates in the dependent portions of the lungs. The cortical lung is remarkably free of interstitial edema, a finding that may suggest either direct alveolar damage from the inhaled water or edema following laryngospasm rather than secondary damage from the associated hypoxia. The laryngospasm was probably the major component given the rapid clearing of the areas of increased opacity.
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Figure 13c. Pulmonary edema in a 5-year-old boy who was admitted 1 hour after nearly drowning in chlorinated water. (a) Chest radiograph obtained at the time of admission reveals cardiac enlargement, diffuse confluent alveolar patterns of pulmonary edema, and peribronchial cuffing. (b, c) Chest radiograph (b) and high-resolution CT scan (c) obtained 3 hours later demonstrate a marked decrease in pulmonary edema, although it still predominates in the dependent portions of the lungs. The cortical lung is remarkably free of interstitial edema, a finding that may suggest either direct alveolar damage from the inhaled water or edema following laryngospasm rather than secondary damage from the associated hypoxia. The laryngospasm was probably the major component given the rapid clearing of the areas of increased opacity.
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Figure 14a. ARDS associated with DAD in a 20-year-old man involved in a motor vehicle accident who underwent massive bronchoaspiration during tracheal intubation. (a-c) Chest radiograph (a) and supine unenhanced CT scans (10-mm section thickness) (b, c) (c obtained caudad to b) reveal characteristic bilateral diffuse airspace consolidations with a marked anteroposterior gradient. In addition, bilateral peripheral areas of hyperlucency representing trapped air are seen. Kerley lines are notably absent, and pleural effusions are minor compared with the extent of the airspace lesions. (d, e) High-resolution CT scans (e obtained caudad to d) obtained 1 day later after the patient had been maintained in a prone position for 12 hours demonstrate markedly decreased posterior airspace consolidations with small, posterior pleural effusions. Note the residual inter- and intralobular septal thickening. A posteroanterior gradient is now present, clearly demonstrating the importance of dependent atelectasis in ARDS. Note also the presence of numerous dilated small bronchi and bronchioles.
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Figure 14b. ARDS associated with DAD in a 20-year-old man involved in a motor vehicle accident who underwent massive bronchoaspiration during tracheal intubation. (a-c) Chest radiograph (a) and supine unenhanced CT scans (10-mm section thickness) (b, c) (c obtained caudad to b) reveal characteristic bilateral diffuse airspace consolidations with a marked anteroposterior gradient. In addition, bilateral peripheral areas of hyperlucency representing trapped air are seen. Kerley lines are notably absent, and pleural effusions are minor compared with the extent of the airspace lesions. (d, e) High-resolution CT scans (e obtained caudad to d) obtained 1 day later after the patient had been maintained in a prone position for 12 hours demonstrate markedly decreased posterior airspace consolidations with small, posterior pleural effusions. Note the residual inter- and intralobular septal thickening. A posteroanterior gradient is now present, clearly demonstrating the importance of dependent atelectasis in ARDS. Note also the presence of numerous dilated small bronchi and bronchioles.
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Figure 14c. ARDS associated with DAD in a 20-year-old man involved in a motor vehicle accident who underwent massive bronchoaspiration during tracheal intubation. (a-c) Chest radiograph (a) and supine unenhanced CT scans (10-mm section thickness) (b, c) (c obtained caudad to b) reveal characteristic bilateral diffuse airspace consolidations with a marked anteroposterior gradient. In addition, bilateral peripheral areas of hyperlucency representing trapped air are seen. Kerley lines are notably absent, and pleural effusions are minor compared with the extent of the airspace lesions. (d, e) High-resolution CT scans (e obtained caudad to d) obtained 1 day later after the patient had been maintained in a prone position for 12 hours demonstrate markedly decreased posterior airspace consolidations with small, posterior pleural effusions. Note the residual inter- and intralobular septal thickening. A posteroanterior gradient is now present, clearly demonstrating the importance of dependent atelectasis in ARDS. Note also the presence of numerous dilated small bronchi and bronchioles.
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Figure 14d. ARDS associated with DAD in a 20-year-old man involved in a motor vehicle accident who underwent massive bronchoaspiration during tracheal intubation. (a-c) Chest radiograph (a) and supine unenhanced CT scans (10-mm section thickness) (b, c) (c obtained caudad to b) reveal characteristic bilateral diffuse airspace consolidations with a marked anteroposterior gradient. In addition, bilateral peripheral areas of hyperlucency representing trapped air are seen. Kerley lines are notably absent, and pleural effusions are minor compared with the extent of the airspace lesions. (d, e) High-resolution CT scans (e obtained caudad to d) obtained 1 day later after the patient had been maintained in a prone position for 12 hours demonstrate markedly decreased posterior airspace consolidations with small, posterior pleural effusions. Note the residual inter- and intralobular septal thickening. A posteroanterior gradient is now present, clearly demonstrating the importance of dependent atelectasis in ARDS. Note also the presence of numerous dilated small bronchi and bronchioles.
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Figure 14e. ARDS associated with DAD in a 20-year-old man involved in a motor vehicle accident who underwent massive bronchoaspiration during tracheal intubation. (a-c) Chest radiograph (a) and supine unenhanced CT scans (10-mm section thickness) (b, c) (c obtained caudad to b) reveal characteristic bilateral diffuse airspace consolidations with a marked anteroposterior gradient. In addition, bilateral peripheral areas of hyperlucency representing trapped air are seen. Kerley lines are notably absent, and pleural effusions are minor compared with the extent of the airspace lesions. (d, e) High-resolution CT scans (e obtained caudad to d) obtained 1 day later after the patient had been maintained in a prone position for 12 hours demonstrate markedly decreased posterior airspace consolidations with small, posterior pleural effusions. Note the residual inter- and intralobular septal thickening. A posteroanterior gradient is now present, clearly demonstrating the importance of dependent atelectasis in ARDS. Note also the presence of numerous dilated small bronchi and bronchioles.
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Figure 15a. Atypical ARDS secondary to septic shock in a 47-year-old man who had undergone endoscopic sclerotherapy for esophageal varices. Supine high-resolution CT scans (b obtained caudad to a) demonstrate bilateral airspace consolidations that predominate anteriorly. This distribution is of unknown origin because the patient was never placed in the prone position during the course of the disease.
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Figure 15b. Atypical ARDS secondary to septic shock in a 47-year-old man who had undergone endoscopic sclerotherapy for esophageal varices. Supine high-resolution CT scans (b obtained caudad to a) demonstrate bilateral airspace consolidations that predominate anteriorly. This distribution is of unknown origin because the patient was never placed in the prone position during the course of the disease.
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Figure 16a. Heroin-induced pulmonary edema in a 19-year-old male addict with ARDS. (a) Chest radiograph reveals massive diffuse pulmonary edema. (b) Chest radiograph obtained 27 hours later reveals substantial resolution of the pulmonary edema, which is only possible in the absence of DAD. Intubation and positive pressure ventilation may have partially influenced the edematous change.
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Figure 16b. Heroin-induced pulmonary edema in a 19-year-old male addict with ARDS. (a) Chest radiograph reveals massive diffuse pulmonary edema. (b) Chest radiograph obtained 27 hours later reveals substantial resolution of the pulmonary edema, which is only possible in the absence of DAD. Intubation and positive pressure ventilation may have partially influenced the edematous change.
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Figure 17a. Heroin-induced pulmonary edema in a 24-year-old male addict who was admitted with a Glasgow coma score of 3. (a) Chest radiograph obtained at the time of admission demonstrates confluent right pulmonary edema due to the right lateral decubitus position the patient had maintained for the previous 24 hours. (b) Chest radiograph obtained 28 hours later demonstrates rapid resolution of the infiltrates.
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Figure 17b. Heroin-induced pulmonary edema in a 24-year-old male addict who was admitted with a Glasgow coma score of 3. (a) Chest radiograph obtained at the time of admission demonstrates confluent right pulmonary edema due to the right lateral decubitus position the patient had maintained for the previous 24 hours. (b) Chest radiograph obtained 28 hours later demonstrates rapid resolution of the infiltrates.
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Figure 18. Pulmonary edema following administration of a cytokine in a 37-year-old woman with malignant melanoma. The patient was admitted for intraarterial extracorporeal tumor necrosis factor perfusion of the right lower limb. Chest radiograph obtained 48 hours after treatment demonstrates bilateral diffuse pulmonary edema with peribronchial cuffing (arrow), enlarged hila, ill-defined vessels, and pleural effusions. Note the absence of alveolar areas of increased opacity. The infiltrates disappeared within 5 days.
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Figure 19a. High-altitude pulmonary edema in an experienced 30-year-old female mountain climber who developed acute mountain sickness and brain edema at an altitude of 4,500 meters. After resting at this height for 24 hours, she experienced progressive dyspnea and a productive cough. Immediate descent by helicopter was arranged. Chest radiograph (a) and CT scan (2-mm section thickness) (b) obtained at the time of admission demonstrate numerous small, confluent airspace consolidations that spare the apices and most of the lung cortex. No Kerley lines or pleural effusions are seen. The heterogeneity of the airspace disease may reflect the heterogeneity of the pulmonary vascular constriction. The patient recovered in less than 24 hours, at which time radiologic findings were normal.
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Figure 19b. High-altitude pulmonary edema in an experienced 30-year-old female mountain climber who developed acute mountain sickness and brain edema at an altitude of 4,500 meters. After resting at this height for 24 hours, she experienced progressive dyspnea and a productive cough. Immediate descent by helicopter was arranged. Chest radiograph (a) and CT scan (2-mm section thickness) (b) obtained at the time of admission demonstrate numerous small, confluent airspace consolidations that spare the apices and most of the lung cortex. No Kerley lines or pleural effusions are seen. The heterogeneity of the airspace disease may reflect the heterogeneity of the pulmonary vascular constriction. The patient recovered in less than 24 hours, at which time radiologic findings were normal.
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Figure 20a. Neurogenic pulmonary edema in a 54-year-old woman who was admitted for intracranial hemorrhage due to arterial hypertension. (a) Chest radiograph obtained at the time of admission shows airspace consolidations predominantly at the apices. There are no pleural effusions or Kerley lines, and heart size is normal. (b) High-resolution CT scan obtained at the same time demonstrates confluent alveolar consolidations in the central portions of the lungs. A few thickened interlobular septa are also seen (arrows).
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Figure 20b. Neurogenic pulmonary edema in a 54-year-old woman who was admitted for intracranial hemorrhage due to arterial hypertension. (a) Chest radiograph obtained at the time of admission shows airspace consolidations predominantly at the apices. There are no pleural effusions or Kerley lines, and heart size is normal. (b) High-resolution CT scan obtained at the same time demonstrates confluent alveolar consolidations in the central portions of the lungs. A few thickened interlobular septa are also seen (arrows).
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Figure 21a. Reperfusion pulmonary edema in the same patient as in Figure 14 following bilateral pulmonary thromboendarterectomy. (a, b) Chest radiographs obtained 1 (a) and 2 (b) days after surgery demonstrate increased areas of airspace consolidation, particularly in the territories of the recanalized lobar and segmental arteries. (c) On a chest radiograph obtained 4 days after surgical intervention, the reperfusion pulmonary edema has mostly resolved.
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Figure 21b. Reperfusion pulmonary edema in the same patient as in Figure 14 following bilateral pulmonary thromboendarterectomy. (a, b) Chest radiographs obtained 1 (a) and 2 (b) days after surgery demonstrate increased areas of airspace consolidation, particularly in the territories of the recanalized lobar and segmental arteries. (c) On a chest radiograph obtained 4 days after surgical intervention, the reperfusion pulmonary edema has mostly resolved.
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Figure 21c. Reperfusion pulmonary edema in the same patient as in Figure 14 following bilateral pulmonary thromboendarterectomy. (a, b) Chest radiographs obtained 1 (a) and 2 (b) days after surgery demonstrate increased areas of airspace consolidation, particularly in the territories of the recanalized lobar and segmental arteries. (c) On a chest radiograph obtained 4 days after surgical intervention, the reperfusion pulmonary edema has mostly resolved.
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Figure 22a. Pulmonary edema in a 34-year-old man who had undergone bilateral lung transplantation for end-stage cystic fibrosis. (a) Chest radiograph obtained 48 hours after transplantation demonstrates diffuse, confluent alveolar areas of increased opacity. (b) On a chest radiograph obtained 2 days later, the areas of increased opacity have decreased markedly. The heart and vascular axes are normal in size.
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Figure 22b. Pulmonary edema in a 34-year-old man who had undergone bilateral lung transplantation for end-stage cystic fibrosis. (a) Chest radiograph obtained 48 hours after transplantation demonstrates diffuse, confluent alveolar areas of increased opacity. (b) On a chest radiograph obtained 2 days later, the areas of increased opacity have decreased markedly. The heart and vascular axes are normal in size.
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Figure 23. Reexpansion pulmonary edema in a 57-year-old man who was admitted for massive left-sided carcinomatous pleural effusion. Three liters of fluid were drained within 3 hours. Control chest radiograph obtained 2 hours later demonstrates extensive left pulmonary edema. The radiologic signs disappeared within 5 days.
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Figure 24a. Postreduction pulmonary edema in a 64-year-old woman who had undergone bilateral lung reduction for emphysema. (a) Chest radiograph obtained 18 hours after surgery demonstrates the appearance of pulmonary edema that was observed in 14% of affected patients. Kerley lines are the most prominent finding. The heart and vascular structures are normal. (b) High-resolution CT scan obtained 2 hours later demonstrates numerous thickened interlobular septa, predominantly in the right lung field (arrows). Areas of ground-glass attenuation are observed bilaterally, predominantly in the lung cortex. These findings were not present preoperatively and disappeared within 48 hours.
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Figure 24b. Postreduction pulmonary edema in a 64-year-old woman who had undergone bilateral lung reduction for emphysema. (a) Chest radiograph obtained 18 hours after surgery demonstrates the appearance of pulmonary edema that was observed in 14% of affected patients. Kerley lines are the most prominent finding. The heart and vascular structures are normal. (b) High-resolution CT scan obtained 2 hours later demonstrates numerous thickened interlobular septa, predominantly in the right lung field (arrows). Areas of ground-glass attenuation are observed bilaterally, predominantly in the lung cortex. These findings were not present preoperatively and disappeared within 48 hours.
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Figure 25a. Pulmonary edema due to air embolism in a 72-year-old woman immediately following coronary artery bypass graft surgery. One liter of air was inadvertently injected during flushing of the extracorporeal circulation device. (a) Intraoperative transesophageal echocardiogram demonstrates a large quantity of air bubbles passing through the right side of the heart (arrows). RA = right atrium, RV = right ventricle. (Courtesy of D. Bettex, MD, Zurich, Switzerland.) (b) Chest radiograph obtained 2 hours later after the patient had become markedly hypoxic demonstrates severe pulmonary edema with a large number of Kerley lines predominating in the left lung and subpleural edema in the minor fissure.
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Figure 25b. Pulmonary edema due to air embolism in a 72-year-old woman immediately following coronary artery bypass graft surgery. One liter of air was inadvertently injected during flushing of the extracorporeal circulation device. (a) Intraoperative transesophageal echocardiogram demonstrates a large quantity of air bubbles passing through the right side of the heart (arrows). RA = right atrium, RV = right ventricle. (Courtesy of D. Bettex, MD, Zurich, Switzerland.) (b) Chest radiograph obtained 2 hours later after the patient had become markedly hypoxic demonstrates severe pulmonary edema with a large number of Kerley lines predominating in the left lung and subpleural edema in the minor fissure.
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Copyright © 1999 by the Radiological Society of North America.