From the Archives of the AFIP
Pulmonary Vasculature: Hypertension and Infarction1 (CME available in print version and on RSNA Link)
Aletta Ann Frazier, MD,
Jeffrey R. Galvin, MD ,
Teri J. Franks, MD and
Melissa L. Rosado-de-Christenson, Col, USAF, MC
1 From the Departments of Radiologic Pathology (A.A.F., J.R.G., M.L.R.) and Pulmonary and Mediastinal Pathology (T.J.F.), Armed Forces Institute of Pathology, 6825 16th St NW, Bldg 54, Room M-121, Washington, DC, 20306-6000; the Department of Radiology, University of Maryland Medical System, Baltimore (J.R.G.); and the Department of Radiology and Nuclear Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD (M.L.R.). Received October 26, 1999; revisions requested November 24 and received December 28; accepted December 29. Address reprint requests to A.A.F. (e-mail: frazier@afip.osd.mil).
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Figure 1. Cross-sectional drawings depict normal pulmonary vascular anatomy. Arterial vessels are located adjacent to a schematic airway (A). The walls of elastic arteries (a) contain multiple parallel elastic lamellae, smooth muscle cells, and collagen fibrils. The muscular arteries (b) contain a media of smooth muscle fibers, bordered by distinct internal and external elastic laminae. Arterioles (c) are distinguished by the absence of a distinct external elastic lamina. Veins (d) are identified by their septal location (S) and a media of loosely organized smooth muscle fibers.
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Figure 2. Schematic illustrates how the bronchial arteries (ba) supply the visceral pleura, airways, vasa vasora of pulmonary arteries, lymph nodes, and bronchovascular and neural bundles. Extrapulmonary bronchial veins (ev) drain to the right side of the heart, and intrapulmonary veins (iv) anastomose with pulmonary arteries and return to the left side of the heart.
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Figure 3. Contrast material-enhanced chest computed tomographic (CT) scan (mediastinal window) of a patient with corrected transposition demonstrates thrombosis of the right pulmonary artery (*) secondary to slow flow. There is compensatory enlargement and tortuosity of bronchial arteries within the mediastinum and along central airways (arrows).
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Figure 4. Schematics show the anastomosis of a bronchial artery (b) and pulmonary arteriole (p) at an alveolar capillary loop (9). Normal (nl) antegrade flow in both vessels is shown in A. Occlusion of the pulmonary arteriole by thrombus, with recruitment of bronchial flow and consequent extravasation of blood cells into alveoli (arrows), is seen in B. Elevated postcapillary pulmonary pressure (P), combined with arterial occlusion, causes more significant intraalveolar hemorrhage (arrows), as illustrated in C. This higher degree of hemorrhage predisposes the patient to infarction.
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Figure 5a. Pulmonary hemorrhage and infarction. (a) Photograph of a gross specimen with pleural-based pulmonary hemorrhage shows thrombosis of the feeding vessel (arrow) and preservation of the underlying lung architecture. Scale is in millimeters. (b) Low-power photomicrograph (original magnification, x4; hematoxylin-eosin [H-E] stain) of a subpleural pulmonary infarct shows the triangular area of coagulation necrosis (*) surrounded by hemorrhage (arrows). (c) Photograph of a gross specimen with a wedge-shaped pulmonary infarct shows necrotic destruction of the affected parenchyma, surrounded by inflammatory infiltrates (solid arrows) and a rim of reactive hyperemia from bronchial arterial collateral flow (open arrows). (Fig 5a and 5c reprinted, with permission, from reference 13.)
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Figure 5b. Pulmonary hemorrhage and infarction. (a) Photograph of a gross specimen with pleural-based pulmonary hemorrhage shows thrombosis of the feeding vessel (arrow) and preservation of the underlying lung architecture. Scale is in millimeters. (b) Low-power photomicrograph (original magnification, x4; hematoxylin-eosin [H-E] stain) of a subpleural pulmonary infarct shows the triangular area of coagulation necrosis (*) surrounded by hemorrhage (arrows). (c) Photograph of a gross specimen with a wedge-shaped pulmonary infarct shows necrotic destruction of the affected parenchyma, surrounded by inflammatory infiltrates (solid arrows) and a rim of reactive hyperemia from bronchial arterial collateral flow (open arrows). (Fig 5a and 5c reprinted, with permission, from reference 13.)
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Figure 5c. Pulmonary hemorrhage and infarction. (a) Photograph of a gross specimen with pleural-based pulmonary hemorrhage shows thrombosis of the feeding vessel (arrow) and preservation of the underlying lung architecture. Scale is in millimeters. (b) Low-power photomicrograph (original magnification, x4; hematoxylin-eosin [H-E] stain) of a subpleural pulmonary infarct shows the triangular area of coagulation necrosis (*) surrounded by hemorrhage (arrows). (c) Photograph of a gross specimen with a wedge-shaped pulmonary infarct shows necrotic destruction of the affected parenchyma, surrounded by inflammatory infiltrates (solid arrows) and a rim of reactive hyperemia from bronchial arterial collateral flow (open arrows). (Fig 5a and 5c reprinted, with permission, from reference 13.)
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Figure 6. Diagram provides an anatomic overview of precapillary or arterial hypertension (left) and postcapillary or venous hypertension (right).
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Figure 7. Schematics demonstrate the vascular changes of pulmonary arterial hypertension. In cross-section A, medial hypertrophy produces marked thickening of the medial smooth muscle in between internal and external elastic laminae. In cross-section B, intimal proliferation thickens the intima in concentric layers. In cross-section C, a plexiform lesion is characterized by intimal proliferation and interruption of the media by a "glomeruloid" proliferation of small vascular channels.
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Figure 8a. Microscopic features of pulmonary arterial hypertension. (a) Medium-power photomicrograph (original magnification, x20; Movat pentachrome elastic stain) of a muscular artery shows medial hypertrophy of the vessel wall (arrows). (b) Medium-power photomicrograph (original magnification, x20; Movat pentachrome elastic stain) of a muscular artery shows intimal proliferation (arrow). (c) Medium-power photomicrograph (original magnification, x20; Movat pentachrome elastic stain) of a plexiform lesion in a muscular artery shows intimal proliferation with aneurysmal disruption of the wall (*) by proliferative vascular channels (arrows). (d) Medium-power photomicrograph (original magnification, x10; H-E stain) of a muscular artery shows a plexiform lesion, identified by the glomeruloid proliferation (curved arrow) and dilatation (straight arrows) of vascular channels.
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Figure 8b. Microscopic features of pulmonary arterial hypertension. (a) Medium-power photomicrograph (original magnification, x20; Movat pentachrome elastic stain) of a muscular artery shows medial hypertrophy of the vessel wall (arrows). (b) Medium-power photomicrograph (original magnification, x20; Movat pentachrome elastic stain) of a muscular artery shows intimal proliferation (arrow). (c) Medium-power photomicrograph (original magnification, x20; Movat pentachrome elastic stain) of a plexiform lesion in a muscular artery shows intimal proliferation with aneurysmal disruption of the wall (*) by proliferative vascular channels (arrows). (d) Medium-power photomicrograph (original magnification, x10; H-E stain) of a muscular artery shows a plexiform lesion, identified by the glomeruloid proliferation (curved arrow) and dilatation (straight arrows) of vascular channels.
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Figure 8c. Microscopic features of pulmonary arterial hypertension. (a) Medium-power photomicrograph (original magnification, x20; Movat pentachrome elastic stain) of a muscular artery shows medial hypertrophy of the vessel wall (arrows). (b) Medium-power photomicrograph (original magnification, x20; Movat pentachrome elastic stain) of a muscular artery shows intimal proliferation (arrow). (c) Medium-power photomicrograph (original magnification, x20; Movat pentachrome elastic stain) of a plexiform lesion in a muscular artery shows intimal proliferation with aneurysmal disruption of the wall (*) by proliferative vascular channels (arrows). (d) Medium-power photomicrograph (original magnification, x10; H-E stain) of a muscular artery shows a plexiform lesion, identified by the glomeruloid proliferation (curved arrow) and dilatation (straight arrows) of vascular channels.
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Figure 8d. Microscopic features of pulmonary arterial hypertension. (a) Medium-power photomicrograph (original magnification, x20; Movat pentachrome elastic stain) of a muscular artery shows medial hypertrophy of the vessel wall (arrows). (b) Medium-power photomicrograph (original magnification, x20; Movat pentachrome elastic stain) of a muscular artery shows intimal proliferation (arrow). (c) Medium-power photomicrograph (original magnification, x20; Movat pentachrome elastic stain) of a plexiform lesion in a muscular artery shows intimal proliferation with aneurysmal disruption of the wall (*) by proliferative vascular channels (arrows). (d) Medium-power photomicrograph (original magnification, x10; H-E stain) of a muscular artery shows a plexiform lesion, identified by the glomeruloid proliferation (curved arrow) and dilatation (straight arrows) of vascular channels.
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Figure 9a. Complications of pulmonary arterial hypertension. (a) Photograph of a sagittal cut section of the right pulmonary hilum shows golden atherosclerotic plaques (arrows) and thrombosis (*) within the central arteries. (b) Photograph of an opened central pulmonary artery reveals pale tan intimal atherosclerotic plaques (arrows). Scale is in centimeters. (c) Photograph of the heart (coronal cut section) shows marked right ventricular hypertrophy (arrow), in this case accompanied by left ventricular hypertrophy (*).
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Figure 9b. Complications of pulmonary arterial hypertension. (a) Photograph of a sagittal cut section of the right pulmonary hilum shows golden atherosclerotic plaques (arrows) and thrombosis (*) within the central arteries. (b) Photograph of an opened central pulmonary artery reveals pale tan intimal atherosclerotic plaques (arrows). Scale is in centimeters. (c) Photograph of the heart (coronal cut section) shows marked right ventricular hypertrophy (arrow), in this case accompanied by left ventricular hypertrophy (*).
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Figure 9c. Complications of pulmonary arterial hypertension. (a) Photograph of a sagittal cut section of the right pulmonary hilum shows golden atherosclerotic plaques (arrows) and thrombosis (*) within the central arteries. (b) Photograph of an opened central pulmonary artery reveals pale tan intimal atherosclerotic plaques (arrows). Scale is in centimeters. (c) Photograph of the heart (coronal cut section) shows marked right ventricular hypertrophy (arrow), in this case accompanied by left ventricular hypertrophy (*).
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Figure 10a. Microscopic features of pulmonary venous hypertension. (a) Low-power photomicrograph (original magnification, x4; H-E stain) shows a dilated vein (*) surrounded by a collar of fibrosis within a thickened interlobular septum (arrows). (b) Medium-power photomicrograph (original magnification, x20; Movat pentachrome elastic stain) demonstrates marked capillary congestion and proliferation (arrows). (c) Low-power photomicrograph (original magnification, x4; H-E stain) shows a venous infarct (*) within the interlobular septum, secondary to pulmonary venous obstruction.
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Figure 10b. Microscopic features of pulmonary venous hypertension. (a) Low-power photomicrograph (original magnification, x4; H-E stain) shows a dilated vein (*) surrounded by a collar of fibrosis within a thickened interlobular septum (arrows). (b) Medium-power photomicrograph (original magnification, x20; Movat pentachrome elastic stain) demonstrates marked capillary congestion and proliferation (arrows). (c) Low-power photomicrograph (original magnification, x4; H-E stain) shows a venous infarct (*) within the interlobular septum, secondary to pulmonary venous obstruction.
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Figure 10c. Microscopic features of pulmonary venous hypertension. (a) Low-power photomicrograph (original magnification, x4; H-E stain) shows a dilated vein (*) surrounded by a collar of fibrosis within a thickened interlobular septum (arrows). (b) Medium-power photomicrograph (original magnification, x20; Movat pentachrome elastic stain) demonstrates marked capillary congestion and proliferation (arrows). (c) Low-power photomicrograph (original magnification, x4; H-E stain) shows a venous infarct (*) within the interlobular septum, secondary to pulmonary venous obstruction.
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Figure 11a. Progression of PPH. (a) Frontal chest radiograph of a 34-year-old man who presented with mild symptoms of dyspnea and fatigue shows minimal prominence of the main pulmonary artery. (b) On a chest radiograph obtained 10 years later, when the patient returned with severe dyspnea and elevated right ventricular pressure (120 mm Hg), marked enlargement of the main pulmonary artery and hilar vessels is seen.
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Figure 11b. Progression of PPH. (a) Frontal chest radiograph of a 34-year-old man who presented with mild symptoms of dyspnea and fatigue shows minimal prominence of the main pulmonary artery. (b) On a chest radiograph obtained 10 years later, when the patient returned with severe dyspnea and elevated right ventricular pressure (120 mm Hg), marked enlargement of the main pulmonary artery and hilar vessels is seen.
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Figure 12a. PPH in a young adult woman. (a, b) Posteroanterior (a) and lateral (b) radiographs of the chest show an enlarged pulmonary trunk and right ventricular dilatation. (c) Contrast-enhanced chest CT scan (mediastinal window) demonstrates a widened pulmonary trunk. (d) Contrast-enhanced chest CT scan (mediastinal window) obtained at a lower level shows right ventricular dilatation and thickening of the free right ventricular wall (arrow). (e) Chest CT scan (lung window) shows large-caliber central pulmonary arteries (arrows) with abrupt tapering of the peripheral vessels (arrowheads).
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Figure 12b. PPH in a young adult woman. (a, b) Posteroanterior (a) and lateral (b) radiographs of the chest show an enlarged pulmonary trunk and right ventricular dilatation. (c) Contrast-enhanced chest CT scan (mediastinal window) demonstrates a widened pulmonary trunk. (d) Contrast-enhanced chest CT scan (mediastinal window) obtained at a lower level shows right ventricular dilatation and thickening of the free right ventricular wall (arrow). (e) Chest CT scan (lung window) shows large-caliber central pulmonary arteries (arrows) with abrupt tapering of the peripheral vessels (arrowheads).
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Figure 12c. PPH in a young adult woman. (a, b) Posteroanterior (a) and lateral (b) radiographs of the chest show an enlarged pulmonary trunk and right ventricular dilatation. (c) Contrast-enhanced chest CT scan (mediastinal window) demonstrates a widened pulmonary trunk. (d) Contrast-enhanced chest CT scan (mediastinal window) obtained at a lower level shows right ventricular dilatation and thickening of the free right ventricular wall (arrow). (e) Chest CT scan (lung window) shows large-caliber central pulmonary arteries (arrows) with abrupt tapering of the peripheral vessels (arrowheads).
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Figure 12d. PPH in a young adult woman. (a, b) Posteroanterior (a) and lateral (b) radiographs of the chest show an enlarged pulmonary trunk and right ventricular dilatation. (c) Contrast-enhanced chest CT scan (mediastinal window) demonstrates a widened pulmonary trunk. (d) Contrast-enhanced chest CT scan (mediastinal window) obtained at a lower level shows right ventricular dilatation and thickening of the free right ventricular wall (arrow). (e) Chest CT scan (lung window) shows large-caliber central pulmonary arteries (arrows) with abrupt tapering of the peripheral vessels (arrowheads).
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Figure 12e. PPH in a young adult woman. (a, b) Posteroanterior (a) and lateral (b) radiographs of the chest show an enlarged pulmonary trunk and right ventricular dilatation. (c) Contrast-enhanced chest CT scan (mediastinal window) demonstrates a widened pulmonary trunk. (d) Contrast-enhanced chest CT scan (mediastinal window) obtained at a lower level shows right ventricular dilatation and thickening of the free right ventricular wall (arrow). (e) Chest CT scan (lung window) shows large-caliber central pulmonary arteries (arrows) with abrupt tapering of the peripheral vessels (arrowheads).
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Figure 13. PPH in a young adult man. Lung perfusion scans (anterior view, left; posterior view, right) demonstrate multiple, bilateral subsegmental perfusion defects. Such a nonspecific pattern is also seen with many secondary causes of precapillary pulmonary hypertension.
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Figure 14. PPH. Pulmonary arteriogram of the right upper lobe shows pruning of the peripheral vascularity (arrows).
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Figure 15. PPH. Radiograph of a whole lung specimen in which contrast material had been injected shows a corkscrew configuration of peripheral pulmonary arteries (arrows).
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Figure 16a. Pulmonary arterial hypertension in a 39-year-old woman with atrial septal defect. (a, b) Posteroanterior (a) and lateral (b) radiographs of the chest show enlargement of the pulmonary trunk and hilar vessels and a prominent right ventricle. (c) Contrast-enhanced chest CT scan (mediastinal window) demonstrates marked enlargement of the central pulmonary arteries, which contain extensive thrombus and calcified atherosclerotic plaques. (d) Radiograph of the right lung specimen reveals linear calcific deposits compatible with advanced atherosclerosis of the central pulmonary arteries. (e) Low-power photomicrograph (original magnification, x4; Movat pentachrome elastic stain) of a large elastic pulmonary artery shows organizing intraluminal thrombus (*).
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Figure 16b. Pulmonary arterial hypertension in a 39-year-old woman with atrial septal defect. (a, b) Posteroanterior (a) and lateral (b) radiographs of the chest show enlargement of the pulmonary trunk and hilar vessels and a prominent right ventricle. (c) Contrast-enhanced chest CT scan (mediastinal window) demonstrates marked enlargement of the central pulmonary arteries, which contain extensive thrombus and calcified atherosclerotic plaques. (d) Radiograph of the right lung specimen reveals linear calcific deposits compatible with advanced atherosclerosis of the central pulmonary arteries. (e) Low-power photomicrograph (original magnification, x4; Movat pentachrome elastic stain) of a large elastic pulmonary artery shows organizing intraluminal thrombus (*).
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Figure 16c. Pulmonary arterial hypertension in a 39-year-old woman with atrial septal defect. (a, b) Posteroanterior (a) and lateral (b) radiographs of the chest show enlargement of the pulmonary trunk and hilar vessels and a prominent right ventricle. (c) Contrast-enhanced chest CT scan (mediastinal window) demonstrates marked enlargement of the central pulmonary arteries, which contain extensive thrombus and calcified atherosclerotic plaques. (d) Radiograph of the right lung specimen reveals linear calcific deposits compatible with advanced atherosclerosis of the central pulmonary arteries. (e) Low-power photomicrograph (original magnification, x4; Movat pentachrome elastic stain) of a large elastic pulmonary artery shows organizing intraluminal thrombus (*).
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Figure 16d. Pulmonary arterial hypertension in a 39-year-old woman with atrial septal defect. (a, b) Posteroanterior (a) and lateral (b) radiographs of the chest show enlargement of the pulmonary trunk and hilar vessels and a prominent right ventricle. (c) Contrast-enhanced chest CT scan (mediastinal window) demonstrates marked enlargement of the central pulmonary arteries, which contain extensive thrombus and calcified atherosclerotic plaques. (d) Radiograph of the right lung specimen reveals linear calcific deposits compatible with advanced atherosclerosis of the central pulmonary arteries. (e) Low-power photomicrograph (original magnification, x4; Movat pentachrome elastic stain) of a large elastic pulmonary artery shows organizing intraluminal thrombus (*).
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Figure 16e. Pulmonary arterial hypertension in a 39-year-old woman with atrial septal defect. (a, b) Posteroanterior (a) and lateral (b) radiographs of the chest show enlargement of the pulmonary trunk and hilar vessels and a prominent right ventricle. (c) Contrast-enhanced chest CT scan (mediastinal window) demonstrates marked enlargement of the central pulmonary arteries, which contain extensive thrombus and calcified atherosclerotic plaques. (d) Radiograph of the right lung specimen reveals linear calcific deposits compatible with advanced atherosclerosis of the central pulmonary arteries. (e) Low-power photomicrograph (original magnification, x4; Movat pentachrome elastic stain) of a large elastic pulmonary artery shows organizing intraluminal thrombus (*).
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Figure 17a. Pulmonary arterial hypertension secondary to long-standing ventricular septal defect (VSD). (a) Axial spin-echo T1-weighted MR image (cardiac gated) demonstrates a large VSD (*) and biventricular hypertrophy (arrows). (b) Axial spin-echo T1-weighted MR image (cardiac gated) shows dilatation of the main pulmonary artery (*) and mixed signal intensity within the bifurcation compatible with flow-related artifact (arrow).
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Figure 17b. Pulmonary arterial hypertension secondary to long-standing ventricular septal defect (VSD). (a) Axial spin-echo T1-weighted MR image (cardiac gated) demonstrates a large VSD (*) and biventricular hypertrophy (arrows). (b) Axial spin-echo T1-weighted MR image (cardiac gated) shows dilatation of the main pulmonary artery (*) and mixed signal intensity within the bifurcation compatible with flow-related artifact (arrow).
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Figure 18. Microscopic features of CTEPH. High-power photomicrograph (original magnification, x40; Movat pentachrome elastic stain) of a muscular artery shows eccentric intimal thickening (*) and organized thrombus (T) containing recanalized vascular channels (arrows).
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Figure 19a. Pulmonary embolism in a 60-year-old woman with atrial fibrillation. (a) Frontal chest radiograph reveals a rounded homogeneous opacity in the right lower lung. (b) Collimated chest CT scan (lung window) demonstrates a pulmonary infarct as a wedge-shaped, pleural-based area of high attenuation.
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Figure 19b. Pulmonary embolism in a 60-year-old woman with atrial fibrillation. (a) Frontal chest radiograph reveals a rounded homogeneous opacity in the right lower lung. (b) Collimated chest CT scan (lung window) demonstrates a pulmonary infarct as a wedge-shaped, pleural-based area of high attenuation.
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Figure 20a. Pulmonary embolism in a 22-year-old man with right atrial myxoma. (a) Frontal chest radiograph shows ill-defined bibasilar opacities (arrows). (b) Contrast-enhanced chest CT scan demonstrates a filling defect in the right atrium (arrow) and a wedge-shaped consolidation in the right lower lobe, confirmed as being a pulmonary infarction at biopsy.
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Figure 20b. Pulmonary embolism in a 22-year-old man with right atrial myxoma. (a) Frontal chest radiograph shows ill-defined bibasilar opacities (arrows). (b) Contrast-enhanced chest CT scan demonstrates a filling defect in the right atrium (arrow) and a wedge-shaped consolidation in the right lower lobe, confirmed as being a pulmonary infarction at biopsy.
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Figure 21. Chest CT scan (lung window) of a patient with multiple pulmonary emboli demonstrates sharply defined areas of variable lung attenuation compatible with mosaic perfusion.
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Figure 22a. Microscopic features of tumor embolism. (a) Low-power photomicrograph (original magnification, x4; H-E stain) shows a muscular pulmonary artery distended by thrombus that contains tumor cells (arrow). (b) Low-power photomicrograph (original magnification, x4; H-E stain) reveals tumor cells (*) filling subpleural lymphatic vessels, with secondary edema of the adjacent interlobular septum (arrow).
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Figure 22b. Microscopic features of tumor embolism. (a) Low-power photomicrograph (original magnification, x4; H-E stain) shows a muscular pulmonary artery distended by thrombus that contains tumor cells (arrow). (b) Low-power photomicrograph (original magnification, x4; H-E stain) reveals tumor cells (*) filling subpleural lymphatic vessels, with secondary edema of the adjacent interlobular septum (arrow).
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Figure 23a. Tumor embolism in a middle-aged woman with severe dyspnea and adenocarcinoma of unknown origin. Frontal chest radiograph was normal. (a) Chest CT scan (lung window) demonstrates bibasilar subpleural wedge-shaped areas of consolidation compatible with areas of pulmonary infarction. (b) Lung perfusion scans show multiple subsegmental perfusion defects.
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Figure 23b. Tumor embolism in a middle-aged woman with severe dyspnea and adenocarcinoma of unknown origin. Frontal chest radiograph was normal. (a) Chest CT scan (lung window) demonstrates bibasilar subpleural wedge-shaped areas of consolidation compatible with areas of pulmonary infarction. (b) Lung perfusion scans show multiple subsegmental perfusion defects.
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Figure 24a. Tumor embolism in a 42-year-old man with dyspnea, hemoptysis, and hematuria secondary to transitional cell carcinoma of the bladder. (a) Chest CT scan (lung window) reveals nodular thickening of the minor fissure (white arrow), thickening of the bronchovascular bundles and interlobular septa (black arrow), and a masslike consolidation in the right lower lobe. (b) Photograph of a cut section of the lung demonstrates subpleural and peribronchovascular tan masses (arrows) consistent with capillary and lymphangitic spread of tumor.
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Figure 24b. Tumor embolism in a 42-year-old man with dyspnea, hemoptysis, and hematuria secondary to transitional cell carcinoma of the bladder. (a) Chest CT scan (lung window) reveals nodular thickening of the minor fissure (white arrow), thickening of the bronchovascular bundles and interlobular septa (black arrow), and a masslike consolidation in the right lower lobe. (b) Photograph of a cut section of the lung demonstrates subpleural and peribronchovascular tan masses (arrows) consistent with capillary and lymphangitic spread of tumor.
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Figure 25. Microscopic features of schistosomal embolism. High-power photomicrograph (original magnification, x40; H-E stain) shows a cluster of S mansoni eggs that has obliterated the pulmonary artery lumen (arrows) and is surrounded by interstitial fibrosis and inflammation.
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Figure 26. Schistosomiasis with pulmonary arterial hypertension in a 25-year-old Asian woman. Frontal chest radiograph shows mild cardiomegaly and prominence of the main pulmonary artery and hilar vessels.
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Figure 27a. Microscopic features of pulmonary talcosis. (a) Electron microscopic image shows irregular crystalline plates of talc (arrow) embedded in the lung parenchyma. (b) Low-power photomicrograph (original magnification, x4; H-E stain) under polarized light reveals a central deposition of birefringent talc particles and obliteration of the surrounding pulmonary architecture by dense fibrosis. (c) Photograph of the cut lung surface shows a large fibrotic mass (*) emanating from the hilum (arrow) that exerts traction on the upper lobe.
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Figure 27b. Microscopic features of pulmonary talcosis. (a) Electron microscopic image shows irregular crystalline plates of talc (arrow) embedded in the lung parenchyma. (b) Low-power photomicrograph (original magnification, x4; H-E stain) under polarized light reveals a central deposition of birefringent talc particles and obliteration of the surrounding pulmonary architecture by dense fibrosis. (c) Photograph of the cut lung surface shows a large fibrotic mass (*) emanating from the hilum (arrow) that exerts traction on the upper lobe.
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Figure 27c. Microscopic features of pulmonary talcosis. (a) Electron microscopic image shows irregular crystalline plates of talc (arrow) embedded in the lung parenchyma. (b) Low-power photomicrograph (original magnification, x4; H-E stain) under polarized light reveals a central deposition of birefringent talc particles and obliteration of the surrounding pulmonary architecture by dense fibrosis. (c) Photograph of the cut lung surface shows a large fibrotic mass (*) emanating from the hilum (arrow) that exerts traction on the upper lobe.
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Figure 28a. Pulmonary talcosis in a 37-year-old woman with a history of chronic intravenous injection of crushed pentazocine lactate (Talwin) and methylphenidate hydrochloride (Ritalin) tablets. (a) Frontal chest radiograph reveals micronodular opacities in the upper lungs and irregular perihilar masses, with upward hilar retraction and marked hyperlucency at the lung bases. (b) High-resolution CT scan (lung window) reveals fine, scattered, bilateral interstitial nodules. (c) Chest CT scan (mediastinal window) of the left lung shows an irregular, high-attenuation perihilar mass.
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Figure 28b. Pulmonary talcosis in a 37-year-old woman with a history of chronic intravenous injection of crushed pentazocine lactate (Talwin) and methylphenidate hydrochloride (Ritalin) tablets. (a) Frontal chest radiograph reveals micronodular opacities in the upper lungs and irregular perihilar masses, with upward hilar retraction and marked hyperlucency at the lung bases. (b) High-resolution CT scan (lung window) reveals fine, scattered, bilateral interstitial nodules. (c) Chest CT scan (mediastinal window) of the left lung shows an irregular, high-attenuation perihilar mass.
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Figure 28c. Pulmonary talcosis in a 37-year-old woman with a history of chronic intravenous injection of crushed pentazocine lactate (Talwin) and methylphenidate hydrochloride (Ritalin) tablets. (a) Frontal chest radiograph reveals micronodular opacities in the upper lungs and irregular perihilar masses, with upward hilar retraction and marked hyperlucency at the lung bases. (b) High-resolution CT scan (lung window) reveals fine, scattered, bilateral interstitial nodules. (c) Chest CT scan (mediastinal window) of the left lung shows an irregular, high-attenuation perihilar mass.
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Figure 29. Frontal chest radiograph of a young man, following a suicide attempt with intravenous injection of mercury, shows bibasilar high-density branching structures that represent extensive intravascular accumulation of the liquid metal.
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Figure 30. Hallmark microscopic features of PVOD. High-power photomicrograph (original magnification, x40; elastic stain) shows an intralobular vein obstructed by connective tissue (*) that contains multiple recanalization channels (arrows).
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Figure 31a. PVOD in a 20-year-old man with progressive dyspnea. (a) Frontal chest radiograph shows central pulmonary arterial enlargement and diffuse reticular opacities. (b) Collimated view of the right lower lobe shows prominent septal lines. (c) High-resolution CT scan (lung window) demonstrates enlarged central arteries, peribronchovascular thickening, and prominent interlobular septa.
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Figure 31b. PVOD in a 20-year-old man with progressive dyspnea. (a) Frontal chest radiograph shows central pulmonary arterial enlargement and diffuse reticular opacities. (b) Collimated view of the right lower lobe shows prominent septal lines. (c) High-resolution CT scan (lung window) demonstrates enlarged central arteries, peribronchovascular thickening, and prominent interlobular septa.
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Figure 31c. PVOD in a 20-year-old man with progressive dyspnea. (a) Frontal chest radiograph shows central pulmonary arterial enlargement and diffuse reticular opacities. (b) Collimated view of the right lower lobe shows prominent septal lines. (c) High-resolution CT scan (lung window) demonstrates enlarged central arteries, peribronchovascular thickening, and prominent interlobular septa.
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Figure 32a. Mediastinal fibrosis and focal pulmonary venous constriction in a 45-year-old woman with dyspnea and hemoptysis. (a) CT scan (mediastinal window) reveals a perihilar soft-tissue mass containing coarse calcifications. (b) CT scan (lung window) shows a pleural-based area of high attenuation corresponding to macroscopic venous infarction.
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Figure 32b. Mediastinal fibrosis and focal pulmonary venous constriction in a 45-year-old woman with dyspnea and hemoptysis. (a) CT scan (mediastinal window) reveals a perihilar soft-tissue mass containing coarse calcifications. (b) CT scan (lung window) shows a pleural-based area of high attenuation corresponding to macroscopic venous infarction.
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Figure 33. Venous changes of postcapillary pulmonary hypertension, secondary to obstructive left atrial neoplasm. Low-power photomicrograph (original magnification, x4; H-E stain) shows a thick-walled, dilated vein (*) within a fibrotic interlobular septum (arrow).
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Figure 34a. Severe pulmonary venous hypertension secondary to a left atrial mass in an 82-year-old woman. (a) Frontal chest radiograph shows cardiomegaly and diffuse bilateral air-space opacities representing pulmonary edema. (b) Echocardiogram demonstrates a left atrial mass (*) that is adherent to the mitral valve. (c) CT scan (mediastinal window) reveals a large soft-tissue mass filling the left atrial chamber (*). (d) Photograph of a cut section shows a large bosselated fibrosarcoma resected from the left atrium. Scale is in centimeters.
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Figure 34b. Severe pulmonary venous hypertension secondary to a left atrial mass in an 82-year-old woman. (a) Frontal chest radiograph shows cardiomegaly and diffuse bilateral air-space opacities representing pulmonary edema. (b) Echocardiogram demonstrates a left atrial mass (*) that is adherent to the mitral valve. (c) CT scan (mediastinal window) reveals a large soft-tissue mass filling the left atrial chamber (*). (d) Photograph of a cut section shows a large bosselated fibrosarcoma resected from the left atrium. Scale is in centimeters.
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Figure 34c. Severe pulmonary venous hypertension secondary to a left atrial mass in an 82-year-old woman. (a) Frontal chest radiograph shows cardiomegaly and diffuse bilateral air-space opacities representing pulmonary edema. (b) Echocardiogram demonstrates a left atrial mass (*) that is adherent to the mitral valve. (c) CT scan (mediastinal window) reveals a large soft-tissue mass filling the left atrial chamber (*). (d) Photograph of a cut section shows a large bosselated fibrosarcoma resected from the left atrium. Scale is in centimeters.
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Figure 34d. Severe pulmonary venous hypertension secondary to a left atrial mass in an 82-year-old woman. (a) Frontal chest radiograph shows cardiomegaly and diffuse bilateral air-space opacities representing pulmonary edema. (b) Echocardiogram demonstrates a left atrial mass (*) that is adherent to the mitral valve. (c) CT scan (mediastinal window) reveals a large soft-tissue mass filling the left atrial chamber (*). (d) Photograph of a cut section shows a large bosselated fibrosarcoma resected from the left atrium. Scale is in centimeters.
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Figure 35a. Severe mitral stenosis with secondary pulmonary venous hypertension in a middle-aged woman. Posteroanterior (a) and lateral (b) radiographs of the chest show marked left atrial dilatation, prominent upper lobe vessels, and an enlarged pulmonary trunk.
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Figure 35b. Severe mitral stenosis with secondary pulmonary venous hypertension in a middle-aged woman. Posteroanterior (a) and lateral (b) radiographs of the chest show marked left atrial dilatation, prominent upper lobe vessels, and an enlarged pulmonary trunk.
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Copyright © 2000 by the Radiological Society of North America.
