(Radiographics. 1999;19:1507-1531.)
© RSNA, 1999
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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Abstract
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Pulmonary edema may be classified as increased hydrostatic pressure edema, permeability edema with diffuse alveolar damage (DAD), permeability edema without DAD, or mixed edema. Pulmonary edema has variable manifestations. Postobstructive pulmonary edema typically manifests radiologically as septal lines, peribronchial cuffing, and, in more severe cases, central alveolar edema. Pulmonary edema with chronic pulmonary embolism manifests as sharply demarcated areas of increased ground-glass attenuation. Pulmonary edema with veno-occlusive disease manifests as large pulmonary arteries, diffuse interstitial edema with numerous Kerley lines, peribronchial cuffing, and a dilated right ventricle. Stage 1 near drowning pulmonary edema manifests as Kerley lines, peribronchial cuffing, and patchy, perihilar alveolar areas of airspace consolidation; stage 2 and 3 lesions are radiologically nonspecific. Pulmonary edema following administration of cytokines demonstrates bilateral, symmetric interstitial edema with thickened septal lines. High-altitude pulmonary edema usually manifests as central interstitial edema associated with peribronchial cuffing, ill-defined vessels, and patchy airspace consolidation. Neurogenic pulmonary edema manifests as bilateral, rather homogeneous airspace consolidations that predominate at the apices in about 50% of cases. Reperfusion pulmonary edema usually demonstrates heterogeneous airspace consolidations that predominate in the areas distal to the recanalized vessels. Postreduction pulmonary edema manifests as mild airspace consolidation involving the ipsilateral lung, whereas pulmonary edema due to air embolism initially demonstrates interstitial edema followed by bilateral, peripheral alveolar areas of increased opacity that predominate at the lung bases. Familiarity with the spectrum of radiologic findings in pulmonary edema from various causes will often help narrow the differential diagnosis.
Index Terms: Lung, diseases, 60.91 • Lung, edema, 60.45, 60.644, 60.7112, 60.7115 • Respiratory distress syndrome, adult (ARDS), 60.413
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INTRODUCTION
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Pulmonary edema is defined as an abnormal accumulation of fluid in the extravascular compartments of the lung. The relative amounts of intravascular and extravascular fluid in the lung are mostly controlled by the permeability of the capillary membrane as well as the oncotic pressure (1). This relation is described by the Starling equation, which is used to determine the theoretic amount of fluid Qfilt filtered per unit area per unit of time:
In this equation, HPiv and HPev represent the intravascular and extravascular hydrostatic pressure, respectively, and OPiv and OPev represent the intravascular and extravascular oncotic pressure, respectively. Kfilt represents the conductance of the capillary wall and expresses the water resistance created by the capillary endothelial cell junctions with changes in HPiv and HPev. t represents the oncotic reflection coefficient and expresses the permeability of the capillary membrane to macromolecules. The greater this reflection coefficient is, the more the passage of macromolecules will be restricted, thus decreasing overall fluid filtration. The net flow Fnet is defined as Qfilt - Qlymph, where Qfilt represents fluid transudation or exudation and Qlymph represents lymphatic absorption. Pulmonary edema develops when the equilibrium between fluid transudation or exudation Qfilt and lymphatic absorption Qlymph is disturbed. Thus, although under normal conditions the endothelial cells are relatively impermeable to protein but remain permeable to water and solutes, the tight intercellular junctions of the alveolar epithelium remain nearly impermeable to water and solutes, thus constituting an effective barrier that is a major factor in preventing the development of pulmonary edema. Lymphatic drainage (Qlymph) represents another way of eliminating excess lung water. A manifold increase in lymphatic flow has been observed with chronically increased hydrostatic pressure. This increase in lymphatic flow is very efficient in eliminating excess water, especially when there is diminished oncotic pressure due to hypoalbuminemia (2). However, its impact requires time; thus, it may not be as effective in acute settings.
Pulmonary edema can be divided into four main categories on the basis of pathophysiology: (a) increased hydrostatic pressure edema, (b) permeability edema with diffuse alveolar damage (DAD), (c) permeability edema without DAD, and (d) mixed edema due to simultaneous increased hydrostatic pressure and permeability changes (3,4). This classification scheme is helpful because pulmonary edema is often seen in the clinical setting, especially in the intensive care unit and emergency department. The clinical and radiologic manifestations of acute pulmonary edema are generally well established. However, pulmonary edema may also demonstrate unusual findings.
In this article, we describe the clinical and radiologic features of pulmonary edema in a series of 80 patients who were seen over a 10-year period in the intensive care units and emergency department at our institution. Pulmonary edema in these patients was categorized according to the classification scheme described earlier. Atypical pulmonary edema is defined as lung edema with an unusual radiologic appearance but with clinical findings that are usually associated with well-known causes of pulmonary edema. Unusual forms of pulmonary edema are defined as lung edema from unusual causes (ie, rare diseases or rare manifestations of common diseases).
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INCREASED HYDROSTATIC PRESSURE EDEMA
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Two pathophysiologic and radiologic phases are recognized in the development of pressure edema: interstitial edema and alveolar flooding or edema. These phases are virtually identical for left-sided heart failure and fluid overload, the two most frequently observed causes of pressure edema in intensive care and emergency patients. The intensity and duration of both phases are clearly related to the degree of increased pressure, which is determined by the hydrostatic-oncotic pressure ratio.
Interstitial edema occurs with an increase of 15–25 mm Hg in mean transmural arterial pressure and results in the early loss of definition of subsegmental and segmental vessels, mild enlargement of the peribronchovascular spaces, the appearance of Kerley lines, and subpleural effusions (5,6). If the quantity of extravascular fluid continues to increase, the edema will migrate centrally with progressive blurring of vessels, first at the lobar level and later at the level of the hilum. At this point, lung radiolucency decreases markedly, making identification of small peripheral vessels difficult. Peribronchial cuffing becomes apparent, particularly in the perihilar areas (4,7). With increases in transmural pressure greater than 25 mm Hg, fluid drainage from the extravascular compartment is at maximum capacity and the second phase (alveolar flooding) commences, leading to a sudden extension of edema into the alveolar spaces and thus creating tiny nodular or acinar areas of increased opacity that coalesce into frank consolidations (Fig 1). Some investigators have observed that, with such pressure increases, the onset of alveolar edema may also be associated with direct pressure-induced damage to the alveolar epithelium (8).
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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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Pulmonary artery catheters are frequently used to assess hydrostatic pressure in intensive care patients. Pulmonary capillary wedge pressure has been shown to reflect left atrial pressure and correlates well with the radiologic features of congestive heart failure and pulmonary venous hypertension (Table) (4,9). However, in acute heart failure, a time lag is often observed between the increased pulmonary capillary wedge pressure and the radiologic manifestation of pulmonary edema due to the relatively slow movement of water through the widened capillary endothelial cell junctions (10). Similarly, as pulmonary edema resolves, the radiologic findings will persist with decreasing or even normal pulmonary capillary wedge pressure (Fig 2).
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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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Bat Wing Edema
Bat wing edema refers to a central, nongravitational distribution of alveolar edema. It is seen in less than 10% of cases of pulmonary edema (4) and generally occurs with rapidly developing severe cardiac failure as seen in acute mitral insufficiency (associated with papillary muscle rupture, massive myocardial infarct, and valve leaflet destruction due to septic endocarditis) or renal failure (Figs 3, 4). In bat wing edema, the lung cortex is free of alveolar or interstitial fluid. This pathologic condition develops so rapidly that it is initially observed as an alveolar infiltrate, and the preceding interstitial phase that is typically seen in pulmonary edema goes undetected radiologically.
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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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Several theories have been proposed to explain the pathophysiology of bat wing edema. One such theory involves an increase in hydraulic conductivity. Mucopolysaccharides fill the spaces in the perivascular cytoskeleton and, under normal conditions, inhibit the flow of liquid. However, with increased tissue hydration, this extracellular matrix allows water to easily flow centrally (4). Other investigators have suggested a pumping effect of the respiratory cycle, which is more pronounced in the lung cortex (10) and causes overall fluid flow toward the hilum. Another probable contributing factor is the contractile property of alveolar septa, which allows them to expel interstitial edema toward the hilum (4).
Asymmetric Distribution of Increased Pressure Edema
The most frequent cause of asymmetric distribution of pressure edema is morphologic changes in the lung parenchyma in chronic obstructive pulmonary disease. In cardiac failure, extensive lung emphysema of the apices (seen in heavy smokers) or marked destruction and fibrosis of the upper and middle portions of the lungs (seen in end-stage tuberculosis, sarcoidosis, or asbestosis) will result in pulmonary edema that predominates in the regions that are less affected by these disease processes (Figs 5, 6).
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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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Hemodynamic factors can also cause asymmetric distribution of pulmonary edema. Edema associated with mitral regurgitation has been shown to predominate in the right upper lobe as a result of flow impairment caused by the reflux stream that is directed toward the right upper pulmonary vein (Fig 7) (11,12). Such asymmetric distribution occurs in 9% of adults and 22% of children with grade 3 or 4 mitral regurgitation (13,14).\.
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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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Finally, the position of the patient also influences intra- and extravascular fluid distribution (Fig 8). In supine patients, axial CT usually demonstrates an anteroposterior gradient, whereas more asymmetric distribution of edema secondary to prolonged surgery or immobilization is frequently observed in the lung fields in recumbent patients. This distribution is typically seen in congestive heart failure but is also observed in overhydration.
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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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Pulmonary Edema with Acute Asthma
Pulmonary edema with acute asthma is a rare pathologic condition because the associated trapped air tends to maintain a positive intraalveolar pressure, thus decreasing the hydrostatic pressure gradient. Its pathogenesis can be associated with the severity of the Müller maneuver (ie, forced inspiration as the patient struggles to inhale). Pulmonary edema with acute asthma has been reported in one series of eight children (15). During tidal inspiration, children with episodes of acute asthma have been shown to have very high negative peak inspiratory pressures (mean, -29 cm of water) compared with those in healthy subjects (mean, -7 cm). Furthermore, it has been demonstrated that the mean pleural pressure is markedly decreased over the entire tidal respiration, reaching -25.5 cm of water compared with -5 cm in healthy subjects (15). This high negative pleural pressure during acute asthmatic episodes helps maintain the patency of the narrowed airways.
On the other hand, the lowered pleural pressure results in decreased interstitial pressure, whereas intravascular pressures are only minimally influenced. The airway obstruction in acute asthma is not uniform throughout the lungs, resulting in heterogeneous extravascular fluid accumulation. During the past 5 years, pulmonary edema with acute asthma was documented radiologically only once at our institution. In that case, chest radiography demonstrated Kerley lines, peribronchial cuffing, ill-defined pulmonary vessels, and diffuse alveolar areas of increased opacity in both lungs (Fig 9). These radiologic findings could not be differentiated from those in other causes of cardiogenic 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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Postobstructive Pulmonary Edema
Postobstructive pulmonary edema occurs after relief from an upper airway obstruction and represents a pure form of hydrostatic edema (3,4). It is most frequently caused by an impacted foreign body, laryngospasm, epiglottitis, or strangulation.
If the obstruction occurs primarily with forced inspiration as the patient struggles to inhale (Müller maneuver), it causes a high negative intrathoracic pressure that increases venous return. The resulting edema is caused by a sudden, marked decrease in the negative pleural pressure, which leads to a high hydrostatic pressure gradient between the intravascular and extravascular compartments (16,17). An obstruction that prevents both inspiration and expiration may create a high positive intrathoracic pressure that impairs the development of edema initially. Later, edema develops as the obstruction is relieved and the intrathoracic pressure suddenly drops.
At chest radiography and CT, postobstructive pulmonary edema typically manifests as septal lines, peribronchial cuffing, and, in more severe cases, central alveolar edema (Fig 10). These findings are similar to those in pressure edema. Cardiac size is usually normal, indicating a pressure edema that is not related to overhydration. Resolution of clinical symptoms and radiologic findings is rapid and usually occurs within 2–3 days.
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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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Edema with Acute and Chronic Pulmonary Embolism
For many years, pulmonary edema has been seen occasionally at chest radiography in acute pulmonary embolism (18). Even with the generalized use of helical CT for the assessment of acute pulmonary embolism, pulmonary edema is seen in less than 10% of cases (19,20). Pulmonary edema usually appears at CT as heterogeneous areas of increased ground-glass attenuation localized in the territories of the patent segmental or subsegmental arteries. However, some authors have suggested that in chronic pulmonary embolism these areas of increased attenuation may also represent relatively normal lung parenchyma with no underlying pulmonary edema (with the area of increased attenuation being evident only when compared with the adjacent hypoperfused lung). Thus, some authors have suggested that this is the reason why other high-resolution CT features of pulmonary edema (eg, septal thickening) are not seen in these high-attenuation areas (ie, because they do not actually represent territorial increases in extravascular fluid) (21). If this is true, then pulmonary edema (when present) may be due primarily to hydrostatic causes superimposed on the underlying embolic disease.
On the other hand, it is believed that the mechanism of pulmonary edema in massive acute pulmonary embolism is directly related to pulmonary hypertension (18,22). This hypertension is caused by the occlusion of more than 50% of the pulmonary arterial bed. Because the right-sided cardiac output is then directed through a reduced arterial network, the capillary hydrostatic pressure increases markedly. The resulting increased perfusion of the areas not involved by the vascular thrombosis leads to edema (23).
In our experience, pulmonary edema is seen in many patients with chronic pulmonary embolism, a finding that has also been described by many other investigators (22,24–26). In this setting, pulmonary edema manifests as areas of increased ground-glass attenuation that are sharply demarcated from areas of regional transparency distal to the occluded arteries and thus deprived of blood flow (Fig 11a) (27). Areas of ground-glass attenuation are closely associated with dilated pulmonary arteries in more than 70% of cases of chronic pulmonary embolism (Fig 11b) (28–30). Therefore, these areas are probably of mixed origin and are associated with both simple overperfusion or hyperemia and a component of extravascular fluid accumulation within the perfused regions. The pathogenesis of these focal areas of pulmonary edema has been demonstrated with single-photon emission CT and scintigraphy of the lung (28). Juxtaposition of areas of increased ground-glass attenuation with areas of hypoperfusion produces a familiar mosaic pattern known as mosaic oligemia.
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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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Edema with Pulmonary Veno-occlusive Disease
Pulmonary veno-occlusive disease is a lethal condition associated with the narrowing or occlusion of small pulmonary veins and venules by organized thrombi (30–32). This disease process demonstrates widespread involvement of the lungs but does not involve the large pulmonary veins. Pulmonary veno-occlusive disease has no sex or age predilection and causes a type of hydrostatic edema due to the increased hydrostatic pressure that is directly associated with the resulting increase in peripheral resistance. Its pathogenesis remains unclear, although striking similarities with veno-occlusive disease of the liver have been reported (31–33). The use of oral contraceptives may play a role in both pulmonary and hepatic veno-occlusive disease because they have been found to dramatically reduce the endothelial cell production and metabolism of prostaglandin and prostacyclin, both of which are strong inhibitors of coagulation (34). Patients present with rapidly progressive dyspnea, orthopnea, and acute pulmonary edema with or without hemoptysis. The main diagnostic features include a normal or low pulmonary capillary wedge pressure reflecting the patency of the large pulmonary veins, pulmonary arterial hypertension, and edema. Chest radiography and CT reveal enlarged pulmonary arteries, diffuse interstitial edema with numerous Kerley lines, peribronchial cuffing, and a dilated right ventricle (Fig 12) (31).
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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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Near Drowning Pulmonary Edema
Near drowning is defined as asphyxiation due to water inhalation followed by survival for a minimum of 24 hours (35). Three stages of near drowning are currently recognized (35,36). Stage 1 manifests as acute laryngospasm that occurs after inhalation of a small amount of water. In patients in whom the laryngospasm persists, thereby preventing outright flooding of the lungs, one observes "dry drowning." As in postobstructive pulmonary edema, the resulting lesions are due to negative pressure edema arising from a prolonged episode of the Müller maneuver (35). Kerley lines, peribronchial cuffing, and patchy, perihilar alveolar areas of airspace consolidation are the most important radiologic findings (Fig 13a). These findings disappear completely within 24–48 hours following appropriate therapy (Fig 13b, 13c). In stage 2, the victim still usually presents with laryngospasm but may begin to swallow water into the stomach. In stage 3, 10%–15% of patients still present with dry drowning caused by persistence of the associated laryngospasm; in the remaining 85%–90% of patients, the laryngospasm relaxes secondary to hypoxia and large amounts of water are aspirated (35). In such cases, the lung lesions are no longer associated with pressure edema but mainly with hypoxia, which leads to cytokine release and subsequent permeability edema (36–38). In addition to causing hypoxia, inhaled water has a deleterious effect on the capillary endothelium, alveolar pneumocytes, and surfactant production. This in turn leads to permeability edema with DAD, atelectasis, and shunting, thereby causing adult respiratory distress syndrome (ARDS). This situation is often worsened by the aspiration of gastric fluid and by infections due to fresh-water saprophytic bacteria, which may cause further alveolar damage. Stage 2 and 3 lesions are radiologically nonspecific, varying from tiny, ill-defined lesions to large, lobar airspace consolidations. Lesion size depends on the volume of inhaled water, the duration of the ensuing hypoxia, and on whether fresh or salt water is involved (35,37,38). Clearing of the lungs begins slowly and continues at a rate that depends on the severity of capillary and alveolar damage. This process occurs several days after the incident if the situation remains uncomplicated by gastric aspiration, infection, or other causes of additional alveolar damage (37,38).
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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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PERMEABILITY EDEMA WITH DAD
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ARDS is the term used for various acute or subacute, diffuse pulmonary lesions that cause severe hypoxemia. These lesions are associated with a variety of precipitating factors and are not caused or influenced by concurrent cardiac insufficiency. Therefore, ARDS occurs without an increase in pulmonary capillary pressure. ARDS represents the most severe form of permeability edema associated with DAD (2). DAD may be the direct result of a local precipitating factor or may occur secondary to some systemic condition. Primary or direct injuries to the alveolar and vascular endothelium of the lung usually result from the exposure of these cells to chemical agents, infectious pathogens, gastric fluid, or toxic gas, which destroy or severely damage the cells. Secondary damage is due to a systemic biochemical cascade creating oxidating agents, inflammatory mediators, and enzymes, which also harm these endothelial cells during sepsis, pancreatitis, severe trauma, or blood transfusion. On the basis of these etiologic differences, two major pathophysiologic mechanisms in the development of ARDS have been described: (a) ARDS due to an underlying pulmonary disease, which is associated with pulmonary consolidation, and (b) ARDS secondary to extrapulmonary disease, which manifests as interstitial edema and alveolar collapse (39). These mechanisms are based on physiologic ventilation mechanics, and, although they have not yet been pathologically proved, they do have distinct implications for the treatment of affected patients.
ARDS encompasses three often overlapping stages. The first (exudative) stage is characterized by interstitial edema with a high protein content that rapidly fills the alveolar spaces and is associated with hemorrhage and ensuing hyaline membrane formation. The rapid extension of edema into the alveolar spaces probably explains why findings that are typically seen in interstitial edema (eg, Kerley lines) are not prominent in ARDS. The second (proliferative) stage manifests as organization of the fibrinous exudate. Following this organization, one observes the regeneration of the alveolar lining and thickening of the alveolar septa. The third (fibrotic) stage is characterized by varying degrees of scarring and formation of subpleural and intrapulmonary cysts.
Initially, most patients present with few if any clinical symptoms. Soon, however, they develop rapidly progressive dyspnea, tachypnea, and cyanosis. Hypoxemia is present and remains unresponsive to oxygen therapy mainly due to the presence of arteriovenous shunting. Mechanical ventilatory assistance with positive end-expiratory pressure is often necessary to adequately expand the lung parenchyma and increase oxygen diffusion.
The early exudative stage demonstrates 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 hydrostatic edema, the alveolar edema in ARDS usually has a more peripheral or cortical distribution. Radiologic signs that are typically seen in cardiogenic edema (eg, cardiomegaly, apical vascular redistribution, Kerley lines) are absent. Despite the presence of diffuse, homogeneous DAD, ARDS usually displays a gravitational gradient that is easily visualized at CT and can be modified by changing the patient's position (Fig 14) (40). This suggests that atelectasis is also an important factor in the inhomogeneous regional distribution of ARDS. Furthermore, this gravitational pattern can help exclude concomitant infectious processes because such dependent atelectasis is more common in patients with early ARDS without pneumonia (41).
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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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With progression of the disease into the proliferative stage, an inhomogeneous pattern of ground-glass areas of increased opacity is seen, along with early modifications due to fibrosis. During the fibrotic stage, subpleural and intrapulmonary cystic lesions may be observed and may be the direct cause of pneumothoraces (2,42). Recurrent exudative episodes can still occur in the proliferative and fibrotic stages of ARDS, resulting in mixed radiologic findings that demonstrate parts of all three stages simultaneously.
Atypical ARDS, which is characterized by a predominance of anterior airspace consolidations in supine patients, was observed in about 5% of patients who underwent CT during the exudative stage (Fig 15). The pathophysiologic explanation for this finding remains unclear but may involve regional differences in mechanically assisted ventilation pressures.
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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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PERMEABILITY EDEMA WITHOUT DAD
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As the name implies, permeability edema without DAD refers to pulmonary edema in which permeability changes are not primarily associated with DAD. The absence of cellular damage is often not proved pathologically but may be inferred from the clinical and radiologic course of the disease because rapid regression is often observed, with ventilatory improvements occurring within a short period of time. Although some degree of DAD may occur, damage remains minor and usually only partially affects patient outcome.
Heroin-induced Pulmonary Edema
Pulmonary edema directly associated with an overdose of opiates occurs almost exclusively with heroin but is also rarely encountered with the use of cocaine and "crack." Heroin-induced pulmonary edema is seen in about 15% of cases of heroin overdose with an overall mortality rate of 10% (43–45). Heroin overdose is believed to directly cause depression of the medullary respiratory center and lead to hypoxia and acidosis, both of which cause permeability edema without DAD (46). This absence of DAD can be directly inferred from the rapid resolution of the disorder observed in all cases that are not complicated by aspiration of gastric contents or by infection. Unlike cocaine, heroin has no direct deleterious effect on myocardial function (47).
Often, a patient who overdoses on heroin may lie motionless in a given position for hours or even days. These recumbent positions give rise to a markedly asymmetric distribution of edema associated with gravity dependency and may lead to extensive crush injuries with associated muscle damage and ensuing renal insufficiency. At radiology, heroin-induced pulmonary edema is indistinguishable from other types of edema without DAD. It manifests as widespread, patchy, bilateral airspace consolidations, ill-defined vessels, and peribronchial cuffing and is frequently complicated by edema due to fluid overload associated with renal insufficiency (Fig 16). When heroin-induced pulmonary edema is not associated with renal insufficiency or other complications such as aspiration of gastric contents, rapid resolution of the infiltrates is observed within 1 or 2 days with no parenchymal sequelae (Fig 17).
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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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Pulmonary Edema Following Administration of Cytokines
Interleukin (IL)–2 is an endogenous glycoprotein that enhances the in vivo and in vitro tumoricidal activity of natural killer cells. It is used in patients with metastatic melanoma and metastatic renal cell adenocarcinoma. Another cytokine known as tumor necrosis factor may be administered by intraarterial infusion and subsequently increases the production and release of IL-2 via cytokine cascades with intermediary products such as IL-8. Both IL-2 and tumor necrosis factor may cause permeability disruptions without DAD and lead to pulmonary edema. They predominantly affect the capillary endothelial cells, although the precise underlying pathophysiologic process has yet to be established (2,48,49). Most patients undergoing therapy with IL-2 and tumor necrosis factor demonstrate a mild increase in pulmonary capillary wedge pressure due to the direct toxic effect of these cytokines on the myocardial cells and on the heart's conduction system. Although this toxic effect may lead to arrhythmia and a decreased ejection fraction, it is not sufficient to explain the onset of pulmonary edema from pressure gradients: Two studies have demonstrated that pulmonary capillary wedge pressure increases by only about 12 mm Hg (50,51).
About 75% of patients undergoing intravenous IL-2 therapy and about 15%–20% of those treated with intraarterial tumor necrosis factor infusions will demonstrate radiologic signs of pulmonary edema (3,49). In contrast, only 25% of patients treated with recombinant IL-2 will develop clinical signs and symptoms of pulmonary disease (eg, cough, dyspnea, tachypnea, fever). Approximately 5%–7% of this subgroup will require respiratory assistance (3). Radiologic signs are usually seen at conventional chest radiography 1–5 days after the start of cytokine therapy (Fig 18) and include bilateral, symmetric interstitial edema with thickened septal lines. Peribronchial cuffing is observed in 75% of cases (3,49). No alveolar edema is observed unless there is associated cardiac insufficiency. Interstitial edema is associated with small pleural effusions in about 40% of cases and, like other types of permeability edema without DAD, regresses rapidly.
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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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High-Altitude Pulmonary Edema
High-altitude pulmonary edema is a potentially fatal condition that occurs in a previously healthy individual. It is caused by prolonged exposure to an environment with a lower partial oxygen atmospheric pressure. High-altitude pulmonary edema occurs most frequently in young males 24–48 hours after they have made a rapid ascent to heights greater than 3,000 meters and have remained in that environment (52-54). Numerous cases of high-altitude pulmonary edema have been described in the literature, often demonstrating individual susceptibility (54). High-altitude pulmonary edema usually follows acute mountain sickness, which actually represents a milder form of the disease and can act as an indicator of impending high-altitude pulmonary edema (2). Clinical manifestations include dyspnea at rest, cough with frothy pink sputum production, and neurologic disturbances associated with concomitant brain edema. Arterial oxygen saturation levels correspond directly to the severity of the disorder and may be as low as 38% (52).
The pathophysiology of high-altitude pulmonary edema remains controversial. However, there is general agreement that this condition results from acute, persistent hypoxia, which induces heterogeneous vasoconstriction leading to marked pulmonary hypertension (52). This in turn induces endothelial leakage, which results in interstitial and alveolar edema without DAD. This vascular leakage creates edema with a high protein content, which explains the frothy appearance of the sputum (2,52,55). The clinical manifestations of high-altitude pulmonary edema will resolve rapidly if the patient quickly descends to a low altitude and undergoes adequate therapy with oxygen and pulmonary vasodilators (56).
The radiologic features of high-altitude pulmonary edema vary with the degree of hypoxemia that is present. Usually, this condition manifests as central interstitial edema associated with peribronchial cuffing, ill-defined vessels, and a patchy, frequently asymmetric pattern of airspace consolidation (Fig 19) (57). A few Kerley lines may also be visible. In mild high-altitude pulmonary edema, the airspace consolidations may be subtle or even absent with little or no involvement of the lung periphery. In severe cases, they have a tendency to become confluent and eventually involve the entire lung parenchyma (58).
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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 dyspne | |
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Abstract
INTRODUCTION
