DOI: 10.1148/rg.1103035043
(Radiographics. 2003;23:1521-1539.)
© RSNA, 2003
Thrombotic and Nonthrombotic Pulmonary Arterial Embolism: Spectrum of Imaging Findings1
Daehee Han, MD2,
Kyung Soo Lee, MD,
Tomas Franquet, MD,
Nestor L. Müller, MD,
Tae Sung Kim, MD,
Hojoong Kim, MD,
O Jung Kwon, MD and
Hong Sik Byun, MD
1 From the Department of Radiology and Center for Imaging Science (D.H., K.S.L., T.S.K., H.S.B.) and the Division of Pulmonary and Critical Care Medicine (H.K., O.J.K.), Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Ilwon-Dong, Kangnam-Ku, Seoul 135–710, Korea; and the Department of Radiology, Vancouver Hospital and Health Sciences Center, Vancouver, British Columbia, Canada (T.F., N.L.M.). Presented as an education exhibit at the 2002 RSNA scientific assembly. Received February 25, 2003; revision requested March 24 and received April 17; accepted April 21. Address correspondence to K.S.L. (e-mail: melon2@samsung.co.kr).
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Abstract
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Along with clinical examination and laboratory tests, imaging plays a key role in the diagnosis of pulmonary embolism. Multi–detector row helical computed tomography (CT) is particularly helpful in the diagnosis of acute pulmonary thromboembolism (PTE) owing to its capacity to directly show emboli as intravascular filling defects. Although parenchymal abnormalities at CT are nonspecific for acute PTE, they may contribute to a correct diagnosis of chronic PTE, the characteristic helical CT features of which are similar to its angiographic features and include webs or bands, intimal irregularities, abrupt narrowing or complete obstruction of the pulmonary arteries, and "pouching defect." Nonthrombotic pulmonary embolism is an uncommon condition but is sometimes associated with specific imaging findings, including discrete nodules with cavitation (septic embolism), widespread homogeneous and heterogeneous areas of increased opacity or attenuation that typically appear 12–24 hours after trauma (fat embolism), and fine miliary nodules that subsequently coalesce into large areas of increased opacity or attenuation (talcosis). Knowledge of appropriate imaging methods and familiarity with the specific imaging features of pulmonary embolism should facilitate prompt, effective diagnosis.
© RSNA, 2003
Index Terms: Embolism, 60.72 • Embolism, fat, 60.724 • Embolism, oil • Embolism, pulmonary, 60.72 • Pulmonary arteries, CT, 944.1211 • Pulmonary arteries, thrombosis, 944.7229
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LEARNING OBJECTIVES FOR TEST 5
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After reading this article and taking the test, the reader will be able to:
- List the imaging modalities currently being used to diagnose pulmonary thromboembolism.
- Describe the imaging features of acute and chronic pulmonary thromboembolism.
- Correlate the typical clinical manifestations with the imaging features of nonthrombotic pulmonary embolism.
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Introduction
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Pulmonary thromboembolism (PTE) is a common cause of morbidity and mortality. Imaging plays a critical role in the diagnosis of this potentially fatal condition. Although various imaging modalities can be used, helical computed tomography (CT) is rapidly becoming the imaging method of choice. Due to recent advances in multi–detector row scanning, CT has become at least as important as scintigraphy in the diagnosis of PTE. Although nonthrombotic pulmonary embolism is a relatively uncommon condition, it often manifests with specific imaging features that lead to a correct diagnosis. In this article, we discuss and illustrate the imaging findings in acute and chronic PTE and in nonthrombotic pulmonary embolism and correlate these findings with clinical and pathologic findings.
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Pulmonary Thromboembolism
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Extrapolation from limited data reported by Dalen and Alpert (1) in 1975 indicates that there are 630,000 cases of PTE annually in the United States. According to a recent investigation, the prevalence of unsuspected PTE is 1.5% on routine helical CT scans and is highest among inpatients with cancer (2).
Acute Pulmonary Embolism
Clinical Manifestations.—
PTE has a wide spectrum of clinical manifestations ranging from absence of symptoms to patient death. Although most patients with PTE are asymptomatic, some present with dyspnea, tachypnea, or pleuritic chest pain (3). In one study, a combination of sudden onset of dyspnea, chest pain, and syncope in association with electrocardiographic evidence of right ventricular overload had a sensitivity of 84% and a specificity of 95% for the diagnosis of the disease (4). In addition, the disease can safely be excluded with use of simple scoring systems for clinical features (pretest probability) combined with modern D-dimer tests in up to one-half of outpatients with suspected venous thromboembolism without the need for imaging (5). However, in the majority of patients, the combination of clinical and laboratory findings is insufficient for reliable diagnosis of acute PTE.
Radiographic Findings.—
Chest radiography has relatively low specificity and sensitivity in the diagnosis of PTE. The main role of radiography is to exclude other diseases such as pneumonia and pneumothorax that may mimic PTE clinically. Radiography is also helpful in the interpretation of ventilation-perfusion (V-P) lung scans (6–8). Radiographic signs with a relatively high specificity but low sensitivity for PTE include decreased vascularity in the peripheral lung (Westermark sign), enlargement of the central pulmonary artery (Fleischner sign), pleura-based areas of increased opacity (Hampton sign), and hemidiaphragm elevation (6). Other findings that may be associated with PTE include focal areas of increased opacity, linear atelectasis, and pleural effusion. However, these findings are nonspecific and are commonly seen in both patients with and patients without PTE (6).
Scintigraphic Findings.—
Until recently, V-P scintigraphy has been the main imaging method used in the diagnosis of acute and chronic PTE. The radiopharmaceuticals of choice are technetium-99m–labeled human albumin microsphere or macroaggregated albumin for perfusion scans (9,10) and xenon-133 for ventilation scans (8).
A major limitation of V-P scintigraphy is the high percentage of nondiagnostic intermediate probability scans. This percentage has been reduced with use of the revised Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) criteria. In one study, the application of the revised PIOPED criteria in 104 patients with suspected PTE reduced the percentage of intermediate probability scans from 75% (78 of 104 patients) to 60% (62 of 104 patients) (9).
Recently, several scintigraphic abnormalities have been identified as having a positive predictive value (PPV) of less than 10% for the diagnosis of PTE (11), including nonsegmental perfusion abnormalities (PPV = 8%), perfusion defects smaller than the corresponding regions of increased opacity at radiography (PPV = 8%), the "stripe sign" (PPV = 7%), triple matched defects in the upper or middle lung zone (PPV = 4%), matched V-P abnormalities in two or three zones of one lung (PPV = 3%), and one to three small segmental perfusion defects (PPV = 1%) (11).
However, even expert interpretation of V-P scans results in uncertain diagnosis in up to 73% of cases. In addition, only 41% of patients with documented pulmonary embolism had high-probability scans (12).
Findings at Helical CT Angiography and Indirect CT Venography.—
Having been introduced in the late 1980s, helical CT is rapidly replacing scintigraphy as the imaging modality of choice in the assessment of patients with suspected PTE. It is more accurate than scintigraphy and is rapid, noninvasive, and readily available (13). Helical CT directly demonstrates intraluminal clot as a filling defect (Fig 1). In addition, in patients without PTE, helical CT often provides alternative diagnoses (14–17). With the advent of multi–detector row helical CT scanners, even the subsegmental pulmonary arteries can now be evaluated (18). Therefore, it is likely that multi–detector row helical CT will allow more reliable identification of subsegmental emboli than does single-detector helical CT (19).
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Figure 1a. Acute pulmonary embolism and deep venous thrombosis (DVT) in a 48-year-old woman. (a) Contrast material-enhanced pulmonary CT arteriogram (1.25-mm collimation) obtained at the level of the basal subsegmental pulmonary artery shows multifocal low-attenuation emboli (arrows) in segmental and subsegmental arteries in the right lower lobe. (b) Contrast-enhanced indirect CT venogram (5-mm collimation) obtained at the level of the pelvic inlet 3 minutes after injection shows large low-attenuation thrombi filling the left common iliac vein (arrow).
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Figure 1b. Acute pulmonary embolism and deep venous thrombosis (DVT) in a 48-year-old woman. (a) Contrast material-enhanced pulmonary CT arteriogram (1.25-mm collimation) obtained at the level of the basal subsegmental pulmonary artery shows multifocal low-attenuation emboli (arrows) in segmental and subsegmental arteries in the right lower lobe. (b) Contrast-enhanced indirect CT venogram (5-mm collimation) obtained at the level of the pelvic inlet 3 minutes after injection shows large low-attenuation thrombi filling the left common iliac vein (arrow).
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Another advantage of CT is that it allows evaluation of DVT in the abdomen, pelvis, thighs, and calves (13). Such evaluation can be performed without intravenous injection of additional contrast material by scanning the lower limbs 3–4 minutes after scanning the pulmonary vessels (indirect CT venography). In two recent studies with ultrasonographic correlation, the sensitivity and specificity of CT venography were 93%–97% and 97%–100%, respectively (20,21). Helical CT findings in acute PTE and DVT and the pitfalls of CT angiography and CT venography in the diagnosis of this condition are summarized in Tables 1–4 (22–26).
Optimal technique for pulmonary angiography with a single-detector helical CT scanner includes a 3-mm collimation, 2-mm reconstruction intervals, a pitch of 2, and an average acquisition time of 24 seconds. With a multi–detector row scanner (especially one with eight or 16 detectors), imaging parameters include a total active detector length pitch (beam pitch) of 1.3–1.5, 0.5-second gantry rotation time, and 2.75–5.5 cm/sec table feed (using a 10–20-mm beam width, 1.375 beam pitch, and 0.5-second gantry rotation time; 10–20 x 1.375 x 2 with a 16-detector scanner). Images are reconstructed with a 1.25-mm thickness. A high-volume (100–150-mL) bolus of either diluted or undiluted contrast material is administered with an automated injector. A 15–17-second scan delay with administration of contrast material at a rate of 4 mL/sec is adequate in most patients. CT venography can easily be performed after CT pulmonary angiography without administration of additional contrast material. With single-detector CT, 5- or 10-mm-collimation axial scans are obtained at 20-mm intervals from the knees to the midabdomen (20,21,23,27).
Magnetic Resonance Angiographic Findings.—
Magnetic resonance (MR) imaging can potentially allow visualization of intravascular filling defects and provide physiologic information including the regional distribution of ventilation and perfusion (28). However, because CT is readily available and provides higher spatial resolution than MR imaging, the latter is currently less practical than CT in the diagnosis of PTE (28). To overcome inherent limitations caused by respiratory and cardiac motion artifacts, MR imaging is performed with gradient-recalled echo imaging techniques during suspended respiration. When combined with gadolinium enhancement, these techniques yield high-quality images of the pulmonary arteries (Fig 2) (29). MR angiography is as accurate as CT angiography in demonstrating lobar and segmental emboli (28,29). In a study with angiographic correlation by Erdman et al (30), MR imaging had a sensitivity of 90% and a specificity of 77%, whereas in a study by Gupta et al (29), it had a sensitivity of 85% and a specificity of 96%. Recent MR imaging studies by Hatabu et al (31,32) showed that this modality demonstrates perfusion (31) and ventilation (32) of the lung parenchyma. Although this additional information may be helpful in the assessment of affected patients, MR imaging currently plays a limited role in the diagnosis of PTE.
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Figure 2. Acute pulmonary embolism in a 41-year-old woman. Coronal gadolinium-enhanced three-dimensional pulmonary MR angiogram shows a large embolus (arrows) in the proximal right interlobar artery. (Courtesy of Jin Sung Lee, MD, Asan Medical Center, Seoul, Korea.)
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Pulmonary Angiographic Findings.—
Angiography is the most definitive technique for the diagnosis of PTE and has traditionally been considered the standard of reference in this setting. However, because angiography is an invasive technique, it is seldom performed, even in major academic centers. Complications of angiography include bleeding in the groin, recurrent ventricular arrhythmias, and respiratory arrest requiring ventilatory support (33–35).
The only primary sign of PTE is a filling defect. Secondary signs are the abrupt occlusion of a pulmonary artery and areas of oligemia with pruning of branching vessels (36).
Chronic Pulmonary Embolism
Pathogenesis.—
The majority of pulmonary emboli resolve without sequelae. In a small percentage of patients, particularly those with large emboli, the emboli undergo organization, recanalization, and retraction. The end result is vascular stenosis, which may lead to severe pulmonary hypertension and cor pulmonale (37).
Importance of Diagnosis.—
Recognizing chronic pulmonary embolism is important because, without intervention, the survival rate is low, especially if pulmonary hypertension is severe at the time of diagnosis (38). On the other hand, surgery usually results in good outcome in terms of both functional status (93% in New York Heart Association class I or II) and long-term survival rate (75% for patients who had undergone surgery more than 6 years earlier) (38).
Radiologic Findings.—
The characteristic manifestations of chronic PTE at V-P scintigraphy consist of mismatched, segmental, or lobar defects. These findings allow distinction from primary pulmonary hypertension, which is characterized by normal scintigraphic findings or the presence of patchy nonsegmental perfusion defects (39). Helical CT findings in chronic PTE are summarized in Table 5 (40–42). Direct vascular findings include webs or bands, intimal irregularities, abrupt narrowing or complete obstruction of the pulmonary arteries, and "pouching defect," which is defined as chronic thromboemboli organized in a concave shape that "points" toward the vessel lumen (Fig 3). Similar findings are seen at conventional pulmonary angiography (43). Characteristic pulmonary parenchymal findings in chronic PTE at helical and high-resolution CT consist of areas of decreased attenuation and perfusion adjacent to areas of increased attenuation and perfusion ("mosaic perfusion pattern") (Fig 4). Distinction of a mosaic perfusion pattern due to chronic PTE from one due to small airway disease can readily be made by assessing the diameter of the main pulmonary artery: The main pulmonary artery is typically enlarged in chronic PTE, a finding that reflects the presence of pulmonary arterial hypertension, whereas the main pulmonary artery in patients with airway disease is usually normal (40).
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Figure 3a. Chronic pulmonary embolism in a 55-year-old man. (a) Chest radiograph shows enlargement of the central pulmonary arteries along with cardiomegaly. (b) Contrast-enhanced pulmonary CT arteriogram (1.25-mm collimation) obtained at the level of the bronchus intermedius shows eccentric thrombus along the medial margin of the narrowed right interlobar pulmonary artery (arrows). (c) Perfusion lung scan (right posterior oblique view) obtained after administration of Tc-99m macroaggregated albumin shows multisegmental defects, which did not match the findings seen on a ventilation lung scan obtained with Tc-99m Technegas (not shown). (d) Pulmonary arteriogram shows abrupt cutoff in rounded fashion (pouching defect) of the lower lobar arteries (arrow). (e) Photograph of the thromboembolectomy specimen shows organized emboli filling the enlarged central pulmonary arteries. Note how the central thrombus is organized in concave fashion, creating a pouching defect (arrows).
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Figure 3b. Chronic pulmonary embolism in a 55-year-old man. (a) Chest radiograph shows enlargement of the central pulmonary arteries along with cardiomegaly. (b) Contrast-enhanced pulmonary CT arteriogram (1.25-mm collimation) obtained at the level of the bronchus intermedius shows eccentric thrombus along the medial margin of the narrowed right interlobar pulmonary artery (arrows). (c) Perfusion lung scan (right posterior oblique view) obtained after administration of Tc-99m macroaggregated albumin shows multisegmental defects, which did not match the findings seen on a ventilation lung scan obtained with Tc-99m Technegas (not shown). (d) Pulmonary arteriogram shows abrupt cutoff in rounded fashion (pouching defect) of the lower lobar arteries (arrow). (e) Photograph of the thromboembolectomy specimen shows organized emboli filling the enlarged central pulmonary arteries. Note how the central thrombus is organized in concave fashion, creating a pouching defect (arrows).
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Figure 3c. Chronic pulmonary embolism in a 55-year-old man. (a) Chest radiograph shows enlargement of the central pulmonary arteries along with cardiomegaly. (b) Contrast-enhanced pulmonary CT arteriogram (1.25-mm collimation) obtained at the level of the bronchus intermedius shows eccentric thrombus along the medial margin of the narrowed right interlobar pulmonary artery (arrows). (c) Perfusion lung scan (right posterior oblique view) obtained after administration of Tc-99m macroaggregated albumin shows multisegmental defects, which did not match the findings seen on a ventilation lung scan obtained with Tc-99m Technegas (not shown). (d) Pulmonary arteriogram shows abrupt cutoff in rounded fashion (pouching defect) of the lower lobar arteries (arrow). (e) Photograph of the thromboembolectomy specimen shows organized emboli filling the enlarged central pulmonary arteries. Note how the central thrombus is organized in concave fashion, creating a pouching defect (arrows).
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Figure 3d. Chronic pulmonary embolism in a 55-year-old man. (a) Chest radiograph shows enlargement of the central pulmonary arteries along with cardiomegaly. (b) Contrast-enhanced pulmonary CT arteriogram (1.25-mm collimation) obtained at the level of the bronchus intermedius shows eccentric thrombus along the medial margin of the narrowed right interlobar pulmonary artery (arrows). (c) Perfusion lung scan (right posterior oblique view) obtained after administration of Tc-99m macroaggregated albumin shows multisegmental defects, which did not match the findings seen on a ventilation lung scan obtained with Tc-99m Technegas (not shown). (d) Pulmonary arteriogram shows abrupt cutoff in rounded fashion (pouching defect) of the lower lobar arteries (arrow). (e) Photograph of the thromboembolectomy specimen shows organized emboli filling the enlarged central pulmonary arteries. Note how the central thrombus is organized in concave fashion, creating a pouching defect (arrows).
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Figure 3e. Chronic pulmonary embolism in a 55-year-old man. (a) Chest radiograph shows enlargement of the central pulmonary arteries along with cardiomegaly. (b) Contrast-enhanced pulmonary CT arteriogram (1.25-mm collimation) obtained at the level of the bronchus intermedius shows eccentric thrombus along the medial margin of the narrowed right interlobar pulmonary artery (arrows). (c) Perfusion lung scan (right posterior oblique view) obtained after administration of Tc-99m macroaggregated albumin shows multisegmental defects, which did not match the findings seen on a ventilation lung scan obtained with Tc-99m Technegas (not shown). (d) Pulmonary arteriogram shows abrupt cutoff in rounded fashion (pouching defect) of the lower lobar arteries (arrow). (e) Photograph of the thromboembolectomy specimen shows organized emboli filling the enlarged central pulmonary arteries. Note how the central thrombus is organized in concave fashion, creating a pouching defect (arrows).
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Figure 4a. Chronic pulmonary embolism in a 62-year-old woman. (a) Unenhanced thin-section (1-mm collimation) CT scan obtained at the level of the right inferior pulmonary vein shows calcified thrombi (arrows) in the right middle and lower lobe arteries. (b) CT scan (lung window) obtained at the level of the basal portion of the left lung shows mosaic areas of hypoperfusion (large arrows). Note also the nodular branching structure (small arrow), a finding that suggests bronchiolitis.
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Figure 4b. Chronic pulmonary embolism in a 62-year-old woman. (a) Unenhanced thin-section (1-mm collimation) CT scan obtained at the level of the right inferior pulmonary vein shows calcified thrombi (arrows) in the right middle and lower lobe arteries. (b) CT scan (lung window) obtained at the level of the basal portion of the left lung shows mosaic areas of hypoperfusion (large arrows). Note also the nodular branching structure (small arrow), a finding that suggests bronchiolitis.
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Nonthrombotic Pulmonary Embolism
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Septic Pulmonary Embolism
When fragments of thrombus include micro-organisms, septic embolism can develop. These organisms are typically bacteria or, less commonly, fungi or parasites (44). Common predisposing factors include tricuspid valve endocarditis with or without drug addiction, alcoholism, skin infection, and immunologic deficiencies (particularly lymphoma) (45). Septic embolism is sometimes detected in patients who have infected indwelling catheters or pacemaker wires (46).
Radiographs typically show peripheral, poorly marginated lung nodules bilaterally that often demonstrate cavitary changes (47). These nodules vary greatly in size, which reflects repeated episodes of embolic shower (Fig 5a) (3). Septic embolism is often complicated by empyema (47,48).
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Figure 5a. Septic pulmonary embolism in a 28-year-old intravenous drug abuser with human immunodeficiency viral infection. Repeated blood cultures disclosed a positive culture for Nocardia. (a) Radiograph shows multiple cavitary nodules throughout both lungs. (b) CT scan (10-mm collimation) obtained at the level of the azygos arch demonstrates the feeding vessel sign (vessel leading directly to the nodule) in several nodules (arrows).
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Figure 5b. Septic pulmonary embolism in a 28-year-old intravenous drug abuser with human immunodeficiency viral infection. Repeated blood cultures disclosed a positive culture for Nocardia. (a) Radiograph shows multiple cavitary nodules throughout both lungs. (b) CT scan (10-mm collimation) obtained at the level of the azygos arch demonstrates the feeding vessel sign (vessel leading directly to the nodule) in several nodules (arrows).
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Characteristic CT findings in septic pulmonary embolism consist of discrete nodules with varying degrees of cavitation and subpleural, wedge-shaped heterogeneous areas of increased attenuation with rimlike peripheral enhancement. The nodules tend to be most numerous in the lower lobes. In many cases, a vessel can be seen leading directly to the nodules ("feeding vessel sign") (Fig 5b) (3,46,48).
Hydatid Embolism
Pulmonary embolism is a rare complication of cardiac or hepatic echinococcosis, with only a few cases reported in the English medical literature. Although the liver (75% of cases) and lungs (15%) are the most common sites of infestation, Echinococcus granulosus can affect any part of the body. The sources of pulmonary embolism are either (a) hepatic or abdominal cystic lesions that rupture into the hepatic veins or the inferior vena cava or (b) ruptured cystic lesions in the right cardiac chamber. Typically, the obstruction results from vesicles or daughter cysts; there are no associated blood clots or local thrombosis (49). Cases of hydatid pulmonary embolism are classified into three groups according to clinical manifestation: (a) acute fatal cases, (b) subacute pulmonary hypertension cases resulting in death within 1 year of diagnosis, and (c) chronic pulmonary hypertension cases. The majority of cases appear to follow a course of prolonged pulmonary hypertension punctuated by acute embolic episodes (50). Both helical CT and MR angiography have been reported to demonstrate occlusion of the pulmonary arteries and their branches by cystic lesions (Fig 6) (49).
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Figure 6a. Pulmonary hydatid embolism caused by rupture of a mediastinal hydatid cyst into the right pulmonary artery in a 22-year-old woman. The patient underwent pulmonary transplantation due to severe pulmonary arterial hypertension. (a) CT scan (5-mm collimation, lung window) obtained at the level of the left inferior pulmonary vein shows enlarged or engorged branches of the pulmonary arteries in the bilateral lower lung zones (arrows). (b) Photomicrograph (original magnification, x12; elastic stain) of the pathologic specimen shows a multilayered membrane of a hydatid cyst filling the pulmonary artery lumen.
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Figure 6b. Pulmonary hydatid embolism caused by rupture of a mediastinal hydatid cyst into the right pulmonary artery in a 22-year-old woman. The patient underwent pulmonary transplantation due to severe pulmonary arterial hypertension. (a) CT scan (5-mm collimation, lung window) obtained at the level of the left inferior pulmonary vein shows enlarged or engorged branches of the pulmonary arteries in the bilateral lower lung zones (arrows). (b) Photomicrograph (original magnification, x12; elastic stain) of the pathologic specimen shows a multilayered membrane of a hydatid cyst filling the pulmonary artery lumen.
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Fat Embolism
Fat embolism is an infrequent complication of long bone fracture, occurring in 1%–3% of patients with simple tibial or femoral fractures but in up to 20% of individuals with more severe trauma (51,52). Less common causes include hemoglobinopathy, major burns, pancreatitis, overwhelming infection, tumors, blood transfusion, and liposuction (51,53). The mechanisms are not completely understood but presumably are twofold. The first mechanism is the production of free fatty acids, which initiates a toxic reaction in the endothelium. The process is further complicated by the accumulation of neutrophils and other inflammatory cells, which causes damage to the vasculature (53,54). The second mechanism is the mechanical obstruction of the pulmonary vasculature by fat globules and aggregates of red blood cells and platelets (55).
A combination of pulmonary, cerebral, and cutaneous symptoms typically occur within 12–24 hours of the traumatic event (56,57). The time lapse between the traumatic event and radiographic abnormalities is usually 1–2 days, which allows differentiation from traumatic contusion (3). The radiographic findings resemble those in acute respiratory distress syndrome from any cause and consist of widespread homogeneous and heterogeneous areas of increased opacity (Fig 7) (54). A normal heart size and the absence of other features of cardiogenic edema including septal lines, pleural effusion, and pulmonary venous hypertension allow differentiation from cardiogenic pulmonary edema (47).
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Figure 7a. Fat embolism in a 58-year-old woman who presented with sudden dyspnea. The patient had undergone intramuscular injection of some fatty materials into the buttock several days earlier. (a) Radiograph shows bilateral ground-glass areas of increased opacity. (b) Thin-section (1-mm collimation) CT scan obtained at the level of the aortic arch shows widespread patchy ground-glass attenuation and consolidation. A follow-up radiograph obtained 10 days later (not shown) revealed complete resolution of the ground-glass patterns. (Case courtesy of Jin Sung Lee, MD, Asan Medical Center, Seoul, Korea.)
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Figure 7b. Fat embolism in a 58-year-old woman who presented with sudden dyspnea. The patient had undergone intramuscular injection of some fatty materials into the buttock several days earlier. (a) Radiograph shows bilateral ground-glass areas of increased opacity. (b) Thin-section (1-mm collimation) CT scan obtained at the level of the aortic arch shows widespread patchy ground-glass attenuation and consolidation. A follow-up radiograph obtained 10 days later (not shown) revealed complete resolution of the ground-glass patterns. (Case courtesy of Jin Sung Lee, MD, Asan Medical Center, Seoul, Korea.)
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Amniotic Fluid Embolism
Amniotic fluid embolism is a highly fatal complication of pregnancy, with an 80% maternal mortality rate (58). This condition occurs when amniotic fluid is forced into the bloodstream through small tears in the uterine veins during normal labor (59). However, in some cases, the placenta is disrupted by surgery or trauma (59,60).
Dyspnea, cyanosis, and shock that are abrupt in onset classically progress rapidly to cardiopulmonary collapse and severe pulmonary edema (59,61). In about 70% of patients, these symptoms begin during spontaneous labor; in the remaining 30% (10% with spontaneous delivery and 20% with cesarean section), they occur after parturition (3). Central nervous system irritability (convulsion or hyperflexia) is commonly present (61).
The chief radiographic abnormalities are diffuse bilateral heterogeneous and homogeneous areas of increased opacity, which are indistinguishable from acute pulmonary edema from other causes (Fig 8) (51,62). The principal differential diagnoses include diffuse pulmonary hemorrhage and aspiration pneumonia (3).
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Figure 8a. Amniotic fluid embolism in a 40-year-old woman. The patient experienced sudden respiratory distress shortly after giving birth by cesarean section. (a) Radiograph shows bilateral widespread airspace consolidation. Endotracheal intubation was performed. (b) On a follow-up radiograph obtained 3 days later, the extent of the parenchymal areas of increased opacity has decreased. A chest tube was inserted into the right pleural space to relieve the right pleural effusion.
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Figure 8b. Amniotic fluid embolism in a 40-year-old woman. The patient experienced sudden respiratory distress shortly after giving birth by cesarean section. (a) Radiograph shows bilateral widespread airspace consolidation. Endotracheal intubation was performed. (b) On a follow-up radiograph obtained 3 days later, the extent of the parenchymal areas of increased opacity has decreased. A chest tube was inserted into the right pleural space to relieve the right pleural effusion.
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Tumor Embolism
Pulmonary intravascular tumor emboli are seen in up to 26% of autopsies (63) but are much less frequently identified prior to death. Common extrapulmonary malignancies that cause pulmonary tumor emboli include hepatocellular carcinoma, breast and renal carcinoma, stomach and prostate carcinoma, and choriocarcinoma (63). The radiologic findings are often minimal or nonspecific, making radiologic diagnosis difficult (64). Occasionally, focal or diffuse heterogeneous areas of increased opacity are seen at radiography, findings that may be interpreted as lymphangitic carcinomatosis (47). V-P lung scans may reveal multiple peripheral subsegmental perfusion defects (65). Tumor emboli that are large enough to cause death have rarely been reported (66).
Recently, "tree-in-bud" appearance has been described as a thin-section CT finding in pulmonary tumor embolism (64,67). There are two different pathogenic mechanisms involved in the production of tree-in-bud appearance at thin-section CT in patients with pulmonary tumor embolism. The first mechanism is filling of the centrilobular arteries with tumor cells themselves (Fig 9) (67). The second mechanism is thrombotic microangiopathy of pulmonary tumors, a distinct but rare form of tumor embolism that is seen in only 0.9%–3.3% of autopsies in cases of extrathoracic malignancies (64,68,69). At histopathologic analysis, thrombotic microangiopathy of pulmonary tumors is characterized by extensive fibrocellular intimal hyperplasia of small pulmonary arteries initiated by tumor microemboli (Fig 10) (68). Affected patients present with progressive dyspnea, cough, and signs of hypoxia and pulmonary hypertension (69).
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Figure 9a. Tumor embolism from cholangiocarcinoma in a 62-year-old man. (a) Thin-section (1.5-mm collimation) CT scan obtained at the level of the basal segmental bronchi shows a pleura-based, wedge-shaped area of high attenuation (large arrows) and numerous nodules, some of which demonstrate tree-in-bud appearance (small arrows). (b) Photomicrograph (original magnification, x12; hematoxylin-eosin [H-E] stain) of the biopsy specimen obtained at video-assisted thoracoscopic surgery demonstrates endovascular tumor emboli (thin arrow) surrounded by infarcted lung tissue (thick arrows). (Case courtesy of Eun-Young Kang, MD, Korea University Guro Hospital, Seoul, Korea.)
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Figure 9b. Tumor embolism from cholangiocarcinoma in a 62-year-old man. (a) Thin-section (1.5-mm collimation) CT scan obtained at the level of the basal segmental bronchi shows a pleura-based, wedge-shaped area of high attenuation (large arrows) and numerous nodules, some of which demonstrate tree-in-bud appearance (small arrows). (b) Photomicrograph (original magnification, x12; hematoxylin-eosin [H-E] stain) of the biopsy specimen obtained at video-assisted thoracoscopic surgery demonstrates endovascular tumor emboli (thin arrow) surrounded by infarcted lung tissue (thick arrows). (Case courtesy of Eun-Young Kang, MD, Korea University Guro Hospital, Seoul, Korea.)
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Figure 10a. Pulmonary tumor thrombotic microangiopathy caused by metastatic gastric carcinoma in a 57-year-old man. (a) Thin-section (1.5-mm collimation) CT scan obtained at the level of the left basal trunk shows multifocal tree-in-bud appearances (arrows) caused by tumor emboli. (b) Photograph of the autopsy specimen shows accentuated and enlarged centrilobular axial interstitium in the peripheral lung (arrows), a finding that corresponds to the tree-in-bud appearance seen at CT. (c) Photomicrograph (original magnification, x40; H-E stain) of an arteriole shows small nests of tumor cells (arrows). The vessel lumen is occluded mainly by lamellated fibrointimal proliferation that surrounds the tumor cell nests.
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Figure 10b. Pulmonary tumor thrombotic microangiopathy caused by metastatic gastric carcinoma in a 57-year-old man. (a) Thin-section (1.5-mm collimation) CT scan obtained at the level of the left basal trunk shows multifocal tree-in-bud appearances (arrows) caused by tumor emboli. (b) Photograph of the autopsy specimen shows accentuated and enlarged centrilobular axial interstitium in the peripheral lung (arrows), a finding that corresponds to the tree-in-bud appearance seen at CT. (c) Photomicrograph (original magnification, x40; H-E stain) of an arteriole shows small nests of tumor cells (arrows). The vessel lumen is occluded mainly by lamellated fibrointimal proliferation that surrounds the tumor cell nests.
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Figure 10c. Pulmonary tumor thrombotic microangiopathy caused by metastatic gastric carcinoma in a 57-year-old man. (a) Thin-section (1.5-mm collimation) CT scan obtained at the level of the left basal trunk shows multifocal tree-in-bud appearances (arrows) caused by tumor emboli. (b) Photograph of the autopsy specimen shows accentuated and enlarged centrilobular axial interstitium in the peripheral lung (arrows), a finding that corresponds to the tree-in-bud appearance seen at CT. (c) Photomicrograph (original magnification, x40; H-E stain) of an arteriole shows small nests of tumor cells (arrows). The vessel lumen is occluded mainly by lamellated fibrointimal proliferation that surrounds the tumor cell nests.
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Air Embolism
Iatrogenic causes of venous air embolism include transthoracic needle aspiration and biopsy, barotrauma caused by positive pressure ventilation, hemodialysis, and insertion of subclavian or central venous catheters (70). Small quantities of air can be found in the central veins in up to 23% of patients during contrast material administration for CT (71). The risk of death is affected by both the amount of air and the speed of introduction; the minimum lethal volume and injection rate in humans are about 300–500 mL and 100 mL/sec, respectively (71). Common clinical manifestations include sudden dyspnea, chest pain, hypotension, convulsion, and so on (70,71). Noniatrogenic air embolism sometimes occurs in scuba divers as a result of gas bubble formation in the blood, which occurs due to rapid reduction in the ambient pressure during a diver’s ascent (72).
Although radiographs may be normal, they may also show areas of hyperlucency in the heart, main pulmonary artery, or hepatic veins. Findings of focal pulmonary oligemia, pulmonary edema, or enlargement of the central pulmonary arteries or superior vena cava may be present (70). Small amounts of air may be seen in the systemic veins, right side of the heart, or main pulmonary arteries at CT (Fig 11) (73).
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Figure 11. Incidentally found air embolism in an asymptomatic 59-year-old man. Routine contrast-enhanced chest CT scan (5-mm collimation) shows two small air bubbles in the main pulmonary artery (arrows).
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Talc Embolism
Cellulose and talc granulomatosis are common among drug addicts (74) who grind up and intravenously inject amphetamines, methylphenidate, hydromorphone, or dextropropoxyphene that has been prepared as an oral medication (75). In individuals with talc granulomatosis, the intravascular foreign material and the associated granulomatous reaction in vessel walls cause tree-in-bud appearance (74). Materials responsible for this disorder are insoluble particles such as microcrystalline cellulose, talc, and corn starch, which are used as fillers in tablets taken orally. These substances become trapped in the pulmonary vasculature, causing thrombosis, inflammation, and, eventually, giant cell reaction (74).
Chest radiographic findings progress from initial widespread small nodules (76) to a large area of increased opacity that resembles the progressive massive fibrosis seen in patients with silicosis (Fig 12) (77). Findings of pulmonary hypertension may be present (78). Cellulose granulomatosis has been described as a rare vascular cause of tree-in-bud appearance at thin-section CT (Fig 13) (74).
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Figure 12a. Talc embolism in a 26-year-old woman. The patient had a 4-year history of heroin and methadone abuse. (a) Targeted view of the left lung from a chest radiograph shows widespread involvement of the lung by pinpoint micronodules. (b) CT scan (5-mm collimation, lung window) obtained at the level of the basal trunk shows extensive patchy areas of increased attenuation in both lungs. (c) Follow-up radiograph obtained 6 years later shows coalescent areas of increased opacity (progressive massive fibrosis) in the bilateral middle lung zones (arrows). Note also the emphysematous right upper lung zone. (d) Thin-section (1.5-mm collimation) CT scan (mediastinal window) obtained at the subcarinal level shows coalescent areas of increased attenuation (progressive massive fibrosis) posteriorly in both lungs. Note also the areas of high attenuation within the masses (arrow), a finding that suggests talc deposition.
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Figure 12b. Talc embolism in a 26-year-old woman. The patient had a 4-year history of heroin and methadone abuse. (a) Targeted view of the left lung from a chest radiograph shows widespread involvement of the lung by pinpoint micronodules. (b) CT scan (5-mm collimation, lung window) obtained at the level of the basal trunk shows extensive patchy areas of increased attenuation in both lungs. (c) Follow-up radiograph obtained 6 years later shows coalescent areas of increased opacity (progressive massive fibrosis) in the bilateral middle lung zones (arrows). Note also the emphysematous right upper lung zone. (d) Thin-section (1.5-mm collimation) CT scan (mediastinal window) obtained at the subcarinal level shows coalescent areas of increased attenuation (progressive massive fibrosis) posteriorly in both lungs. Note also the areas of high attenuation within the masses (arrow), a finding that suggests talc deposition.
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Figure 12c. Talc embolism in a 26-year-old woman. The patient had a 4-year history of heroin and methadone abuse. (a) Targeted view of the left lung from a chest radiograph shows widespread involvement of the lung by pinpoint micronodules. (b) CT scan (5-mm collimation, lung window) obtained at the level of the basal trunk shows extensive patchy areas of increased attenuation in both lungs. (c) Follow-up radiograph obtained 6 years later shows coalescent areas of increased opacity (progressive massive fibrosis) in the bilateral middle lung zones (arrows). Note also the emphysematous right upper lung zone. (d) Thin-section (1.5-mm collimation) CT scan (mediastinal window) obtained at the subcarinal level shows coalescent areas of increased attenuation (progressive massive fibrosis) posteriorly in both lungs. Note also the areas of high attenuation within the masses (arrow), a finding that suggests talc deposition.
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Figure 12d. Talc embolism in a 26-year-old woman. The patient had a 4-year history of heroin and methadone abuse. (a) Targeted view of the left lung from a chest radiograph shows widespread involvement of the lung by pinpoint micronodules. (b) CT scan (5-mm collimation, lung window) obtained at the level of the basal trunk shows extensive patchy areas of increased attenuation in both lungs. (c) Follow-up radiograph obtained 6 years later shows coalescent areas of increased opacity (progressive massive fibrosis) in the bilateral middle lung zones (arrows). Note also the emphysematous right upper lung zone. (d) Thin-section (1.5-mm collimation) CT scan (mediastinal window) obtained at the subcarinal level shows coalescent areas of increased attenuation (progressive massive fibrosis) posteriorly in both lungs. Note also the areas of high attenuation within the masses (arrow), a finding that suggests talc deposition.
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Figure 13a. Talc embolism in a 37-year-old male drug abuser. (a) Thin-section (1.5-mm collimation) CT scan obtained at the level of the left interlobar artery shows diffuse pulmonary involvement with ill-defined centrilobular small nodules (arrows). Note also the nodular branching structures (tree-in-bud appearance). (b) Photomicrograph (original magnification, x40; H-E stain) of the pathologic specimen shows necrotizing vasculitis at the center of the secondary pulmonary lobule (arrow).
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Figure 13b. Talc embolism in a 37-year-old male drug abuser. (a) Thin-section (1.5-mm collimation) CT scan obtained at the level of the left interlobar artery shows diffuse pulmonary involvement with ill-defined centrilobular small nodules (arrows). Note also the nodular branching structures (tree-in-bud appearance). (b) Photomicrograph (original magnification, x40; H-E stain) of the pathologic specimen shows necrotizing vasculitis at the center of the secondary pulmonary lobule (arrow).
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Iodinated Oil Embolism
It has been shown that the majority of patients with iodinated oil embolism have undergone lymphangiography (79). Most patients with iodinated oil embolism caused by lymphangiography are asymptomatic (47). Radiography performed immediately after the procedure demonstrates subtle fine nodular areas of increased opacity (47).
Iodinated oil embolism that occurs after transcatheter oil chemoembolization is an uncommon but important complication of treatment for hepatocellular carcinoma. Unlike patients with iodinated oil embolism caused by lymphangiography, these patients may have respiratory symptoms of cough, hemoptysis, and dyspnea. Radiography reveals diffuse bilateral pulmonary parenchymal infiltrates that appear within 2–5 days of chemoembolization for hepatocellular carcinoma (Fig 14) (80).
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Figure 14a. Iodinated oil embolism in a 45-year-old woman with sudden dyspnea. The patient had a large primary liver carcinoma containing arteriovenous shunting and had undergone transarterial hepatic chemoembolization with a mixture of adriamycin and iodinated oil (Lipiodol; Guerbet, Roissy, France) 1 day earlier. (a) Chest radiograph obtained 1 day after chemoembolization shows patchy areas of lung nodules and consolidation bilaterally. Note also the multifocal areas of iodinated oil uptake in the liver (arrows). (b) Thin-section (1-mm collimation) CT scan (lung window) obtained at the level of the inferior pulmonary vein shows multifocal patchy areas of ground-glass attenuation in both lungs. Several high-attenuation nodules are also noted (arrows). (c) Thin-section (1-mm collimation) CT scan (targeted mediastinal window) obtained at the same level as b shows nodules with calcific attenuation in the right lower lobe (arrows), a finding that suggests iodinated oil uptake in metastatic nodules.
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Figure 14b. Iodinated oil embolism in a 45-year-old woman with sudden dyspnea. The patient had a large primary liver carcinoma containing arteriovenous shunting and had undergone transarterial hepatic chemoembolization with a mixture of adriamycin and iodinated oil (Lipiodol; Guerbet, Roissy, France) 1 day earlier. (a) Chest radiograph obtained 1 day after chemoembolization shows patchy areas of lung nodules and consolidation bilaterally. Note also the multifocal areas of iodinated oil uptake in the liver (arrows). (b) Thin-section (1-mm collimation) CT scan (lung window) obtained at the level of the inferior pulmonary vein shows multifocal patchy areas of ground-glass attenuation in both lungs. Several high-attenuation nodules are also noted (arrows). (c) Thin-section (1-mm collimation) CT scan (targeted mediastinal window) obtained at the same level as b shows nodules with calcific attenuation in the right lower lobe (arrows), a finding that suggests iodinated oil uptake in metastatic nodules.
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Figure 14c. Iodinated oil embolism in a 45-year-old woman with sudden dyspnea. The patient had a large primary liver carcinoma containing arteriovenous shunting and had undergone transarterial hepatic chemoembolization with a mixture of adriamycin and iodinated oil (Lipiodol; Guerbet, Roissy, France) 1 day earlier. (a) Chest radiograph obtained 1 day after chemoembolization shows patchy areas of lung nodules and consolidation bilaterally. Note also the multifocal areas of iodinated oil uptake in the liver (arrows). (b) Thin-section (1-mm collimation) CT scan (lung window) obtained at the level of the inferior pulmonary vein shows multifocal patchy areas of ground-glass attenuation in both lungs. Several high-attenuation nodules are also noted (arrows). (c) Thin-section (1-mm collimation) CT scan (targeted mediastinal window) obtained at the same level as b shows nodules with calcific attenuation in the right lower lobe (arrows), a finding that suggests iodinated oil uptake in metastatic nodules.
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Metallic Mercury Embolism
Intravenous injection of mercury is uncommon, and only a few cases of accidental injection, attempted suicide, and iatrogenic injection have been described (81). Surprisingly, most of the individuals who have received intravenous injections of mercury experience only minor toxic effects (82), although death has been reported (83). In fact, many short-term symptoms can be attributed to the mechanical effect of mercury globules, which cause embolism of the pulmonary vasculature and infarction of the lung parenchyma (84).
Radiographs typically show multiple small metallic spherules diffusely scattered throughout both lungs. Recognition of metallic opacity in the heart, abdominal vessels, or extremities may permit differentiation from aspiration of metallic mercury (47). The radiographic abnormalities may be permanent or may resolve gradually (85). The prognosis for individuals with this condition is excellent (47).
Cement (Polymethylmethacrylate) Embolism
Although percutaneous vertebroplasty is regarded as a relatively safe procedure, there is a potential risk of pulmonary embolism via external vertebral venous plexuses. Symptomatic pulmonary embolism caused by acrylic cement is rare (86). Both radiography and CT may demonstrate tubular areas of increased opacity or attenuation outlining the pulmonary arteries (Figs 15, 16) (86). CT may also depict perivertebral leaks (Fig 16) (87).
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Figure 15. Cement embolism in a 29-year-old woman. The patient had recently undergone cyanoacrylate embolization for intracerebral arteriovenous malformation. Targeted view of the right lung from a chest radiograph shows widespread small pulmonary nodules with increased opacity, a finding that represents cement emboli.
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Figure 16a. Polymethylmethacrylate embolism following percutaneous vertebroplasty in a 64-year-old woman. (a) CT scan (7-mm collimation, mediastinal window) obtained at the level of the inferior portion of the left atrium shows radiopaque emboli in the segmental and subsegmental levels of the pulmonary arteries (arrows). (b) CT scan obtained at the level of the pelvic inlet shows tortuous paravertebral veins filled with polymethylmethacrylate (arrows). The vertebral body has been reinforced with this material. (Case courtesy of Joon Beom Seo, MD, Asan Medical Center, Seoul, Korea.)
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Abstract
LEARNING OBJECTIVES FOR TEST...
