June 2000, VOLUME 174

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June 2000, Volume 174, Number 6


Nonthrombotic Pulmonary Emboli

+ Affiliations:
1Department of Radiology, Duke University Medical Center, Box 3808, Erwin St., Durham, NC 27710.

2Present address: Department of Radiology, Fundacion Dr. “Enrique Rossi,” Arenales 2777, C P: 1425, Buenos Aires, Argentina.

3Department of Radiology, Hospital de Sant Pau, Universidad Autonoma de Barcelona, Sant Antoni M. Claret 167, 08025, Barcelona, Spain.

Citation: American Journal of Roentgenology. 2000;174: 1499-1508. 10.2214/ajr.174.6.1741499

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Thrombotic pulmonary embolism is such a significant and commonly considered entity that it has, appropriately, been the focus of most articles dealing with abnormal substances that find their way into pulmonary circulation. Nevertheless, the spectrum of nonthrombotic pulmonary emboli constitutes an interesting and clinically relevant topic of discussion. Not all the effects of the latter are mechanical as is typical with ordinary pulmonary embolism; therefore, the pathogenesis and presentation of these diseases are occasionally more complex and subject to continued speculation. We identify the clinical and radiographic features of nonthrombotic pulmonary emboli.

Septic Embolism
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Septic pulmonary emboli are commonly associated with tricuspid valve endocarditis (e.g., in IV drug users) [1] but are also detected in patients with infections from indwelling catheters and pacemaker wires, peripheral septic thrombophlebitis, and organ transplants [2]. Typically, patients present with fever, cough, and hemoptysis.

Chest radiographs reveal peripheral bilateral poorly marginated lung nodules that have a tendency to form cavities with moderately thick irregular walls (Figs. 1 and 2). Nodules generally range in size from 1 to 3 cm and may increase in number or change in appearance (size or degree of cavitation) from day to day [3]. Empyemas are frequently associated with these predominantly staphylococcal infections. CT may be better than radiography at revealing these lesions because it delineates the extent of disease and potential complications, such as extension into the pleural space [1]; however, chest radiographs are typically adequate for proper patient treatment. On CT, the most characteristic findings of septic embolism include scatered predominantly lower lobe discrete parenchymal nodules that show various stages of cavitation. Nodule-feeding vessels are found in 60-70% of patients [1, 3] (Fig. 3), and heterogeneous subpleural wedge-shaped opacities are identified in 70-75% of patients [3].

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Fig. 1. —34-year-old male IV drug user with septic embolism, shortness of breath, and fever. Posteroanterior chest radiograph shows peripheral bilateral poorly marginated nodules.

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Fig. 2. —33-year-old female IV drug user with septic embolism and fever. Posteroanterior chest radiograph shows bilateral peripheral thick- and irregular-walled cavitary nodules.

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Fig. 3. —56-year-old man with septic embolism and deep venous thrombosis of lower extremities. Patient presented with dyspnea, fever, and chills. CT scan (lung window) shows bilateral peripheral cavitary nodules and confirmed right-sided pleural effusion.

Typically, diagnosis is suggested by radiographic findings, predisposing background or illness, and clinical evidence of infection. Antibiotic treatment is generally successful; however, occasionally the source of emboli must be surgically repaired.

Catheter Embolism
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Catheter emboli, complications of central venous catheterization, were first described in 1954 [4]. Catheter emboli usually develop when a physician attempts to withdraw a catheter through an introducing needle. The catheter catches on the needle and the distal portion is sheared off. The Seldinger technique has reduced the incidence of this problem. Spontaneous catheter breakage accounts for approximately 25% of catheter emboli [5]. Most catheter emboli are found in the basilic vein and the pulmonary arteries, with the remainder in the right heart, great veins, and peripheral aspect of the lungs [4].

Chest radiographs reveal a disconnected catheter fragment overlying an unexpected portion of the lung, mediastinum, or heart. Generally, the course of the catheter corresponds to the expected location of the pulmonary artery. Angiography or CT findings can confirm the position of the catheter (Fig. 4A,4B,4C,4D,4E).

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Fig. 4A. —57-year-old woman with catheter embolism and breast cancer. Patient had part of right subclavian venous line shear off when catheter was being removed. Posteroanterior chest radiograph shows right subclavian central venous catheter with tip in superior vena cava.

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Fig. 4B. —57-year-old woman with catheter embolism and breast cancer. Patient had part of right subclavian venous line shear off when catheter was being removed. Posteroanterior (B) and lateral (C) chest radiographs show catheter fragment (arrows) in posterior segment of right upper lobe.

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Fig. 4C. —57-year-old woman with catheter embolism and breast cancer. Patient had part of right subclavian venous line shear off when catheter was being removed. Posteroanterior (B) and lateral (C) chest radiographs show catheter fragment (arrows) in posterior segment of right upper lobe.

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Fig. 4D. —57-year-old woman with catheter embolism and breast cancer. Patient had part of right subclavian venous line shear off when catheter was being removed. CT scan (mediastinal window) reveals catheter fragment in right pulmonary artery.

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Fig. 4E. —57-year-old woman with catheter embolism and breast cancer. Patient had part of right subclavian venous line shear off when catheter was being removed. Pulmonary angiogram shows catheter fragment in right upper lobe pulmonary artery. Catheter was removed using 35-mm snare device.

Treatment with intravascular retrieval using snares is frequently successful.

Fat Embolism Syndrome
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The first clinical description of fat embolism syndrome appeared in 1873 [6, 7]. This embolism is an uncommon complication of longbone fractures, occurring in 1-20% of trauma patients [6,7,8]. A small number of patients without skeletal trauma have also presented with fat embolism syndrome; the etiology of disease in these patients includes hemoglobinopathy, severe burns, soft-tissue injuries, diabetes, pancreatitis, severe infection, neoplasms, osteomyelitis, blood transfusion, cardiopulmonary bypass, altitude decompression, suction lipectomy, and renal transplantation [6, 7].

The pathogenesis of fat embolism syndrome is not completely understood. One theory proposes that neutral triglycerides are transported to the lung and converted to free fatty acids that instigate a toxic reaction in the capillary endothelium [7, 9]. This injury is compounded by the accumulation of inflammatory cells, particularly neutrophils, that cause further damage to the vasculature. Fat emboli also obstruct vessels, but this mechanical effect is thought to be less important in the lungs [9]. Fat emboli circulating through a patent foramen ovale, atrial septal defect, or intapulmonary shunt bypass the lungs and appear in the microvasculature of the brain and other organs, in which vascular obstruction may be more critical.

Clinically, fat embolism syndrome appears as a combination of pulmonary, cerebral, and cutaneous symptoms that may occur immediately or may develop up to 3 days after trauma [6, 10]. This delay is probably related to continuous embolization from the fracture site and the time required to convert fat globules into free fatty acids. Pulmonary manifestations include dyspnea, tachypnea, hyperpnea, and hemoptysis. Patients also present with tachycardia, chest pain, cyanosis, and fever [6, 7, 9, 10]. Neurologic symptoms occur in up to 85% of patients and include confusion, restlessness, stupor, and coma. Neurologic abnormalities may be the first indication of fat embolism; however, they are generally reversible [9]. Dermatologic features occur in 20-50% of patients and include petechiae of the skin and mucous membranes, particularly in the anterior thorax, anterior axillary folds, head, and neck [7]. Skin findings coincide with the onset of neurologic symptoms and generally resolve in 5-7 days [6]. The anterior distribution of petechiae is probably caused by the differential streaming of fat globules to the upper aorta and its more ventral branches [7].

Chest radiographic abnormalities usually appear 1-2 days after trauma and resolve within 1 week. Typically, patients with fat embolism syndrome develop bilateral homogeneous and heterogeneous opacities that resemble those of pulmonary edema or acute respiratory distress syndrome [6, 9] (Fig. 5A,5B,5C). Differentiation from cardiogenic edema can be determined by identifying a normal heart size and lack of vascular redistribution. Pleural effusions are uncommon. Fat embolism syndrome should be considered when patients have suggestive chest radiographic findings, a history of trauma 1-3 days before their present complaints, and appropriate physical signs and symptoms; however, fat in the conjunctivae and retinal infarcts may be suggestive of fat embolism syndrome. Fat in the urine, serum, or sputum does not have a high enough specificity or sensitivity on which to base the diagnosis of fat embolism syndrome [6].

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Fig. 5A. —34-year-old man with fat embolism and many injuries from motor vehicle collision. Patient experienced new respiratory problems 72 hr later. Anteroposterior radiograph of right femur reveals transverse fracture.

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Fig. 5B. —34-year-old man with fat embolism and many injuries from motor vehicle collision. Patient experienced new respiratory problems 72 hr later. Anteroposterior chest radiographs obtained 24 (B) and 72 hr (C) after A show increase in diffuse heterogeneous opacities in both lungs, consistent with edema caused by fat embolism.

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Fig. 5C. —34-year-old man with fat embolism and many injuries from motor vehicle collision. Patient experienced new respiratory problems 72 hr later. Anteroposterior chest radiographs obtained 24 (B) and 72 hr (C) after A show increase in diffuse heterogeneous opacities in both lungs, consistent with edema caused by fat embolism.

Supportive therapy usually results in recovery. Early surgical correction of fractures may reduce the incidence of fat embolism syndrome by decreasing tissue pressure and halting fat globule release [6].

Venous Air Embolism
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Venous air embolism is a well-known complication of thoracic trauma, surgery, and a variety of diagnostic and therapeutic procedures [11]. These emboli have been reported after transthoracic needle aspiration and biopsy, penetrating injuries to the lung, barotrauma caused by positive pressure ventilation, and hemodialysis; and in patients with asthma, neonates with respiratory distress, and scuba divers [12, 13]. Small amounts of air can be identified in the larger systemic intrathoracic veins in 23% of patients undergoing IV injection of contrast material for CT and in 1/47-1/3000 patients after the insertion of subclavian or central venous catheters [14] (Fig. 6). The amount and speed of air introduction, body position, and general clinical health influence the risk of death from venous air embolism [15]. In humans, the lethal volume of air is usually between 300 and 500 ml injected at a rate of 100 ml/sec [14]. Large volumes of rapidly infused air are most likely to cause major hemodynamic compromise [14]; however, injections of air in amounts as small as 100 ml have caused death [16]. The major effect of venous air embolism is the obstruction of the right ventricular pulmonary outflow tract or obstruction of the pulmonary arterioles by a mixture of air bubbles and fibrin clots formed in the heart. The result in either situation is cardiovascular dysfunction and failure [14]. Interstitial and alveolar edema (caused by high regional pressures) may also occur in unobstructed areas of the pulmonary circulation.

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Fig. 6. —40-year-old asymptomatic man with incidental air embolism. CT scan (mediastinal window) shows air in left brachiocephalic vein (arrow) after IV contrast injection for contrast-enhanced chest CT.

The clinical manifestations of venous air embolism are variable and nonspecific. Typically, patients experience the sudden onset of air hunger, dyspnea, cough, dizziness, chest pain, and a feeling of impending death [6, 11, 14]. Tachycardia, tachypnea, and hypotension are frequently discovered on physical examination, and occasionally, a relatively specific drumlike or “mill wheel” heart murmur is heard [6, 11, 14, 17]. A gasp reflex consisting of a short cough followed by brief expiration and several seconds of forced inspiration may be observed after IV infusion of air. Neurologic symptoms such as altered mental status, convulsions, and coma occur in 42% of patients [14]. Additional symptoms include increased central venous or pulmonary artery pressure, signs of ischemia or cor pulmonale on electrocardiography, and decreased end tidal CO2 fraction [11].

Chest radiographic findings of venous air embolism include normal findings; radiolucency (air) in the main pulmonary artery, heart (Fig. 7), and hepatic veins; focal pulmonary oligemia; pulmonary edema; enlarged central pulmonary arteries; dilatation of the superior vena cava; and subsegmental atelectasis [11]. Air in the distal main pulmonary artery may appear in a characteristic bell shape [11] (Fig. 8). Air in the more distal pulmonary vessels is rarely detected on chest radiographs. Chest CT may reveal small amounts of air in the axillary, subclavian, internal jugular, or brachiocephalic veins; superior vena cava; right heart; or main pulmonary arteries [18]. Diminished pulmonary vascularity or focal oligemia may be more frequent in the upper lobes.

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Fig. 7. —48-year-old man with air embolism and trauma to right chest, causing communication between large bronchus and adjacent pulmonary vein. Posteroanterior chest radiograph reveals radiolucency representing air in heart. Patient died soon after scanning.

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Fig. 8. —32-year-old man with air embolism that disconnected patient's central venous line. Anteroposterior chest radiograph shows bell- or coned-shaped radiolucency (arrow) in main pulmonary artery. Hyperlucent upper lobes result from oligemia caused by obstruction of pulmonary artery by air emboli. (Reprinted with permission from [11])

The diagnosis of venous air embolism is generally suspected when an appropriate clinical situation is coupled with consistent physical examination features and typical radiographic findings.

The treatment of venous air embolism is initially directed at restoring cardiopulmonary circulation and promoting reabsorption of intravascular air. Patients with suspected venous air embolism should be placed in a left lateral decubitus head-down position because it causes right-sided cardiac air bubbles to rise to the periphery of the right atrium and out of the blood flow through the right heart. Occasionally, intraoperative needle aspiration is performed to relieve large air bubbles. Oxygen should be administered because it creates a favorable environment for decreasing the partial pressure of nitrogen in the air bubbles, thus reducing their size.

Amniotic Fluid Embolism
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Amniotic fluid emboli were first described in 1926. In 1954, after the autopsy descriptions of eight women who had amniotic fluid debris (e.g., squamous cells and mucin) in their pulmonary arteries were published, amniotic fluid embolism became widely recognized as a cause of postpartum death [6, 19]. Amniotic emboli are a rare phenomenon, occurring in 1/8000-1/80,000 pregnancies; however, the emboli result in high maternal and fetal mortality rates, 80% and 40%, respectively [19,20,21]. Amniotic fluid embolism ranks third in incidence of non-abortion-related maternal mortality during labor (after pulmonary embolism and hypertension) [22]. Risk factors associated with the development of amniotic fluid emboli include advanced maternal age, multiparity, prolonged gestation, intrauterine demise, use of uterine stimulants, large fetal size, premature rupture of membranes, and meconium staining of the amniotic fluid [23]. Furthermore, amniotic fluid emboli have been associated with first-trimester curettage abortion [6]; second-trimester abortions by hysterotomy or prostaglandin, saline and urea injections [6, 24]; blunt abdominal trauma [24]; amniocentesis; hysterectomy; and cesarean delivery [6]. Most amniotic fluid emboli develop during the first stage of labor [25], but delayed symptoms can occur up to 48 hr after delivery [19]. Uterine contractions during normal labor force amniotic fluid into the maternal venous circulation through small tears in the lower uterine segment or high endocervical canal [23]. Aside from normal labor, some amniotic fluid emboli occur during surgical or traumatic events that disrupt the placenta [23, 26].

The pathophysiology of amniotic fluid emboli remains unclear. Two main theories have been postulated [21]. The conventional explanation states that particulate matter such as fetal squamous cells, lanugo, and meconium contained in the amniotic fluid produce pulmonary vascular obstructions that lead to pulmonary hypertension, right- and left-sided heart failure, hypotension, and death [21, 24]. However, current evidence suggests that a mechanical origin is less likely than an immunologic reaction [19, 24]. In this model, pulmonary vasospasm causes a physiologic pulmonary artery obstruction as a reaction to abnormal substances (e.g., leukotrienes and metabolites of arachnoid acid such as prostaglandins) in the amniotic fluid [19]. Subsequent severe pulmonary hypertension and marked hypoxia result in the death of 50% of patients within the first hour [21, 24, 25]. Most deaths occur within the first 2 hr of the onset of symptoms [25]. Survivors display a mild to moderate increase in mean pulmonary arterial pressure, a variable increase in central venous pressure, and a high pulmonary capillary wedge pressure caused by acute left-sided ventricular failure [21].

The classic clinical presentation of amniotic fluid embolism is that of abrupt dyspnea, cyanosis, and shock, followed (within minutes) by cardiorespiratory arrest and severe pulmonary edema, which occur in 70% of patients [19, 23, 24]. Some patients present with an anaphylactic reaction caused by a hypersensitivity to the leukotrienes and arachnoid metabolites present in amniotic fluid [26]. Central nervous system irritability that produces convulsions is typical. Additionally, 40% of patients suffer a consumptive coagulopathy (e.g., disseminated intravascular coagulation) [21]. This latter effect may be explained by the role of amniotic fluid in initiating fibrinogen consumption and in releasing tissue activators of the fibrinolytic system [21, 24]. Excessive bleeding caused by the consumptive coagulopathy may complicate the clinical situation but can usually be treated successfully.

In patients who live long enough to undergo chest radiography, pulmonary edema or acute respiratory distress syndrome is most commonly revealed [6] (Fig. 9). Chest radiographs reveal diffuse bilateral heterogeneous and homogeneous opacities.

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Fig. 9. —33-year-old woman with amniotic fluid embolism. Patient was not responsive to induction of labor and proceeded to cesarean delivery. While uterus was being sutured, patient had tonic-clonic seizure followed by cardiac arrest. Supportive measures were instituted, but patient died 3 weeks later. Anteroposterior chest radiograph obtained shortly after cesarean delivery reveals mild cardiomegaly and bilateral lung opacities that are denser on left side. Findings were attributed to asymmetric pulmonary edema caused by presumed amniotic fluid embolism.

The clinical diagnosis of amniotic fluid embolism relies heavily on the patient's risk factors and presentation. At autopsy, fetal squamous cells, mucin, hair, and meconium are revealed in the pulmonary vasculature [21, 23].

Treatment is supportive, including maintenance of oxygenation, cardiac output, and blood pressure. Bleeding from disseminated intravascular coagulopathy is usually self-limited but can be treated with transfusions [6, 19, 21].

Tumor Embolism
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Embolism of tumor cells from a distant primary neoplasm to the pulmonary vasculature was first described in 1897 [6, 27]. The incidence of tumor emboli is difficult to establish, but autopsy series reveal a range between 2.4% and 26% of patients [28]. Common sources of tumor emboli include liver, breast, stomach, renal, and prostatic cancers and choriocarcinoma [27, 28]. Pulmonary involvement includes occlusion of the main pulmonary artery by a large amount of tumor material, microscopic arteriolar emboli, diffuse alveolar septal capillary involvement, lymphangitic carcinomatosis, or a combination of these entities [6, 27, 29].

Clinically, the most common symptom of patients with tumor emboli is dyspnea that slowly develops over days or weeks (reported in as many as 70% of patients) [6, 27]. Pleuritic chest pain [6, 29], cough [6], hemoptysis [6, 27, 29], fatigue, and weight loss [27] are also seen. Physical examination typically reveals signs of pulmonary hypertension and right-sided ventricular overload [6, 27, 29].

Chest radiographs usually reveal normal findings, but occasional, focal or diffuse heterogeneous opacities are observed, which may be interpreted as lymphangitic carcinomatosis, especially in patients with known cancer [6, 27]. Cardiac enlargement and prominent pulmonary arteries are infrequent findings despite the elevation of pulmonary artery pressure [27]. CT may reveal dilated and beaded peripheral pulmonary arteries. Additionally, bilateral peripheral wedge-shaped opacities, suggestive of pulmonary infarcts, have also been reported [30, 31] (Fig. 10). Radionuclide perfusion scans may reveal small peripheral subsegmental mottled perfusion defects, whereas ventilation scans are usually normal [32] (Fig. 11A,11B). Pulmonary angiography is usually unrevealing but may show the delayed filling of the segmental arteries, pruning and tortuosity of the third- to fifth-order vessels, and occasional subsegmental filling [6, 33].

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Fig. 10. —48-year-old woman with tumor embolism and history of stage IIIB carcinoma of uterine cervix. Patient presented with increasing dyspnea on exertion, cough, and occasional hemoptysis. CT scan (lung window) shows bilateral peripheral pulmonary opacities, some wedge-shaped, suggesting pulmonary infarcts. Autopsy confirmed multiple tumor emboli in pulmonary circulation. (Courtesy of Haramati LB, Bronx, NY)

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Fig. 11A. —70-year-old woman with tumor embolism and adenocarcinoma of unknown primary source. Patient presented with acute dyspnea and shortness of breath. Anteroposterior chest radiograph shows mild cardiomegaly and normal lungs.

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Fig. 11B. —70-year-old woman with tumor embolism and adenocarcinoma of unknown primary source. Patient presented with acute dyspnea and shortness of breath. 99mTc macroaggregated albumin radionuclide perfusion scan reveals numerous peripheral wedge-shaped perfusion defects, characteristic of tumor emboli. Autopsy confirmed tumor emboli in pulmonary circulation. LPO = left posterior oblique, POST = posterior, RPO = right posterior oblique, RAO = right anterior oblique, ANT = anterior, LAO = left anterior oblique.

Diagnosis is usually made at autopsy; however, tumor embolism is occasionally confirmed with positive cytology findings in aspirated pulmonary arteriolar blood [6].

Talc Embolism
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Many substances, such as magnesium trisilicate (talc), starch, and cellulose, are used as fillers in drug manufacturing [34]. Some of these drugs (prepared as oral medications) such as amphetamines, methylphenidate, hydromorphone, and dextropropoxyphene are ground by drug users, mixed in liquid, and injected IV [35]. In this way, talc particles reach small pulmonary arterioles and capillaries where a foreign body giant cell granulomatous reaction occurs. Confluence of the granulomas and subsequent fibrosis and distortion of lung architecture, especially in the upper lobes, may follow. Pulmonary hypertension may develop as a result of chronic lung changes [36].

Most patients with talc emboli are asymptomatic; however, dyspnea and persistent cough occur with severe talc exposure. Clinical features appear to be dose-related and may progress even after stopping drug injections [36].

Initially, chest radiographs reveal several small (1 mm in diameter) nodular and reticular opacities throughout the lungs [36] (Fig. 12A,12B). Later, homogeneous upper lobe opacities resembling progressive massive fibrosis may be identified. Large pulmonary arteries and a large right heart may be observed in patients with pulmonary hypertension [37]. Lymphadenopathy is rare.

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Fig. 12A. —26-year-old female drug user with talc embolism. Patient had injected dissolved methylphenidate hydrochloride tablets IV and presented with long-standing pulmonary hypertension. Posteroanterior chest radiograph shows fine reticular opacities in lower lobes and large central pulmonary arteries.

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Fig. 12B. —26-year-old female drug user with talc embolism. Patient had injected dissolved methylphenidate hydrochloride tablets IV and presented with long-standing pulmonary hypertension. Coned-down radiograph of left lower lobe shows fine reticular pattern.

Mercury Embolism
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Pulmonary emboli caused by the accidental or intentional IV injection of metallic mercury is rare [38]. Clinical manifestations include dyspnea, cough, and mild hypoxia, which develop shortly after injection [39]. Pulmonary function testing may show restricted ventilation and reduced diffusing capacity [39]. Mercury levels in the blood and urine are usually elevated, but there is no correlation between mercury levels and signs and symptoms of intoxication [38, 40]. Renal damage can also occur, but the resulting proteinuria and pyuria are transient [40].

Chest radiographic findings are striking and should immediately suggest the diagnosis of mercury emboli. Multiple small metallic spherules diffusely distributed throughout the lungs, or occasionally restricted to one or more dependent areas, are most common [38]. The opacities may be scattered, may be of different size, or may appear as beaded chains following the course of the pulmonary arteries, simulating the appearance of an angiogram [38, 41] (Fig. 13A). Metallic mercury may also be identified in the heart and coronary arteries [38]. Abnormal findings on chest radiographs may gradually resolve or may remain permanently [38]. Aspiration of metallic mercury is the main condition requiring differentiation from mercury embolism [38, 40, 41]. Aspirated mercury produces predominately lower lobe linear rather than nodular opacities [42]. Radionuclide ventilation-perfusion scans with 99mTc-labelled macroaggregate albumin and 81Kr can differentiate aspirated intrabronchial mercury from pulmonary artery mercury emboli [40]. If intracardiac, abdominal vessel, or extremity subcutaneous tissue mercury is observed, then mercury embolization, not aspiration, is responsible (Fig. 13B).

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Fig. 13A. —31-year-old man with mercury embolism. Patient injected mercury IV. Posteroanterior chest radiograph shows multiple fine round metallic opacities in both lungs. In medial right lung, round opacities line up in direction of right lower lobe pulmonary artery.

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Fig. 13B. —31-year-old man with mercury embolism. Patient injected mercury IV. Anteroposterior abdominal radiograph with patient supine shows multiple metallic opacities in liver, kidneys, ureters, and bladder.

The prognosis for patients with mercury emboli is good. After several weeks, symptoms and functional impairments will diminish [39].

Iodinated Oil Embolism
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Iodinated oily emboli are almost always caused by lymphangiography performed in patients with lymphatic obstruction [43]. In one study, 44 of 80 such patients developed this complication [44]. Occlusion of the flow of lymph presumedly causes contrast material to enter systemic veins. Ultimately, the contrast material enters the pulmonary circulation, where lipid and oil droplets are widely distributed [45]. Clearance of contrast material into the interstitial and occasionally the alveolar spaces occurs over several days.

Although fever may develop within 2 days of lymphangiography, most patients with iodinated contrast emboli are asymptomatic. Rarely, cough, dyspnea, and hypotension occur.

Chest radiographs reveal subtle fine nodular opacities immediately after lymphangiography (Fig. 14). As resolution occurs, the pattern becomes more reticular and may last for several weeks [43, 44].

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Fig. 14. —53-year-old man with iodinated contrast embolism. After lymphangiography, patient complained of shortness of breath. Coned-down radiograph of left upper lobe shows fine diffuse reticulonodular opacities. Contrast material is also present in left supraclavicular lymph nodes.

Cotton Embolism
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Cotton emboli were first described in 1949 [46]. Cotton emboli occur when IV drug users inject narcotics through cotton swabs and fibers enter systemic venous circulation. Additionally, these emboli can occur when cotton fibers remain on angiographic guidewires or catheters after they have been wiped with moist cotton gauze [46]. In experimental animal studies, cotton fibers incite a granulomatous reaction in the wall of the pulmonary artery. This reaction occludes the artery and causes a disruption of the vessel wall, with passage of the cotton fibers into the alveoli and pulmonary interstitium [47].

Chest radiographs usually show normal findings, but inflammatory reaction, granulomatous changes, or both may produce poorly marginated homogeneous opacities in both lungs (Fig. 15).

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Fig. 15. —22-year-old female IV drug user with cotton embolism and shortness of breath. Patient typically used cotton balls to clean her skin and inserted needle through cotton while injecting narcotics. Posteroanterior chest radiograph reveals multiple poorly marginated hazy and homogeneous opacities in both lungs. Open lung biopsy results revealed chronic inflammatory reaction and refractile cotton fibers.

Hydatid Embolism
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Hydatid disease is a tapeworm parasitosis caused by the larval stage of Echinococcus granulosus [48]. In the United States, fewer than 100 cases are identified annually. Although these lesions are reported in almost all organs, the liver and lungs are most commonly involved [49]. Hydatid pulmonary emboli are caused by the direct passage of hydatid material (vesicles, daughter cysts, scolises) through pulmonary vessels. Hydatid pulmonary emboli have three clinical presentations: massive embolization followed by sudden death, pulmonary hypertension followed by death within 1 year, or a protracted course of pulmonary hypertension [48].

Clinical manifestations include chest pain, cough, exertional dyspnea, hemoptysis, and rare anaphylactic reactions.

Chest radiographs are usually not helpful because they do not reveal intravascular parasites; however, radiographic findings may suggest the diagnosis of pulmonary infection by showing lung parenchymal hydatid cysts [50]. CT findings include pulmonary artery enlargement resulting from intravascular hydatid material (Fig. 16A,16B). Pulmonary angiography reveals segmental or lobar perfusion defects caused by occlusion of the large pulmonary arteries [48].

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Fig. 16A. —22-year-old woman with hydatid embolism and history of pulmonary hydatid disease. Patient presented with 6-month history of dyspnea on exertion and hemoptysis. Contrast-enhanced CT scan (mediastinal window) reveals hypodense material in lower lobe pulmonary arteries. (Reprinted with permission from [48])

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Fig. 16B. —22-year-old woman with hydatid embolism and history of pulmonary hydatid disease. Patient presented with 6-month history of dyspnea on exertion and hemoptysis. Contrast-enhanced CT scan (lung window) reveals marked dilatation of pulmonary arteries resulting from intravascular embolized material.

Serum immunoelectrophoresis is the most reliable laboratory test for hydatidosis. The prognosis of patients with hydatid embolism is poor, and lung transplantation is the treatment of choice in selected cases [48].

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Nonthrombotic pulmonary emboli can be caused by a wide range of substances. Radiologic diagnosis is important because clinical findings are often nonspecific. Although many radiologic manifestations exist, findings are often characteristic and enable a confident diagnosis. Knowledge of nonthrombotic pulmonary emboli and awareness of their radiologic findings is essential in suggesting the correct diagnosis and hastening appropriate treatment.

Address correspondence to P. C. Goodman.

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