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Computed tomography of the normal aorta and thoracic aneurysms
Computed
Tomography Thoracic
of the Normal Aneurysms
By Harold V. Posniak, Terrence
S
ANATOMY
The ascending aorta is subdivided into the aortic root, or aortic bulb, and the tubular segment. The aortic root comprises the three sinuses of Valsalva and extends from the aortic valve to the superior margin of the sinuses. The coronary arteries arise from the right and left sinuses. The tubular aorta extends from the aortic root to the origin of the innominate artery. Most of the ascending aorta is intrapericardial. Posteriorly the ascending aorta is related successively to the left atrium, the right pulmonary artery, and the right main bronchus. On its right is the superior vena cava and right atria1 appendage; on its left is the pulmonary trunk. The aortic arch extends from the origin of the innominate artery to the site of insertion of the ligamentum arteriosum. Several important structures lie within the concavity of the arch, including the bifurcation of the pulmonary trunk, the left main bronchus, and the left recurrent laryngeal nerve. Posteriorly and to the right are the trachea and esophagus. The descending aorta extends from the ligamentum arteriosum to the aortic hiatus in the diaphragm. The esophagus is on the right of the proximal and middle thirds of the descending .?6minarS in Roentgenolog~,
Vol XXIV,
NO 1 (January),
1989:
and
C. Demos, and Richard E. Marsan
INCE 1929, when dos Santos et al first described visualization of the aorta by means of a translumbar injection in an opaque medium,’ aortography has been accepted as the method of choice for the evaluation of suspected aortic disease. Despite the continual evolution of methods and equipment, there remains a small but significant risk for patients undergoing aortography even with the most careful technique in experienced hands.2-s CT has been used since the late 1970s in the investigation of aortic pathology. 6-14The major advantages of this technique include noninvasiveness, and the ability to demonstrate more of the aorta than just the contrast column. CT is more sensitive than plain radiographs and angiography for detecting intimal calcification and intraluminal thrombus. In addition, the periaortic structures are clearly demonstrated. NORMAL
Aorta
pp 7-2 1
aorta. More distally, the esophagus crosses the aorta anteriorly and is related to its left side. The ascending aorta measures approximately 5.0 cm in length, the arch 4.5 cm, and the descending aorta 20.0 cm. The diameter of the thoracic aorta is largest at the aortic root and gradually decreases distally.15 Aronberg et alI6 measured coronal diameters at several levels of the thoracic aorta. The average diameter of the aortic root was 3.6 cm, ascending aorta 1.O cm proximal to the arch 3.5 cm, proximal descending aorta 2.6 cm, mid-descending aorta 2.5 cm, and distal descending aorta 2.4 cm. The largest diameter was 4.7 cm in the ascending aorta and the smallest was 1.4 cm in the distal descending aorta. At no level was the normal descending aorta larger than the ascending aorta. The ratio of ascending to descending diameter was as high as 2.2 in young women, but for older groups it was about 1.2. Similar measurements were obtained by Guthaner et al” in a smaller series. The diameter increases progressively with age. Growth is maximal during the first and second decades.‘* In adults the diameter increases approximately 0.1 cm per decade. The aorta is smaller in females and also varies with body size.j6 Dilatation of a normal aorta may occur as the result of increased pressure.* It is common with systemic hypertension, aortic stenosis, and proxi-
fl----
MRI, magnetic resonance imaging
From Medical
the Department Center, Maywood,
of Radiology, Loyola University IL. Harold V. Posniak: Assistant Professor of Radiology: Terrence C. Demos: Professor of Radiology; Richard E. Marsan: Associate Professor of Radiology. Address reprint requests to Harold V. Posniak. MD, Department of Radiology, Loyola University Medical Center, 2160 S First Ave. Maywood. IL 60153. 0 I989 by Grune & Stratton, Inc. 0037-198X/89/2401-0001$5.00/0
POSNIAK,
DEMOS,
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MARSAN
ma1 to a coarctation. Similarly, an abnormal volume load may also lead to aortic dilatation. This is most striking in patients with severe aortic regurgitation. An aneurysm is defined as a permanent dilatation due to disease of the vessel wall. A true aneurysm results from weakening of all layers of the aortic wall, with the layers remaining intact. In false aneurysm, the wall is normal except for a focal perforation through which blood escapes. The blood is contained by the adventitia or perivascular connective tissue and organized blood clot.2.19 The aneurysm may be fusiform, involving the full circumference of the vessel wall, or saccular, involving only a portion of the wall. ETIOLOGY
Atherosclerosis is now the leading cause of true thoracic aortic aneurysm.‘9‘21 Although once common, the incidence of syphilitic aneurysm has dramatically declined in the last 40 years. Other causes include degeneration of the medial layer of the aortic wall (with or without the stigmata of Marfan syndrome) and aortitis. Bacterial infection, tuberculosis, and congenital aneurysm also occur. Traumatic false aneurysm and aortic dissection are discussed elsewhere in this Seminar. Atherosclerotic Aneurysm
The basis of atherosclerotic aneurysm formation is degeneration and fibrous replacement of the media beneath the atherosclerotic intimal lesions. Once aortic dilatation has occurred, the wall is exposed to increasing tension due to the increasing lateral hydrostatic pressure as the velocity of blood flow diminishes. Both of these factors compromise mural vascular nutrition. This combination of increased mechanical stress and poor nutrition leads to further degeneration and progressive enlargement of the aneurysm. Ultimately the aneurysm wall consists solely of dense ^^ acellular and avascular connective tissue.LL Atherosclerotic aneurysm affects the elderly and is more common in men.20P23V24 It occurs most frequently in the descending aorta, usually beginning just distal to the left subclavian artery (Fig 1). It is relatively uncommon in the ascending aorta (Fig 2). The majority of athero-
Fig 1. Fusiform atherosclerotic aneurysm. (A) The aneurysm (‘1 arises in the proximal descending aorta. The esophagus (arrow) is displaced anteriorly and to the right. IB) Three centimeters cephalad. The esophagus is slightly dilated and the wall thickened (arrows) due to esophagitis.
sclerotic aneurysms are fusiform, but they are saccular in up to 20% of patients (Fig 3). Aneurysms of the lower thoracic aorta may extend into the abdomen (Fig 4). A second aneurysm involving the infrarenal aorta is said to be present in 29% of patients.24 The prognosis for patients with untreated thoracic aortic aneurysm is poor. Survival rates of 1, 3, and 5 years of 57%, 26%, and 19%, respectively, have been reported.*’ The most serious
THORACIC
ANEURYSMS
Fig 2. Fusiform rysm. The aneurysm (arrows).
atherosclerotic (*f arises
just
ascending aortic above the aortic
aneuroot
complication is rupture.3 This is the cause of death in up to 5 1% of patients.zo*2’324Large size at the time of discovery and increasing size are bad prognostic signs. Of nine patients with ruptured aneurysm reported by McNamara and Pressler,23 eight had an aortic diameter >lO cm, and seven had an increase in diameter of >2 cm in the year preceding the rupture. Unlike rupture of an abdominal aortic aneurysm, which may be contained by the retroperitoneal structures, rupture of a thoracic aneurysm is usually free and rapidly fatal.” The second most common cause of death is associated cardiovascular disease.24*2s Degenerative
Antwysms
Medial degeneration is the most common cause of aneurysm in the ascending aorta.22S26It may be associated with genetically transmitted metabolic disorders, such as Marfan or EhlersDanlos syndrome, or may be due to acquired weakness or defect in the aortic media. The cause of medial degeneration is unknown. It is considered to be the result of an ongoing process of repetitive aortic injury and repair that occurs in the aging aorta. Inborn errors of metabolism, such as Marfan syndrome, may accelerate this process. Cardiovascular manifestations are present in 98% of patients with Marfan syndrome, and may be the cause of death in more than 90%.27*28
Fig 3. Saccular aneurysm of the inferior aspect of the aortic arch. The patient presented with hoarseness due to involvement of the left recurrent laryngeal nerve. (A) Thoracic aortogram demonstrates the aneurysm (*j. W CT image at the level of the aorticopulmonary window. The true size of the aneurysm is apparent because of visualization of the mural thrombus (Tj, which is not seen on the angiogram.
Aortic aneurysm and dissection, and mitral and aortic valve regurgitation are the most common. Involvement of the sinuses of Valsalva is frequent (Fig 5). Aortic regurgitation is present in 8 1% of patients with an aortic root diameter >5 cm, and in 100% of those with a diameter 16 cm.5 Aortic wall calcification is seldom present.3 The aneurysmal dilatation generally diminishes higher in
POSNIAK,
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root and aortic valve regurgitation due to dilatation of the aortic annulus. The name was originally reserved for patients with medial degeneration, but may be applied to all patients with this combination of lesions irrespective of the basic etiology.30 Syphilis
Thoracoabdominal aortic aneurysm. l , patent Fig 4. aortic lumen; T, thrombus. (A) At the level of the right pulmonary artery (PA). (Bl In the upper abdomen.
the ascending aorta, and the aortic arch is usually normal. The aortic lesion in patients with Marfan syndrome is identical to that in idiopathic medial degeneration. However, there is a striking difference in the behavior of the disease in the two groups of patients. The onset of degeneration occurs earlier in life and progresses more rapidly in patients with Marfan syndrome.29 Annuloaortic ectasia is a term that describes the combination of an aneurysm of the aortic
About 12% of patients with untreated syphilis develop cardiovascular disease.3’ Problems usually occur 10 to 30 years after the primary infection, and include aortic aneurysm, aortic insufficiency, and aortitis. Aortitis is characterized histologically by chronic inflammatory changes in the adventitia and media. There is focal destruction of the media, loss of elastic and smooth muscle fibers, and scarring. Contracture of the aortic wall produces intimal wrinkling, known as “tree-barking.” Medial destruction may result in aortic dilatation and aneurysm formation. This occurs in up to 40% of patients with aortitis.32 The ascending aorta is involved in 36% of syphilitic aneurysms, the arch in 34%, the proximal descending aorta in 25%, and the distal descending thoracic aorta in 5%. Less than 1% involve the sinuses of Valsalva.33 In syphilis, there is asymmetric enlargement of the sinuses in contradistinction to symmetrical enlargement found in medial degeneration. Most aneurysms are saccular, but about one fourth are fusiform. Fine, pencil-thin dystrophic aortic wall calcification is found in up to 40% of patients.34 This is most severe in the ascending aorta or entirely confined to it. The delicate calcification is frequently altered by superimposition of secondary atherosclerosis which produces thick, irregular, coarse calcification (Fig 6). Aortic insufficiency may be secondary to the aneurysm due to dilatation of the aortic annulus. The prognosis for untreated luetic aneurysm is poor, with death occurring within months of the onset of symptoms. Death is due to aortic rupture in about 40% of cases.33 Mycotic Aneurysms
An aneurysm arising from nonsyphilitic infection of the arterial wall is known as a mycotic aneurysm. This type is frequently saccular (Fig 7). Mycotic aneurysm is often insidious; if untreated, it often leads to uncontrolled sepsis and aortic rupture. Predisposing factors include
THORACIC
ANEURYSMS
Fig 5. Annuloaortic ectasia in a patient with Marfan syndrome. the aortic sinuses (S). The heart is displaced to the left because The ascending aorta (AA) is normal in size. (C) and (DI Another Felson, Cincinnati.)
contiguous bacterial endocarditis, atherosclerosis, drug abuse, and aortic trauma caused by accidents, surgical manipulation, or arterial catheterization. There is an increased incidence in immunocompromised patients.35 The normal arterial intima is extremely resistant to infection, and it is generally felt that the development of a mycotic aneurysm requires prior damage to the aortic wall in addition to a source of infection. Infection of the aortic wall is thought to occur in one of four ways: (1) embolization of infected material directly to the diseased intima or vasa vasorum; (2) direct exten-
11
(A) Large aneurysm of pectus excavatum. patient with Marfan
of the ascending aorta. (‘1, involving lB) Fiie centimeters cephatad to IA). syndrome (Courtesy of Dr Benjamin
sion from an intravascular source, such as infective endocarditis; (3) invasion of the aortic wall from contiguous extravascular source; or (4) lymphangitic spread.” The ascending aorta is the most frequent site of involvement, probably reflecting the proximity to endocarditis. The infectious agents usually responsible for mycotic aneurysm include nonhemolytic streptococcus, pneumococcus, and staphylococcus. Gonococcus and salmonella have also been reported.” Mycotic aneurysm from contiguous spread is most commonly due to tuberculosis extending from the spine or lymph nodes.36
POSNIAK,
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true aneurysms, but tuberculous false aneurysm does occur.36
Fig 6. Syphilitic ascending aortic hancad CT image demonstrates the extensive intimal calcification (arrows). calcification in a normal size descending
aneurysm. Unananeurysm (‘1 with Note absence of aorta (DA).
Tuberculosis may also cause a stenotic aortic lesion or perivascular fibrosis.37 Histologically, mycotic aneurysm is characterized by loss of intima and destruction of the internal elastic lamella produced by the infection. The muscularis of the media and the adventitia also show varying degrees of destruction. Bacteria are often demonstrable in pathologic sections. The majority of mycotic aneurysms are
Aortitis Associated With Aneurysm There are several causes of aortitis associated with aneurysm (Table 1). All show a similar type of inflammatory process pathologically. In most, the inflammation is confined to the media and adventitia. An exception to this is aortitis associated with rheumatic fever, and probably also that of rheumatoid arthritis, in which there is evidence of fibrinoid necrosis and inflammatory reaction of the intima, media, and adventitia. In advanced disease, the cellular infiltrates resolve and the damaged wall is replaced by fibrous tissue.3’ Characteristically, the intima in advanced aortitis is obscured by premature atherosclerosis. At times this may be severe enough to give a misleading appearance. Calcification in aortitis may be dystrophic or due to secondary atherosclerosis. In the former, there is deposition of calcium in the scarred media and intima. This calcification is thin and pencil-like. The calcification due to atherosclerosis is more irregular and coarse.31 Aortitis in rheumatic fever is rare. It may be segmental, proximal to the origin of the right subclavian artery, or involve the entire aorta. The abdominal aorta is frequently affected, and occasionally a fusiform aneurysm develops here.” Aortitis occurs in approximately 5% of patients with rheumatoid arthritis or ankylosing spondylitis. The ascending aorta is most commonly affected. A small number of these patients develop an aneurysm. There may be associated aortic valve insufficiency.31 Giant cell arteritis affects large vessels in about 10% of patients. Aneurysm usually Table
1.
Noninfective Rheumatic
Causes
of Aortitis
fever
Rheumatoid arthritis Ankylosing spondylitis Giant cell arteritis Relapsing polychondritis Reiter syndrome Systemic lupus erythematosus Scleroderma Psoriasis Ulcerative Fig 7. Saccular mycotic aneurysm (‘1 distal aortic arch. Note lung consolidation rounding the aneurysm.
arising from (arrows)
the sur-
Takayasu Radiation Behcet’s
colitis arteritis disease
With
Aneurysm
THORACIC
ANEURYSMS
involves the ascending aorta, leading to aortic root dilatation and valvular insufficiency.38 Relapsing polychondritis is a disease characterized by an extensive inflammatory and degenerative process that affects multiple cartilaginous structures and eventually results in degeneration and fibrous replacement. Aortic aneurysm occurs in approximately 10% of these patients. These are most frequent in the ascending aorta, where it may lead to dilatation of the aortic root and aortic insufficiency. Multiple aneurysms may occur.39 Takayasu arteritis is an inflammatory process of unknown etiology that characteristically affects the aorta segmentally and may involve the great vessels, including the pulmonary Fig 9. Unanhanced scan of a large fusiform descending aortic aneurysm. The aneurysm (‘1 displaces the left main bronchus (straight arrows) and esophagus (curved arrow). Note lymphadenopathy (N) in this patient, who also had lymphoma.
arteries.3’.40 Arterial stenosis and occlusion are the most common manifestations, but aneurysm may also develop. These changes are due to intimal thickening and extensive destruction of the elastic fibers in the media, with residual fibrosis. The aneurysm is usually fusiform and may occur anywhere in the aorta. Aortic calcification occurs in about 15% of the patients and
(Al Fig 8. Atherosclerotic aneurysm of the aortic arch. Unenhancad scan reveals peripheral location of intimal calcification (arrowheads). (8) CT image at sama level ss (A) after intravenous contrast. The intimal calcification is diicult to detect.
Fig 10. Large descending the left atrium (straight arrows) vain (curved arrow) anteriorly. thrombus.
aortio aneurysm and left inferior l , patent aortic
displacing pulmonary lumen.
T,
POSNIAK,
characteristically is found in the arch and descending aorta.40 Congenital
Aneurysm
This rare lesion may involve any part of the thoracic aorta but is most frequent in an aortic sinus. It may occur as an isolated lesion or in association with coarctation of the aorta or con-
DEMOS,
AND
MARSAN
genital aortic stenosis. The right, the noncoronary, and the left coronary sinus are involved in decreasing order of frequency. The aneurysm is usually asymptomatic unless rupture occurs.3’5 CLINICAL
MANIFESTATIONS
Most patients with aneurysm are asymptomatic when the aneurysm is detected,20*24but some have nonspecific chest or back pain. The likeli-
Fig 11. Partial SVC obstruction distal to entry of the azygos vain. (A) The WC (curved arrow) is compressed by a large ascending aortic aneurysm (‘1. Note the dense opacification of the azygos vain (straight arrow). indicating retrograde flow of contrast medium secondary to the obstruction. (B) Five centimeters cephalad to (A). Note normal-sized SVC (curved arrow) and dense opacification of the distal azygos arch (open arrow) and azygos vain (straight arrow).
THORACIC
15
ANEURYSMS
hood of an aneurysm becoming symptomatic depends on its relationship to vital structures. An aneurysm of the arch is more likely to produce symptoms sooner than one in the ascending or descending aorta. due to its proximity to important anatomic structures. Dyspnea, dysphagia, or hoarseness may be a presenting symptom due to compression of the bronchial tree, esophagus, or recurrent laryngeal nerve, respectively.20*26 A large aneurysm may erode adjacent bone or compress pulmonary arteries or veins. SVC syndrome may rarely be a presenting feature.22 Patients with impending or actual rupture frequently experience severe chest pain.‘0*23325Rupture is usually into the left pleural cavity but may also extend into the mediastinum, right pleural cavity, pericardium, or adjacent lung. The clinical presentation of mycotic aneurysm is varied and nonspecific. Malaise, weakness, low grade fever, and chills may be present. The clinical picture may be that of the primary underlying process, such as endocarditis, pneumonia, or osteomyelitis. The aneurysm does not usually reach a large enough size to produce intrathoracic signs and symptoms. As with other aneurysms, severe chest pain is usually associated with rapid enlargement or rupture. C:T TECHNIQUE
Initially a scanogram is performed. Axial unenhanced images are directed to specific areas
Fig 12. Aneurysm with ture into the mediastinum. enhanced image at the level the aortic arch demonstrates large aortic arch aneurysm Note the high attenuation diastinal hemstoma (HI.
rupUnof a (‘1. me-
of interest. These initial images are important for identifying and evaluating vascular calcification (Fig 8). Unenhanced scans may be sufficient for follow-up of known aortic disease. In most cases, however, intravenous contrast is needed. Dynamic scans are obtained following a bolus of about 25 mL of contrast material, if an aortic dissection is suspected, or if differentiation from a mediastinal mass is necessary. In a patient being evaluated for aneurysm, incremental l-cm thick images are obtained at 2-cm intervals, from the top of the aortic arch to the diaphragm during rapid drip infusion of intravenous contrast medium. The scans are continued to the aortic bifurcation if the aorta is abnormal at the level of the diaphragm or if a second aneurysm is a possibility. CT Findings
The criteria for the diagnosis of aortic aneurysm are well established.6”4 Focal or diffuse aortic dilatation and deformity, as well as the length of the aneurysm are readily apparent on unenhanced scans. Localization of the calcification relative to the wall of the aorta is important in differentiating dissections from aneurysm. In aortic dissection, the intimal calcification is characteristically displaced internally, whereas calcification is peripheral in aneurysm (Fig calcification has been 8). 7*‘2,‘3 Peripheral reported in about 75% of aortic aneurysms.‘3*4’
16
CT is superior to angiography in evaluating the true diameter of the aneurysm because of better visualization of mural thrombus. Intravenous contrast material is required to differentiate the patent lumen and mural thrombus (Figs 3 and 4). Thrombus may be circumferential or
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crescentic. Fine punctate calcification may occasionally be seen in the thrombus. There is a direct relationship between the size of the aneurysm and the amount of thrombus.13 Knowledge of the position and amount of mural thrombus may be important in surgical planning.4’
Fig 13. Posterior mediastinal toma resembling an aneurysm. a fusiform posterior mediastinal CT image in the lower thorax aorta (A) displaced anteriorly by mass (M). (C) Lateral thoracic aorta.
malignant fibrous histiocy(A) PA chest radiograph shows mass (arrows). (B) Enhanced demonstrates a normal sited an inhomogeneous soft tissue aortogram reveals a normal
THORACIC
ANEURYSMS
CT clearly demonstrates the relationship of the aortic aneurysm to adjacent structures. Subtle erosion of bone may be appreciated by adjusting the window width and level to appropriate values. Compression of the tracheobronchial tree, the pulmonary arteries and veins, as well as the SVC, are easily identified (Figs 9 through 1 1).42,43 Esophageal displacement or obstruction may be seen (Figs 1 and 9). Angiography is required only if the relationship of the aneurysm to the great vessels needs to be evaluated or aortic insufficiency requires demonstration. CT is especially useful in evaluating a patient for impending or actual aortic rupture. The aorta may rupture into the mediastinum, pericardium, or either pleural sac or extrapleural space (Fig
17
12). High attenuation fluid at these sites is suggestive of rupture.‘2*44 Central displacement of peripheral calcification has been described as a sign of early disruption of the aortic wall.13 Aortobronchopulmonary fistula is rare. It is manifested as consolidation of the lung adjacent to the aneurysm.4s CT is the primary method used to differentiate a mediastinal or paramediastinal lung mass from saccular aortic aneurysms (Fig 13).46 Single level dynamic scanning following a rapid bolus injection of contrast medium is imperative in this situation, This is done in order to create as large a density difference as possible between the intraluminal blood and the surrounding soft tissue. With a drip infusion, a para-aortic mass may enhance sufficiently to make the differentiation
Postoperative infection. (A) Unenhancad image three days folFig 14. lowing repair of a descending aortic aneurysm. Note the high density hemorrhage (HI between the graft (A) and the native aortic wall (arrows). (B) Ten days later. The hemorrhage has mostly resolved. A large amount of gas (01 is now present between the graft (A) and aortic wall, indmting infection. This was confirmed at surgery. (Cl Another patient. Fluid (F) and a small amount of gas (small arrows) between the graft (AI and the native aortic wall eight days after surgery. This resolved spontaneously. indicating a normal postoperative appearance.
18
very difficult or impossible. Differentiation may also be difficult following a bolus in the rare patient who has a noncalcified saccular aneurysm which is completely clot-filled. In this situation, however, no enhancement should occur in the thrombus, whereas most tumors demonstrate at least minimal enhancement. CT plays an important role in following a patient after surgical repair of an aneurysm. After making the graft secure, the aortic wall is often wrapped around it and the incision sutured. This leaves a potential space between the graft and the native aorta.47 A small amount of blood and gas may normally be present in this space in
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the immediate postoperative period. Suture dehiscence, either proximally or distally, will result in blood leaking into the space. This is readily apparent on CT. On enhanced singlelevel dynamic images, contrast material will be identified within this space. In more chronic cases, there may be thrombus in the space. Aortic graft infection is a rare but potentially lethal complication of aortic surgery. Although the CT appearance of an infected thoracic aortic graft has not been described, it can be expected to be similar to abdominal aortic graft infection. Any fluid between the graft and native aorta six weeks following surgery is highly suspicious of
Fig 15. Buckled innominate artery. The patient had a palpable pulsating right supraclavicular mass. (A) Right auperior mediastinal mass that stops at the clavicle. indicating an anterior location fcervicothoracic sign). (B) Venous angiogram, of less than optimal quality, was interpreted as showing an aneurysm of the innominate artery. W Retouched copy of (BL illustrating the findings at operation. The cleft created by the U-turn of the innominate artery was not appreciated in (B).
THORACIC
ANEURYSMS
Fig 16. Tuberculous mycotic aneurysm of the aorta, proved at operation. (A) Admission teleroentgenogram. Innumerable miliary lesions are present throughout both lungs. (B) About 5 weeks later, after antituberculous therapy. The miliary lesions have almost disappeared, but a mass is now noted in the vicinity of the aortic knob. It was present but smaller and overlooked in (A). (C) Catheter aortogram shows a bilobed aneurysm in the region of the aortic knob.
19
20
POSNIAK,
graft infection. It has been reported that gas in this space more than 2 weeks after surgery is virtually pathognomonic of infection (Fig 14).48 Postoperative scanning is particularly important in those patients who have multiple aneurysms or who have a predisposition for new aneurysm formation. This is especially important in Marfan syndrome. MRI
Early reports indicate that MRI may have an important role in evaluating patients with aortic and paraaortic pathology.4g-52 However, more experience is required, and it will have to be shown to be significantly better than CT in order to overcome the limitation of the relatively high cost of the examination. EDITOR’S
ADDENDA
A fairly common condition that may closely resemble an aneurysm is the buckled innominate artery. In the patient illustrated in Fig !5 this mistake was actually made from a poor quality venous angiocardiogram (before the days of digital subtraction angiography). The case illustrated in Fig 16 is a fascinating example of a tuberculous mycotic aneurysm of the aortic arch, a component of an even more fascinating series of coincidences. The patient appeared at our institution following onset of weakness, cough, and chest pain. She was an elderly black woman. Despite the lack of fever, the widespread miliary pattern strongly suggested miliary tuberculosis, and this diagnosis was confirmed by bone marrow study. She was started on antituberculous therapy.
DEMOS,
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A few days later, on a visit to Massachusetts General Hospital, I was shown the chest films of an elderly febrile Chinese woman with recent onset of a miliary pattern, associated with a growing mass contiguous with the aortic knob. I raised the question of miliary tuberculosis with mycotic aneurysm of the aortic arch, which proved to be the diagnosis. When I came back to Cincinnati, our case of miliary tuberculosis again crossed my desk. The lungs had cleared, but now there was an enlarging aortic mass! The diagnosis of mycotic tuberculous aneurysm was quickly confirmed by angiography and operation. A month or so later, in Spain, I saw a third case, similar to the first two. The three cases were combined and published in JAMA. Tuberculous mycotic aneurysm of large arteries is not so rare. Well over 100 cases have been reported. If undiagnosed and untreated, the condition is almost uniformly fatal, but if recognized, surgical cure is the rule. The condition is often caused by direct extension from an adjacent tuberculous focus, usually lymphadenitis or Pott’s abscess. Many of the patients have acute miliary tuberculosis. There is considerable evidence to indicate that the miliary dissemination is often the result of the mycotic aneurysm rather than its cause, and follows discharge of organisms from the aneurysm into the bloodstream. Benjamin Felson Editor ACKNOWLEDGMENT Our thanks to Barbara Medley for assistance in preparation of this manuscript.
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aortitis. A clinicopathologic 1950 to 1960. Circulation aneurysm
of the thoracic
aorta. A clinical study of 633 cases. Ann Intern Med 1938;12:624-51 34. Smith WG, Leonard JC: The radiological features of syphilitic aortic incompetence. Br Heart J 1959;2 1: 162-6 35. Johansen K, Devin J: Mycotic aortic aneurysms: A reappraisal. Arch Surg 1983;118:583-8 36. Felson B, Akers PV, Hall GS, et al: Mycotic tuberculous aneurysm of the thoracic aorta. JAMA 1977:237: 11048 37. Gajaraj A, Victor S: Tuberculous aortoarteritis. Clin Radio1 1981;32:461-6 38. Spence RK, Estella F, Gisser S, et al: Thoracic aortic aneurysm secondary to giant cell arteritis: A reappraisal of etiology, treatment and possible prevention. J Curdiovasc Surg 1985;26:492-5 39. Cipriano PR, Alonso DR, Baltaxe HA, et al: Multiple aortic aneurysms in relapsing polychondritis. Am .I Curdiol 1976;37:1097-1102 40. Yamato M, Lecky JW, Hiramatsu K, et al: Takayasu arteritis: Radiographic and angiographic findings in 59 patients. Radiology 1986;161:329-34 41. Machida K, Tasaka A: CT patterns of mural thrombus in aortic aneurysms. J Comput Assist Tomogr 1980;4:840-2 42. Cramer M, Foley WD, Palmer TE, et al: Compression of the right pulmonary artery by aortic aneurysms: CT demonstration. J Comput Assist Tomogr 1985;9:3 10-4 43. Duke RA, Barrett MR, Payne SD, et al: Compression of left main bronchus and left pulmonary artery by thoracic aortic aneurysm. AJR 1987;149:261-3 44. Kucich VA, Vogelzang RL, Hartz RS, et al: Ruptured thoracic aneurysm: Unusual manifestation and early diagnosis using CT. Radiology 1986;160:87-9 45. Coblentz CL, Sallee DS, Chiles C: Aortobronchopulmonary fistula complicating aortic aneurysm: Diagnosis in four cases. AJR 1988;150:535-8 46. Miller GA, Heaston DK, Moore AV, et al: CT differentiation of thoracic aortic aneurysms from pulmonary masses adjacent to the mediastinum. J Comput Assist Tomogr 1984;8:437-42 47. Jacob NM, Godwin JD, Wolfe WG, et al: Evaluation of the grafted ascending aorta with computed tomography. Complications caused by suture dehiscence. Radiology 1982;145:749-53 48. Mark AS, McCarthy SM, Moss AA, et al: Detection of abdominal aortic graft infection: Comparison of CT and In-labelled white blood cell scans. AJR 1985;144:315-8 49. Dinsmore RE, Liberthson RR, Wismer GL. et al: Magnetic resonance imaging of thoracic aortic aneurysms: Comparison with other imaging methods. A/R 1986; 146:309-14 50. Akins EW, Carmichael MJ, Hill JA, et al: Preoperative evaluation of the thoracic aorta using MRI and angiography. Ann Thorac Surg 1987;44:499-507 5 1. Kersting-Sommerhoff BA, Sechtem UP, Schiller NB, et al: MR imaging of the thoracic aorta in Marfan patients. J Comput Assist Tomogr 1987;11:633-9 52. Cook JP, Kazmier FJ, Orszulak TA: The penetrating aortic ulcer: Pathologic manifestations, diagnosis, and management. Mayo Chin Proc 1988;63:718-25
Tomography Thoracic
of the Normal Aneurysms
By Harold V. Posniak, Terrence
S
ANATOMY
The ascending aorta is subdivided into the aortic root, or aortic bulb, and the tubular segment. The aortic root comprises the three sinuses of Valsalva and extends from the aortic valve to the superior margin of the sinuses. The coronary arteries arise from the right and left sinuses. The tubular aorta extends from the aortic root to the origin of the innominate artery. Most of the ascending aorta is intrapericardial. Posteriorly the ascending aorta is related successively to the left atrium, the right pulmonary artery, and the right main bronchus. On its right is the superior vena cava and right atria1 appendage; on its left is the pulmonary trunk. The aortic arch extends from the origin of the innominate artery to the site of insertion of the ligamentum arteriosum. Several important structures lie within the concavity of the arch, including the bifurcation of the pulmonary trunk, the left main bronchus, and the left recurrent laryngeal nerve. Posteriorly and to the right are the trachea and esophagus. The descending aorta extends from the ligamentum arteriosum to the aortic hiatus in the diaphragm. The esophagus is on the right of the proximal and middle thirds of the descending .?6minarS in Roentgenolog~,
Vol XXIV,
NO 1 (January),
1989:
and
C. Demos, and Richard E. Marsan
INCE 1929, when dos Santos et al first described visualization of the aorta by means of a translumbar injection in an opaque medium,’ aortography has been accepted as the method of choice for the evaluation of suspected aortic disease. Despite the continual evolution of methods and equipment, there remains a small but significant risk for patients undergoing aortography even with the most careful technique in experienced hands.2-s CT has been used since the late 1970s in the investigation of aortic pathology. 6-14The major advantages of this technique include noninvasiveness, and the ability to demonstrate more of the aorta than just the contrast column. CT is more sensitive than plain radiographs and angiography for detecting intimal calcification and intraluminal thrombus. In addition, the periaortic structures are clearly demonstrated. NORMAL
Aorta
pp 7-2 1
aorta. More distally, the esophagus crosses the aorta anteriorly and is related to its left side. The ascending aorta measures approximately 5.0 cm in length, the arch 4.5 cm, and the descending aorta 20.0 cm. The diameter of the thoracic aorta is largest at the aortic root and gradually decreases distally.15 Aronberg et alI6 measured coronal diameters at several levels of the thoracic aorta. The average diameter of the aortic root was 3.6 cm, ascending aorta 1.O cm proximal to the arch 3.5 cm, proximal descending aorta 2.6 cm, mid-descending aorta 2.5 cm, and distal descending aorta 2.4 cm. The largest diameter was 4.7 cm in the ascending aorta and the smallest was 1.4 cm in the distal descending aorta. At no level was the normal descending aorta larger than the ascending aorta. The ratio of ascending to descending diameter was as high as 2.2 in young women, but for older groups it was about 1.2. Similar measurements were obtained by Guthaner et al” in a smaller series. The diameter increases progressively with age. Growth is maximal during the first and second decades.‘* In adults the diameter increases approximately 0.1 cm per decade. The aorta is smaller in females and also varies with body size.j6 Dilatation of a normal aorta may occur as the result of increased pressure.* It is common with systemic hypertension, aortic stenosis, and proxi-
fl----
MRI, magnetic resonance imaging
From Medical
the Department Center, Maywood,
of Radiology, Loyola University IL. Harold V. Posniak: Assistant Professor of Radiology: Terrence C. Demos: Professor of Radiology; Richard E. Marsan: Associate Professor of Radiology. Address reprint requests to Harold V. Posniak. MD, Department of Radiology, Loyola University Medical Center, 2160 S First Ave. Maywood. IL 60153. 0 I989 by Grune & Stratton, Inc. 0037-198X/89/2401-0001$5.00/0
POSNIAK,
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ma1 to a coarctation. Similarly, an abnormal volume load may also lead to aortic dilatation. This is most striking in patients with severe aortic regurgitation. An aneurysm is defined as a permanent dilatation due to disease of the vessel wall. A true aneurysm results from weakening of all layers of the aortic wall, with the layers remaining intact. In false aneurysm, the wall is normal except for a focal perforation through which blood escapes. The blood is contained by the adventitia or perivascular connective tissue and organized blood clot.2.19 The aneurysm may be fusiform, involving the full circumference of the vessel wall, or saccular, involving only a portion of the wall. ETIOLOGY
Atherosclerosis is now the leading cause of true thoracic aortic aneurysm.‘9‘21 Although once common, the incidence of syphilitic aneurysm has dramatically declined in the last 40 years. Other causes include degeneration of the medial layer of the aortic wall (with or without the stigmata of Marfan syndrome) and aortitis. Bacterial infection, tuberculosis, and congenital aneurysm also occur. Traumatic false aneurysm and aortic dissection are discussed elsewhere in this Seminar. Atherosclerotic Aneurysm
The basis of atherosclerotic aneurysm formation is degeneration and fibrous replacement of the media beneath the atherosclerotic intimal lesions. Once aortic dilatation has occurred, the wall is exposed to increasing tension due to the increasing lateral hydrostatic pressure as the velocity of blood flow diminishes. Both of these factors compromise mural vascular nutrition. This combination of increased mechanical stress and poor nutrition leads to further degeneration and progressive enlargement of the aneurysm. Ultimately the aneurysm wall consists solely of dense ^^ acellular and avascular connective tissue.LL Atherosclerotic aneurysm affects the elderly and is more common in men.20P23V24 It occurs most frequently in the descending aorta, usually beginning just distal to the left subclavian artery (Fig 1). It is relatively uncommon in the ascending aorta (Fig 2). The majority of athero-
Fig 1. Fusiform atherosclerotic aneurysm. (A) The aneurysm (‘1 arises in the proximal descending aorta. The esophagus (arrow) is displaced anteriorly and to the right. IB) Three centimeters cephalad. The esophagus is slightly dilated and the wall thickened (arrows) due to esophagitis.
sclerotic aneurysms are fusiform, but they are saccular in up to 20% of patients (Fig 3). Aneurysms of the lower thoracic aorta may extend into the abdomen (Fig 4). A second aneurysm involving the infrarenal aorta is said to be present in 29% of patients.24 The prognosis for patients with untreated thoracic aortic aneurysm is poor. Survival rates of 1, 3, and 5 years of 57%, 26%, and 19%, respectively, have been reported.*’ The most serious
THORACIC
ANEURYSMS
Fig 2. Fusiform rysm. The aneurysm (arrows).
atherosclerotic (*f arises
just
ascending aortic above the aortic
aneuroot
complication is rupture.3 This is the cause of death in up to 5 1% of patients.zo*2’324Large size at the time of discovery and increasing size are bad prognostic signs. Of nine patients with ruptured aneurysm reported by McNamara and Pressler,23 eight had an aortic diameter >lO cm, and seven had an increase in diameter of >2 cm in the year preceding the rupture. Unlike rupture of an abdominal aortic aneurysm, which may be contained by the retroperitoneal structures, rupture of a thoracic aneurysm is usually free and rapidly fatal.” The second most common cause of death is associated cardiovascular disease.24*2s Degenerative
Antwysms
Medial degeneration is the most common cause of aneurysm in the ascending aorta.22S26It may be associated with genetically transmitted metabolic disorders, such as Marfan or EhlersDanlos syndrome, or may be due to acquired weakness or defect in the aortic media. The cause of medial degeneration is unknown. It is considered to be the result of an ongoing process of repetitive aortic injury and repair that occurs in the aging aorta. Inborn errors of metabolism, such as Marfan syndrome, may accelerate this process. Cardiovascular manifestations are present in 98% of patients with Marfan syndrome, and may be the cause of death in more than 90%.27*28
Fig 3. Saccular aneurysm of the inferior aspect of the aortic arch. The patient presented with hoarseness due to involvement of the left recurrent laryngeal nerve. (A) Thoracic aortogram demonstrates the aneurysm (*j. W CT image at the level of the aorticopulmonary window. The true size of the aneurysm is apparent because of visualization of the mural thrombus (Tj, which is not seen on the angiogram.
Aortic aneurysm and dissection, and mitral and aortic valve regurgitation are the most common. Involvement of the sinuses of Valsalva is frequent (Fig 5). Aortic regurgitation is present in 8 1% of patients with an aortic root diameter >5 cm, and in 100% of those with a diameter 16 cm.5 Aortic wall calcification is seldom present.3 The aneurysmal dilatation generally diminishes higher in
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root and aortic valve regurgitation due to dilatation of the aortic annulus. The name was originally reserved for patients with medial degeneration, but may be applied to all patients with this combination of lesions irrespective of the basic etiology.30 Syphilis
Thoracoabdominal aortic aneurysm. l , patent Fig 4. aortic lumen; T, thrombus. (A) At the level of the right pulmonary artery (PA). (Bl In the upper abdomen.
the ascending aorta, and the aortic arch is usually normal. The aortic lesion in patients with Marfan syndrome is identical to that in idiopathic medial degeneration. However, there is a striking difference in the behavior of the disease in the two groups of patients. The onset of degeneration occurs earlier in life and progresses more rapidly in patients with Marfan syndrome.29 Annuloaortic ectasia is a term that describes the combination of an aneurysm of the aortic
About 12% of patients with untreated syphilis develop cardiovascular disease.3’ Problems usually occur 10 to 30 years after the primary infection, and include aortic aneurysm, aortic insufficiency, and aortitis. Aortitis is characterized histologically by chronic inflammatory changes in the adventitia and media. There is focal destruction of the media, loss of elastic and smooth muscle fibers, and scarring. Contracture of the aortic wall produces intimal wrinkling, known as “tree-barking.” Medial destruction may result in aortic dilatation and aneurysm formation. This occurs in up to 40% of patients with aortitis.32 The ascending aorta is involved in 36% of syphilitic aneurysms, the arch in 34%, the proximal descending aorta in 25%, and the distal descending thoracic aorta in 5%. Less than 1% involve the sinuses of Valsalva.33 In syphilis, there is asymmetric enlargement of the sinuses in contradistinction to symmetrical enlargement found in medial degeneration. Most aneurysms are saccular, but about one fourth are fusiform. Fine, pencil-thin dystrophic aortic wall calcification is found in up to 40% of patients.34 This is most severe in the ascending aorta or entirely confined to it. The delicate calcification is frequently altered by superimposition of secondary atherosclerosis which produces thick, irregular, coarse calcification (Fig 6). Aortic insufficiency may be secondary to the aneurysm due to dilatation of the aortic annulus. The prognosis for untreated luetic aneurysm is poor, with death occurring within months of the onset of symptoms. Death is due to aortic rupture in about 40% of cases.33 Mycotic Aneurysms
An aneurysm arising from nonsyphilitic infection of the arterial wall is known as a mycotic aneurysm. This type is frequently saccular (Fig 7). Mycotic aneurysm is often insidious; if untreated, it often leads to uncontrolled sepsis and aortic rupture. Predisposing factors include
THORACIC
ANEURYSMS
Fig 5. Annuloaortic ectasia in a patient with Marfan syndrome. the aortic sinuses (S). The heart is displaced to the left because The ascending aorta (AA) is normal in size. (C) and (DI Another Felson, Cincinnati.)
contiguous bacterial endocarditis, atherosclerosis, drug abuse, and aortic trauma caused by accidents, surgical manipulation, or arterial catheterization. There is an increased incidence in immunocompromised patients.35 The normal arterial intima is extremely resistant to infection, and it is generally felt that the development of a mycotic aneurysm requires prior damage to the aortic wall in addition to a source of infection. Infection of the aortic wall is thought to occur in one of four ways: (1) embolization of infected material directly to the diseased intima or vasa vasorum; (2) direct exten-
11
(A) Large aneurysm of pectus excavatum. patient with Marfan
of the ascending aorta. (‘1, involving lB) Fiie centimeters cephatad to IA). syndrome (Courtesy of Dr Benjamin
sion from an intravascular source, such as infective endocarditis; (3) invasion of the aortic wall from contiguous extravascular source; or (4) lymphangitic spread.” The ascending aorta is the most frequent site of involvement, probably reflecting the proximity to endocarditis. The infectious agents usually responsible for mycotic aneurysm include nonhemolytic streptococcus, pneumococcus, and staphylococcus. Gonococcus and salmonella have also been reported.” Mycotic aneurysm from contiguous spread is most commonly due to tuberculosis extending from the spine or lymph nodes.36
POSNIAK,
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true aneurysms, but tuberculous false aneurysm does occur.36
Fig 6. Syphilitic ascending aortic hancad CT image demonstrates the extensive intimal calcification (arrows). calcification in a normal size descending
aneurysm. Unananeurysm (‘1 with Note absence of aorta (DA).
Tuberculosis may also cause a stenotic aortic lesion or perivascular fibrosis.37 Histologically, mycotic aneurysm is characterized by loss of intima and destruction of the internal elastic lamella produced by the infection. The muscularis of the media and the adventitia also show varying degrees of destruction. Bacteria are often demonstrable in pathologic sections. The majority of mycotic aneurysms are
Aortitis Associated With Aneurysm There are several causes of aortitis associated with aneurysm (Table 1). All show a similar type of inflammatory process pathologically. In most, the inflammation is confined to the media and adventitia. An exception to this is aortitis associated with rheumatic fever, and probably also that of rheumatoid arthritis, in which there is evidence of fibrinoid necrosis and inflammatory reaction of the intima, media, and adventitia. In advanced disease, the cellular infiltrates resolve and the damaged wall is replaced by fibrous tissue.3’ Characteristically, the intima in advanced aortitis is obscured by premature atherosclerosis. At times this may be severe enough to give a misleading appearance. Calcification in aortitis may be dystrophic or due to secondary atherosclerosis. In the former, there is deposition of calcium in the scarred media and intima. This calcification is thin and pencil-like. The calcification due to atherosclerosis is more irregular and coarse.31 Aortitis in rheumatic fever is rare. It may be segmental, proximal to the origin of the right subclavian artery, or involve the entire aorta. The abdominal aorta is frequently affected, and occasionally a fusiform aneurysm develops here.” Aortitis occurs in approximately 5% of patients with rheumatoid arthritis or ankylosing spondylitis. The ascending aorta is most commonly affected. A small number of these patients develop an aneurysm. There may be associated aortic valve insufficiency.31 Giant cell arteritis affects large vessels in about 10% of patients. Aneurysm usually Table
1.
Noninfective Rheumatic
Causes
of Aortitis
fever
Rheumatoid arthritis Ankylosing spondylitis Giant cell arteritis Relapsing polychondritis Reiter syndrome Systemic lupus erythematosus Scleroderma Psoriasis Ulcerative Fig 7. Saccular mycotic aneurysm (‘1 distal aortic arch. Note lung consolidation rounding the aneurysm.
arising from (arrows)
the sur-
Takayasu Radiation Behcet’s
colitis arteritis disease
With
Aneurysm
THORACIC
ANEURYSMS
involves the ascending aorta, leading to aortic root dilatation and valvular insufficiency.38 Relapsing polychondritis is a disease characterized by an extensive inflammatory and degenerative process that affects multiple cartilaginous structures and eventually results in degeneration and fibrous replacement. Aortic aneurysm occurs in approximately 10% of these patients. These are most frequent in the ascending aorta, where it may lead to dilatation of the aortic root and aortic insufficiency. Multiple aneurysms may occur.39 Takayasu arteritis is an inflammatory process of unknown etiology that characteristically affects the aorta segmentally and may involve the great vessels, including the pulmonary Fig 9. Unanhanced scan of a large fusiform descending aortic aneurysm. The aneurysm (‘1 displaces the left main bronchus (straight arrows) and esophagus (curved arrow). Note lymphadenopathy (N) in this patient, who also had lymphoma.
arteries.3’.40 Arterial stenosis and occlusion are the most common manifestations, but aneurysm may also develop. These changes are due to intimal thickening and extensive destruction of the elastic fibers in the media, with residual fibrosis. The aneurysm is usually fusiform and may occur anywhere in the aorta. Aortic calcification occurs in about 15% of the patients and
(Al Fig 8. Atherosclerotic aneurysm of the aortic arch. Unenhancad scan reveals peripheral location of intimal calcification (arrowheads). (8) CT image at sama level ss (A) after intravenous contrast. The intimal calcification is diicult to detect.
Fig 10. Large descending the left atrium (straight arrows) vain (curved arrow) anteriorly. thrombus.
aortio aneurysm and left inferior l , patent aortic
displacing pulmonary lumen.
T,
POSNIAK,
characteristically is found in the arch and descending aorta.40 Congenital
Aneurysm
This rare lesion may involve any part of the thoracic aorta but is most frequent in an aortic sinus. It may occur as an isolated lesion or in association with coarctation of the aorta or con-
DEMOS,
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genital aortic stenosis. The right, the noncoronary, and the left coronary sinus are involved in decreasing order of frequency. The aneurysm is usually asymptomatic unless rupture occurs.3’5 CLINICAL
MANIFESTATIONS
Most patients with aneurysm are asymptomatic when the aneurysm is detected,20*24but some have nonspecific chest or back pain. The likeli-
Fig 11. Partial SVC obstruction distal to entry of the azygos vain. (A) The WC (curved arrow) is compressed by a large ascending aortic aneurysm (‘1. Note the dense opacification of the azygos vain (straight arrow). indicating retrograde flow of contrast medium secondary to the obstruction. (B) Five centimeters cephalad to (A). Note normal-sized SVC (curved arrow) and dense opacification of the distal azygos arch (open arrow) and azygos vain (straight arrow).
THORACIC
15
ANEURYSMS
hood of an aneurysm becoming symptomatic depends on its relationship to vital structures. An aneurysm of the arch is more likely to produce symptoms sooner than one in the ascending or descending aorta. due to its proximity to important anatomic structures. Dyspnea, dysphagia, or hoarseness may be a presenting symptom due to compression of the bronchial tree, esophagus, or recurrent laryngeal nerve, respectively.20*26 A large aneurysm may erode adjacent bone or compress pulmonary arteries or veins. SVC syndrome may rarely be a presenting feature.22 Patients with impending or actual rupture frequently experience severe chest pain.‘0*23325Rupture is usually into the left pleural cavity but may also extend into the mediastinum, right pleural cavity, pericardium, or adjacent lung. The clinical presentation of mycotic aneurysm is varied and nonspecific. Malaise, weakness, low grade fever, and chills may be present. The clinical picture may be that of the primary underlying process, such as endocarditis, pneumonia, or osteomyelitis. The aneurysm does not usually reach a large enough size to produce intrathoracic signs and symptoms. As with other aneurysms, severe chest pain is usually associated with rapid enlargement or rupture. C:T TECHNIQUE
Initially a scanogram is performed. Axial unenhanced images are directed to specific areas
Fig 12. Aneurysm with ture into the mediastinum. enhanced image at the level the aortic arch demonstrates large aortic arch aneurysm Note the high attenuation diastinal hemstoma (HI.
rupUnof a (‘1. me-
of interest. These initial images are important for identifying and evaluating vascular calcification (Fig 8). Unenhanced scans may be sufficient for follow-up of known aortic disease. In most cases, however, intravenous contrast is needed. Dynamic scans are obtained following a bolus of about 25 mL of contrast material, if an aortic dissection is suspected, or if differentiation from a mediastinal mass is necessary. In a patient being evaluated for aneurysm, incremental l-cm thick images are obtained at 2-cm intervals, from the top of the aortic arch to the diaphragm during rapid drip infusion of intravenous contrast medium. The scans are continued to the aortic bifurcation if the aorta is abnormal at the level of the diaphragm or if a second aneurysm is a possibility. CT Findings
The criteria for the diagnosis of aortic aneurysm are well established.6”4 Focal or diffuse aortic dilatation and deformity, as well as the length of the aneurysm are readily apparent on unenhanced scans. Localization of the calcification relative to the wall of the aorta is important in differentiating dissections from aneurysm. In aortic dissection, the intimal calcification is characteristically displaced internally, whereas calcification is peripheral in aneurysm (Fig calcification has been 8). 7*‘2,‘3 Peripheral reported in about 75% of aortic aneurysms.‘3*4’
16
CT is superior to angiography in evaluating the true diameter of the aneurysm because of better visualization of mural thrombus. Intravenous contrast material is required to differentiate the patent lumen and mural thrombus (Figs 3 and 4). Thrombus may be circumferential or
POSNIAK,
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crescentic. Fine punctate calcification may occasionally be seen in the thrombus. There is a direct relationship between the size of the aneurysm and the amount of thrombus.13 Knowledge of the position and amount of mural thrombus may be important in surgical planning.4’
Fig 13. Posterior mediastinal toma resembling an aneurysm. a fusiform posterior mediastinal CT image in the lower thorax aorta (A) displaced anteriorly by mass (M). (C) Lateral thoracic aorta.
malignant fibrous histiocy(A) PA chest radiograph shows mass (arrows). (B) Enhanced demonstrates a normal sited an inhomogeneous soft tissue aortogram reveals a normal
THORACIC
ANEURYSMS
CT clearly demonstrates the relationship of the aortic aneurysm to adjacent structures. Subtle erosion of bone may be appreciated by adjusting the window width and level to appropriate values. Compression of the tracheobronchial tree, the pulmonary arteries and veins, as well as the SVC, are easily identified (Figs 9 through 1 1).42,43 Esophageal displacement or obstruction may be seen (Figs 1 and 9). Angiography is required only if the relationship of the aneurysm to the great vessels needs to be evaluated or aortic insufficiency requires demonstration. CT is especially useful in evaluating a patient for impending or actual aortic rupture. The aorta may rupture into the mediastinum, pericardium, or either pleural sac or extrapleural space (Fig
17
12). High attenuation fluid at these sites is suggestive of rupture.‘2*44 Central displacement of peripheral calcification has been described as a sign of early disruption of the aortic wall.13 Aortobronchopulmonary fistula is rare. It is manifested as consolidation of the lung adjacent to the aneurysm.4s CT is the primary method used to differentiate a mediastinal or paramediastinal lung mass from saccular aortic aneurysms (Fig 13).46 Single level dynamic scanning following a rapid bolus injection of contrast medium is imperative in this situation, This is done in order to create as large a density difference as possible between the intraluminal blood and the surrounding soft tissue. With a drip infusion, a para-aortic mass may enhance sufficiently to make the differentiation
Postoperative infection. (A) Unenhancad image three days folFig 14. lowing repair of a descending aortic aneurysm. Note the high density hemorrhage (HI between the graft (A) and the native aortic wall (arrows). (B) Ten days later. The hemorrhage has mostly resolved. A large amount of gas (01 is now present between the graft (A) and aortic wall, indmting infection. This was confirmed at surgery. (Cl Another patient. Fluid (F) and a small amount of gas (small arrows) between the graft (AI and the native aortic wall eight days after surgery. This resolved spontaneously. indicating a normal postoperative appearance.
18
very difficult or impossible. Differentiation may also be difficult following a bolus in the rare patient who has a noncalcified saccular aneurysm which is completely clot-filled. In this situation, however, no enhancement should occur in the thrombus, whereas most tumors demonstrate at least minimal enhancement. CT plays an important role in following a patient after surgical repair of an aneurysm. After making the graft secure, the aortic wall is often wrapped around it and the incision sutured. This leaves a potential space between the graft and the native aorta.47 A small amount of blood and gas may normally be present in this space in
POSNIAK,
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the immediate postoperative period. Suture dehiscence, either proximally or distally, will result in blood leaking into the space. This is readily apparent on CT. On enhanced singlelevel dynamic images, contrast material will be identified within this space. In more chronic cases, there may be thrombus in the space. Aortic graft infection is a rare but potentially lethal complication of aortic surgery. Although the CT appearance of an infected thoracic aortic graft has not been described, it can be expected to be similar to abdominal aortic graft infection. Any fluid between the graft and native aorta six weeks following surgery is highly suspicious of
Fig 15. Buckled innominate artery. The patient had a palpable pulsating right supraclavicular mass. (A) Right auperior mediastinal mass that stops at the clavicle. indicating an anterior location fcervicothoracic sign). (B) Venous angiogram, of less than optimal quality, was interpreted as showing an aneurysm of the innominate artery. W Retouched copy of (BL illustrating the findings at operation. The cleft created by the U-turn of the innominate artery was not appreciated in (B).
THORACIC
ANEURYSMS
Fig 16. Tuberculous mycotic aneurysm of the aorta, proved at operation. (A) Admission teleroentgenogram. Innumerable miliary lesions are present throughout both lungs. (B) About 5 weeks later, after antituberculous therapy. The miliary lesions have almost disappeared, but a mass is now noted in the vicinity of the aortic knob. It was present but smaller and overlooked in (A). (C) Catheter aortogram shows a bilobed aneurysm in the region of the aortic knob.
19
20
POSNIAK,
graft infection. It has been reported that gas in this space more than 2 weeks after surgery is virtually pathognomonic of infection (Fig 14).48 Postoperative scanning is particularly important in those patients who have multiple aneurysms or who have a predisposition for new aneurysm formation. This is especially important in Marfan syndrome. MRI
Early reports indicate that MRI may have an important role in evaluating patients with aortic and paraaortic pathology.4g-52 However, more experience is required, and it will have to be shown to be significantly better than CT in order to overcome the limitation of the relatively high cost of the examination. EDITOR’S
ADDENDA
A fairly common condition that may closely resemble an aneurysm is the buckled innominate artery. In the patient illustrated in Fig !5 this mistake was actually made from a poor quality venous angiocardiogram (before the days of digital subtraction angiography). The case illustrated in Fig 16 is a fascinating example of a tuberculous mycotic aneurysm of the aortic arch, a component of an even more fascinating series of coincidences. The patient appeared at our institution following onset of weakness, cough, and chest pain. She was an elderly black woman. Despite the lack of fever, the widespread miliary pattern strongly suggested miliary tuberculosis, and this diagnosis was confirmed by bone marrow study. She was started on antituberculous therapy.
DEMOS,
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A few days later, on a visit to Massachusetts General Hospital, I was shown the chest films of an elderly febrile Chinese woman with recent onset of a miliary pattern, associated with a growing mass contiguous with the aortic knob. I raised the question of miliary tuberculosis with mycotic aneurysm of the aortic arch, which proved to be the diagnosis. When I came back to Cincinnati, our case of miliary tuberculosis again crossed my desk. The lungs had cleared, but now there was an enlarging aortic mass! The diagnosis of mycotic tuberculous aneurysm was quickly confirmed by angiography and operation. A month or so later, in Spain, I saw a third case, similar to the first two. The three cases were combined and published in JAMA. Tuberculous mycotic aneurysm of large arteries is not so rare. Well over 100 cases have been reported. If undiagnosed and untreated, the condition is almost uniformly fatal, but if recognized, surgical cure is the rule. The condition is often caused by direct extension from an adjacent tuberculous focus, usually lymphadenitis or Pott’s abscess. Many of the patients have acute miliary tuberculosis. There is considerable evidence to indicate that the miliary dissemination is often the result of the mycotic aneurysm rather than its cause, and follows discharge of organisms from the aneurysm into the bloodstream. Benjamin Felson Editor ACKNOWLEDGMENT Our thanks to Barbara Medley for assistance in preparation of this manuscript.
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by conventional and dynamic CT scanning. Radiology 1980;136:125-33 8. Egan TJ, Neiman HL, Herman RJ, et al: Computed tomography in the diagnosis of aortic aneurysm dissection or traumatic injury. Radiology 1980; 136: 141-6 9. Pond GD, Hillman B: Evaluation of aneurysms by computed tomography. Surgery 1981;89:216-23 10. Godwin JD, Korobkin M: Acute disease of the aorta. Diagnosis by computed tomography and ultrasonography. Radio1
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11. Goodman LR, Teplick SK: Computed tomography in acute cardiopulmonary disease. Radio1 Clin North Am 1983;21:741-58 12. Godwin JD: Examination of the thoracic aorta by computed tomography. Chest 1984;85:564-7 13. Heiberg E, Wolverson MK, Sundaram M, et al: CT characteristics of aortic atherosclerotic aneurysm versus aortic dissection. J Comput Assist Tomogr 1985;9:78-83
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ANEURYSMS
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