CT of aortic dissection

CT of Aortic Dissection By Terrence

C. Demos,

Harold

V. Posniak,

K

ING GEORGE II of England (1683-1760) died suddenly while straining on the commode. At autopsy there was a hematoma of the ascending aortic wall, an intimal tear, and blood in the pericardium. The prosector interpreted this as a saccular aneurysm, but these findings are now considered to be the first description of an aortic dissection (AD).‘*’ Untreated AD causes death in a vast majority of patients; sudden death in 3%, death within one day in 21%, 1 week in 62%, 1 month in 80%, and within 1 year in 95%.2 Since the introduction of surgical intervention in 1955 and medical treatment in 1965, the prognosis of this lethal disease has improved dramatically. An overall actuarial lo-year survival of 40% has been achieved, while 1O-year survival for those leaving the hospital has been about 60%.3*4 Obviously early diagnosis is crucial, and CT has now been established as an accurate noninvasive means of recognizing it.“15

and

Richard

E. Marsan

Traumatic dissection is a term sometimes used in referring to fracture of the aorta produced by blunt trauma. This should not be confused with spontaneous AD. The two most common sites of AD and traumatic injury are the same: the proximal ascending aorta, and the descending aorta just distal to the left subclavian artery. Aside from this similarity, however, AD is quite different than traumatic injury. The traumatized aorta is lacerated, and all layers of the aortic wall are involved to varying degrees. The laceration is usually transverse with only minor longitudinal extension. Saccular false aneurysm commonly occurs at the site of fracture. In spontaneous AD the initiating tear of the aortic wall is confined to the intima. There is major longitudinal dissection selectively involving the media, and the aortic dilation is usually fusiform. External trauma rarely causes a long segment of dissection such as that found in spontaneous AD.2

Definitions Pathogenesis

AD is characterized by longitudinal separation of the wall by circulating blood that has gained access to the media.16 The term dissecting aneurysm has been used for this entity, but is a misnomer. It is the blood in the aortic wall that dissects, and the aorta itself may be only slightly dilated or not dilated at all. Aortic dissection (AD) is a more accurate descriptive designation for this disease.

In the 19th century it was believed that an intimal tear initiated the dissection of the aortic wall. In this century, until the 1970s it was generally believed that an underlying specific, but idiopathic cystic medial necrosis of the aorta was the primary cause of AD. It was hypothesized that the disease of the media led to rupture of the vasa vasorum resulting in hematoma, which then dissected the aortic wa11.2V*6,17 The pendulum has swung back, and it is now increasingly accepted that AD is initiated by an intimal tear, which is the entry site that allows the blood stream access to the aortic media.3,‘7-19 In an extensive literature review of 505 published cases, Hirst et al2 found that 4% of the cases had no entry site to account for the AD. In a careful study of 158 autopsied cases from one institution, 100% had an intimal tear.17 Opinions concerning the nature and importance of aortic wall changes in AD have also changed. Degeneration of the elastic and muscle tissue of the media of the aorta is found in AD, but it is neither cystic nor necrotic.16 More important, the medial degeneration is not specific, but is due to aging, and usually is no different

ABBREVIATIONS AD, aortic dissection AP, anteroposterior GE, General Electric Co. HRCT, High resolution computed tomography

From Medical

of Radiology, Loyola University IL. Terrence. C. Demos: Professor of Radiology; Harold V. Posniak: Assistant Professor of Radiology; Richard E. Marsan: Associate Professor of Radiology. Address reprint requests to Terrence C. Demos, MD, Department of Radiology. Loyola University Medical Center. 2160 S First Ave. Maywood, IL 60153. 0 I989 by Grune & Stratton, Inc. 0037-198X/89/2401-0002$5.00/0

22

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CT OF AORTIC

than in elderly patients without AD. An exception is Marfan syndrome, in which severe changes in the media are found in young patients.‘77’8 Thus degeneration of the media probably plays a secondary role in AD. Dissection may occur even when the media appears histologically normal.” Intimal tears are probably the result of mechanical forces acting on the aorta. The heart is suspended by the great vessels and confined between the sternum and vertebral column, so that motion is primarily from side to side like a pendulum. Resultant flexing strain of the aorta is greatest near two relatively fixed points: at the isthmus between the origin of the left subclavian artery and the insertion of the ligamentum arteriosum, and at the aortic valve. It is precisely at these two sites, in the proximal ascending aorta and just distal to the left subclavian artery, that a large majority of intimal tears occur.2*19 Classification

ADS have been classified by DeBakey as type I, originating in the ascending aorta and extending to the aortic arch and a variable distance beyond; type II, confined to the ascending aorta; and type III, originating in the descending aorta and extending a variable distance distally. More recently, an AD involving the ascending aorta is classified as proximal (type A), whereas one originating in the descending aorta is termed distal (type B) dissection. Since involvement of the ascending aorta is of primary importance in determining treatment and prognosis, the latter classification is now in general use. Proximal AD is almost always treated surgically, while distal AD has a better prognosis and is usually treated medically.3,4 Dissection of the aorta usually extends distally in the direction of blood flow. When it extends proximally, it is termed retrograde dissection. Catheter-induced dissection is often retrograde. An AD less than 2 weeks old is arbitrarily defined as acute, and one present for more than 2 weeks is defined as chronic.‘v3 Predisposing

23

DISSECTION

Factors

Degenerative changes of the aortic media are commonly present and evidence of past or present hypertension, such as left ventricular hypertrophy or cardiomegaly, is reported in up to 90%

of patients.2T’3,‘8 Hypertension may accelerate the degenerative changes in the aortic media.‘7*‘9 About half the patients under age 40 with AD have some underlying abnormality. Congenital bicuspid or unicuspid aortic valve is an important predisposing factor.” The incidence of AD in Marfan syndrome is high; the dissection is often confined to the ascending aorta. Ehlers-Danlos, Turner, and Noonan syndromes; coarctation; and relapsing polychondritis may be complicated by AD. Coarctation is the most common cause in children under age 16.16 Half of the ADS in women under age 40 are associated with pregnancy. ” Other rare associations include systemic lupus erythematosus and giant cell arteritis.16vi7 Arteriosclerosis is not an important factor in spontaneous AD, but does increase the incidence of iatrogenic dissection.2,‘6*21 Iatrogenic dissection has occurred at the sites of aortic incision, cross-clamping, cannulation, catheterization, and aortic valve replacement.‘6*‘9~22’23 We have seen a patient who developed distal AD shortly after an aortic-assist balloon pump was inserted. Gross Pathology

A primary intimal tear in the proximal aorta is referred to as an entry point in order to distinguish it from a secondary tear more distally, which is a point of re-entry. In some cases there is only an entry point, but there may be multiple entry and re-entry points. These communications between the true and false lumen account for the fact that the false lumen usually remains patent following surgical procedures. About 90% of the entry points in proximal AD occur within the first 4 cm of the ascending aorta. More than 90% of entry points in distal AD occur at the aortic isthmus or in the proximal descending aorta.* The longitudinal separation of the aortic wall takes place within the middle to outer third of the media, so that the dissected aorta then has a true and a false lumen. The dissection channel tends to spiral as it follows the outer curve of the aorta. The false lumen is usually anterior and to the right in the ascending aorta, superior and slightly posterior in the arch, and posterior and to the left in the descending aorta. The true lumen is often compressed. The dissection frequently extends for a long distance and often involves branch arteries along the way. At autopsy the arch vessels are involved in about half the patients, the

24

renal arteries in one fourth, and the iliac vessels in about half. The incidence of branch involvement is less in living patients. The involved vessels may be perfused by blood from the false lumen, the true lumen, or both. The arterial branches may also be narrowed or occluded. When chronic, the false lumen becomes endothelialized and may develop atheromas that may calcify.*,16 Death is usually due to rupture of the false lumen. Intrapericardial rupture causing cardiac tamponade is the most common cause of death and was found at autopsy in 70% of those with proximal AD. Distal AD sometimes causes death by rupturing into the left pleural space. Left pleural hemorrhage was found in about 4% of autopsies with distal AD.*,16 Rupture into the right pleural cavity, mediastinum, retroperitoneum, or peritoneal cavity is less common.19 Rupture without exsanguination may occur when the false lumen communicates with the right atrium, right ventricle, or pulmonary artery. Rarely, the false lumen compresses or occludes the right pulmonary artery or superior vena cava.24 Proximal aortic dissection is more common in most autopsy series; while distal dissection is more common in some clinical series. This probably reflects the higher early mortality in patients with proximal AD.2*17*25 Incidence

It is estimated that 2,000 dissections occur yearly in the United States, which is more than all aneurysmal ruptures of the thoracic and abdominal aorta combined. The autopsy incidence is about one in 400. Men are affected more often than women, and the peak incidence is about 60 years of age.*,13 Signs and Symptoms

Chest pain, the most common symptom, is present in 95% of patients.23 The pain is usually acute, severe, and maximal at onset. Proximal AD more often produces anterior chest pain, while posterior chest pain is most frequent with distal dissection. The pain tends to migrate and sometimes corresponds to progression of the dissection. Pain may radiate to the head and neck, low back, or abdomen.2*2’~25 Even though the patient may appear to be in shock, the blood pressure is often elevated, espe-

DEMOS,

POSNIAK,

AND

MARSAN

cially with distal AD. A diminished or absent pulse due to involvement of an aortic branch is an important sign of dissection. A pulse deficit occurs in up to one half of proximal and one sixth of distal dissections.2,25 Appearance of an aortic insufficiency murmur is an important sign of involvement of the aortic valve.23 Patients with proximal AD may present with neurologic findings, including stroke, paraparesis, or paraplegia. Proximal or distal AD may cause peripheral neuropathy due to ischemia. Rare associated conditions include myocardial infarction, superior vena caval syndrome, hemoptysis, hematemesis, vocal cord paralysis, Horner syndrome, and fever of unknown origin. 2*21*25Congestive heart failure is rare, almost always due to aortic insufficiency. Syncope is also rare and may reflect cardiac tamponade. Acute AD has masqueraded as ureteral colic, gastrointestinal disease, and peripheral vascular embolism.2*24V26 RADIOLOGIC

FINDINGS

Plain Chest Radiography

The diagnosis of AD can occasionally be made from chest radiographs. A high incidence of abnormal findings is reported, but the findings are usually nonspecific.*‘-” Mediastinal widening and various aortic abnormalities are commonly seen, but most of these findings are also common in this age group.*’ The chest is normal in up to 25% of patients.30 When a patient presents in the emergency room, it is important to quickly obtain any previous films for comparison. Demonstration of changes in configuration or size of the aorta or mediastinum on serial films is highly suggestive (Fig 1). Internal displacement of intimal calcification more than 1 cm (Fig 2), and marked disparity in the size of the ascending and descending aorta are useful signs, especially when absent on previous films. Displacement of intimal calcification is only reliable if the plaque is in profile. On the PA view, apparent internal displacement of calcification in the aortic knob may be produced when the calcific plaque is in a different coronal plane than the border-forming segment of the aortic knob.** Displaced calcification is a more reliable sign when found on axial CT images.

CT OF AORTIC

DISSECTION

25

Fig 1. Acute distal aortic dissection (type Ill). (A) Emergency room radiograph shows a focal bulge of the proximal descending aorta. A radiograph 6 months earlier had shown only a tortuous aorta. (Bl Unenhanced CT image shows an intimal flap (arrows) in the descending aorta. (Cl Enhanced CT image shows the intimal flap (arrows) between the central compressed true lumen and the surrounding false lumen.

Angiography

Angiography has been the standard for diagnosis of AD for decades. Injection is made directly into the aorta. Right posterior oblique and AP or biplane AP and lateral views are generally obtained.3@‘32 Direct signsof AD are detection of an intimal flap and the presence of two aortic lumens. The flap will not be demonstrated unlessit is tangential to the x-ray beam. Indirect signs of AD include compressionof the true lumen, abnormal catheter position, aortic insufficiency, aortic branch involvement, ulcer-like projections caused by truncated branches, and thickening of the aortic wa11.27S3G34 In about 20% of patients,

only one aortic channel is opacified. The angiographic diagnosis is then based on indirect and sometimes subtle signs. In some casesthe only abnormality is a thickened aortic wall. This is not specific for AD since an identical appearance may be due to thrombus in an aneurysm, aortitis. mediastinal hematoma, or neoplasm contiguous with the aorta.3’.32.34 Advantages and Disadvantages of Angiography (cf CT section) Although 100% accuracy in the angiographic diagnosisof AD has been reported,30*34 one study indicated diagnostic difficulties in ten of 44

26

Fig 2. atheromatous descending

DEMOS,

Chronic distal (type III) aortic dissection. plaques in the aortic knob (arrows). aorta.

(A) (6)

Closeup Lateral

patients.3’ The overall accuracy, averaging several large series, is about 97%.12330*34V35 Falsenegative studies have been reported in at least 16 patients 5*12*13,‘5*31P3s-40; 12 had CT and ten of these were positive. 5~12~13~‘5,35-38 There have been two patients with proximal AD on CT that had been diagnosed as distal AD on angiography.” Angiography is superior to CT in several respects. Spatial resolution is better. Entry and reentry points, aortic insufficiency, coronary arteries, and branch vessel involvement are shown in better detail, and the true lumen can more often be differentiated from the false lumen.‘2,15 The importance of these superiorities in the management of the patient with acute dissection is open to question.‘3*41 The entry and reentry points are identified on only about half the angiograms,27”0,34 and there is evidence that leaving the entry point in situ when a graft is placed does not affect survival.4 It is also well known that the false lumen remains patent in a large majority of patients following any type of surgery.42m45The need for aortic valve

of chest radiograph

PA radiograph shows shows displacement

POSNIAK,

AND

internally displaced of plaques in the

MARSAN

calcified arch and

surgery is determined by the surgeon during the operation.41 The goal of surgery for acute AD is not to cure the dissection, but to prevent life-threatening local complications such as rupture into the pericardium or pleural space and progressive aortic insufficiency. This is done by either primary repair of the entry intimal tear, buttressing of the aorta, and oversewing the true and false lumens, or more often by replacing a relatively short segment of aorta with a graft. If necessary, the aortic valve is replaced or resuspended.334 Many recent articles state that angiography is preferred or even indispensable prior to surA growing number of surgeons, howgery. 9~15,23346 ever, operate after a CT study and believe that angiography is not needed in most cases.1’,‘3*‘4 The radiologist should be familiar with the beliefs and prejudices of his own surgical colleagues so that the patient can be evaluated as efficiently as possible. Delay in surgery and excess intravenous contrast material, the result of doing both CT and angiography, may be

CT OF AORTIC

DISSECTION

27

Fig 3. MRI in postoperative proximal (type I) aortic dissection. MRI is an asymptomatic postoperative patient. Ascending aorta (AA). descending aorta (DA), pulmonary artery (PA), intimal flap (straight arrows). (A) Oblique sagittal TI-weighted image. (B) Axial TI-weighted image. (C) Axial echo gradient (Grass) image. High signal in the true and false lumens confirms the flow and better demonstrates the intervening axillary-femoral bypass graft which is patent also (curved arrow).

significant factors in patient morbidity tality.

and mor-

Sonography

Two-dimensional real time echocardiography may clearly define the anatomy of the ascending aorta. A high percentage of proximal AD can be detected, but the distal aorta cannot be evaluated. Echocardiography has been used for

screening, but the examination is dependent on operator skill. False positive studies are frequent and collective experience is too small to assess accuracy.4’ Transesophageal echocardiography has been used to detect distal dissection4’ MRI

Early results indicate that MRI is as accurate as angiography and CT in diagnosing acute and

DEMOS,

28

chronic AD.“S,48M50 Excellent results, however, do require considerable experience. Coronal and sagittal planes are both useful, and information concerning flow and thrombus in the false lumen can be obtained (Fig 3). Important limitations are the presence of a heart pacer or a life support system that cannot be brought into the magnetic field. CT Technique

In the diagnosis of aortic dissection, the manner in which the CT examination is performed is as important as the interpretation of the images.13 Using a GE 9800 machine, we begin the study with a supine digital scout radiograph. From above the aortic arch to the diaphragm, l-cm thick sections are then obtained at 2-cm intervals. These sections are viewed for evidence of aortic dissection and then used to select three sites for single-level dynamic scanning: the aortic

Fig 4. midascending the aortic brachiocephalic 1).

POSNIAK,

AND

MARSAN

root, midascending aorta, and aortic arch (Fig 4). It is of utmost importance not only to identify AD, but to determine if the ascending aorta is involved since acute proximal AD is generally treated surgically, while distal AD is usually treated medically. Coverage of the aorta with three bolus injections provides three chances to identify a subtle intimal flap and, in addition, decreases the likelihood of missing a short AD confined to the ascending aorta.10*‘3 The patient is coached in end-inspiratory breath holding without the Valsalva maneuver. A 19-gauge butterfly needle is inserted into the basilic vein in the antecubital fossa and taped in place. An axial section is then taken at one of the previously selected levels. After the level has been reaffirmed, a bolus of 25 to 40 mL of 60% contrast material is injected by hand in less than ten seconds. In order to catch the peak of aortic enhancement, six to eight images are made dynamically (Fig 5). The timing of the first

Acute distal (type III) aortic dissection. Three bolus injections are given at: (1) aortic arch (AA) level, (2) aorta (MI level, and (3) aortic root (RI level. These levels are indicated on the digital scout film. The intimal flap in arch is barely visible. The ventral true lumen (black arrow) is more densely opacifiad than the false lumen. The vain (long white arrow) and innominate artery (short white arrow) could be mistaken for dissection (image

CT OF AORTIC

DISSECTION

29

Fig 5. Acute distal (type ill) aortic dissection. Dynamic single level series of CT images at root of aorta. The compressed true lumen (arrows) opacifies before the false lumen (FL Note that the ascending aorta (AA) is densely opacified only on images 3 and 4.

image in relation to the injection depends on the patient’s circulation time and the type of CT machine. The primary goal is to identify involvement of the ascending aorta. If a proximal dissection is found following the first bolus, the aorta is then examined during rapid infusion of contrast material in order to determine the extent of distal and branch involvement (Fig 6). Even if the aorta at the first level is normaI, or if dissection appears to be confined to the descending aorta, bolus injections are still made at the other two levels in order to make certain that dissection involving the ascending aorta is not missed. More caudal sections may be taken after the additional bolus injections in order to determine the extent of distal involvement. The nephrogram will give an indirect indication of blood supply to the kidneys (Fig 6). If there are no clinical signs or symptoms indicating vascular compromise of the viscera or extremities, the extent of distal involvement is seldom important. CT Findings

Table 1 lists the CT signs of aortic dissection on unenhanced and enhanced images. A specific diagnosis can be made when two opacified aortic lumens separated by an intimal flap are identi-

fied (Figs 1, 4 to 7). If the patient is anemic, the intimal flap may be visible on an unenhanced CT (Fig 1).5’ The intimal flap is usually thin and may be missed if flow in the two lumens is nearly equal. In this case, intense opacification of the aorta is crucial. Bolus injection of contrast material gives more intense opacification than does drip infusion, but even then it must be given as rapidly as possible and the scanning timed to catch peak aortic enhancement (Fig 8). The more images made during passage of the bolus, the easier it is to capture this peak (Fig 5). Rapid sequence scans may also depict the changing density of the false lumen compared to the density of the true lumen. Opacification of the false lumen is often delayed (Fig 5). Newer CT scanners may provide high-quality images with rapid drip infusion, but infusion will not depict the serial density changes in the true and false lumen. In addition, the enhancement of the aorta is not as great as with rapid bolus injection. The false lumen is thrombosed in at least 10% of patients so that it does not opacify on either CT or angiography.30*3’*34 Such a lesion may be difficult or impossible to differentiate from an aneurysm containing thrombus. In general, the

DEMOS,

POSNIAK,

AND

MARSAN

Fig 6. Postoperative distal (type Ill) aortic dissection. The patient was asymptomatic. (A) The true lumen (T) is compressed by the false lumen, which contains flowing blood IF) end circumferential thrombus. (B) At the level of the kidneys the true lumen (T) is ventral and the false lumen with thrombus and flowing blood (F) is dorsal. The left renal artery (arrow) comas off the true lumen. Normal nephrograms indicate adequate perfusion of both kidneys. Note that the true lumen has spiraled. (C) Dissection continues to the left common iliac artery which is dilated. The true lumen (arrow) is ventral.

aneurysm is focal, has a dilated lumen, and may contain peripheral calcification; whereas AD usually involves a longer length of aorta, compresses the true lumen, extends in a spiral manner, and may show internal calcification. Internally displaced calcification strongly suggests AD, but may be mimicked by calcium on

the luminal surface or within the clot in aneurysm.52,s3 Conversely, the endothelialized surface of the false lumen in chronic AD may become calcified after some months and produce peripheral calcification. Thus, none of the signs differentiating aneurysm from AD are specific, but a combination of them strongly suggests the

CT OF AORTIC

Table

DISSECTION

1.

31

CT Signs

of Aortic

Dissection

Unenhanced

Enhanced

Displaced calcification Visible intimal flap

lntimal

Two aortic Compressed

High density thrombosed false lumen Pericaridial or pleural fluid (high density) blood Dilated

aorta

flap

or

Branch

lumens true lumen

involvement

Pericardial

or pleural

leakage

of blood

diagnosis of AD. Acute thrombus in the false lumen of an AD may be hyperdense on unenhanced CT (Fig 9); when this finding is noted, a confident diagnosis of acute dissection can be made.j* In some patients it is not possible to differentiate a fusiform aneurysm from AD by any study. Fig 7. Acute proximal (type I) aortic dissection. The pericardium is thickened and there is high attenuation acute intraparicardial hemorrhage (HI. The false lumen (F) in the ascending aorta is aneurysmally dilated and the true lumen compressed. The intimal flap in the ascending aorta is clearly seen (arrows): that in the descending aorta is barely visible. (Courtesy of Dr Joseph Porada. St. James Hospital, Chicago Heights, IL.)

An intimal flap may be invisible at the peak of aortic opacification when the console is viewed with soft tissue settings. The flap will usually become visible with either a very high window level or very wide window width. It is also important to view the region with a narrow window width in order to detect a small density difference between the false and true lumens. 240 240-,

A

1

\\

\

180

A

\

160 140 140 128 -~

\ \ A

188 ‘, \ 80

Fig 8. Graph of sonic attenuation after rapid bolus injection. Peak enhancement lasts for lass than 10 seconds. Dynamic scanning is needed to consistently catch this peak. Drip infusion of contrast material will not produce enhancement to this level.

60-, 40-. l’“‘1’“‘l’“‘l’“‘~“’ 0

5

15

10 SECONDS

20

32

DEMOS,

POSNIAK,

AND

MARSAN

Fig 9. Acute distal (type III) aortic dissection with rupture into mediastinum. A totally thrombosed false lumen (arrows) and mediastinal hemorrhage (‘1 show high attenuation on this unenhanced CT. The patient was not a surgical candidate. Autopsy confirmed the diagnosis.

Streak artifacts due to cardiac movement (Fig lo), calcification, or a high-contrast interface commonly simulate an intimal flap or low attenuation false lumen. They are recognizable as artifacts because they are also present on unenhanced images, are confined to one level, and may be seen as one of many line artifacts that are

Fig 10. Artifact produced by heart motion. The artifact, caused by left ventricular motion, crosses the descending aorta (arrows), and simulates dissection. Note that the aorta on images above and below the artifact is normal.

Fig 11. Left brachiocephalic vein simulating dissection. CT level at bottom of the aortic arch shows a densely opecified vein (arrows) contiguous with the less opacified aorte. Note also the parallel streak artifacts crossing the aorta.

CT OF AORTIC

DISSECTION

Fig 13. Sinus of Valsalva simulating an intimal flap. The curvilinear defects (black arrows) represent the sinuses of Valsalva. The circumflex branch of the left coronary artery (white arrow) indicates that this image is at the level of the sinuses.

parallel or radiate from a point (Fig 11). Artifacts often extend beyond the aorta. Internally displaced calcified plaques indicate dissection (Fig 12). However, volume averaging when a calcified segment of aorta forms a sharp angle with the axial plane may give a false appearance of displacement. This commonly occurs at the top or bottom of the aortic arch or at the margin of a tortuous segment of the aorta. Scanning with narrower collimation will show the true peripheral location of the calcification. Enhanced vessels contiguous with the aorta (Fig 1 l), or a normal sinus of Valsalva (Fig 13) may simulate a false lumen. Demonstration of a proximal coronary artery helps identify the sinus. Knowledge of normal anatomy, tracing the course of the vessel on adjacent sections, and the focal nature of the finding should prevent falsepositive diagnosis. Pericardial or pleural thickening and atelectatic lung may strikingly enhance and simulate a false lumen or even a hemorrhagic leak. Often atelectatic lung will contain some air (Fig 14). The superior preaortic or retroaortic pericardial recess may be mistaken for a false lumen but is recognized by its focal

DEMOS,

POSNIAK,

AND

MARSAN

studies. Our experience over the past 9 years indicates that multiple bolus CT is as accurate as angiography in diagnosing aortic dissection. If the false lumen is totally thrombosed, however, CT is more accurate than angiography. It is our opinion, and that of others, that angiography should be done in any patient whose signs and symptoms strongly suggest AD, even if an adequate CT study is negative.13 Conversely, a negative angiogram should be followed by CT when clinical suspicion is high.

Fig 15. Fluid in the preaortic pericardial recess simulating aortic dissection. CT section at level of bottom of the aortic arch. Fluid in the recess (arrows) curves around the ascending aortic {AA), simulating dissection. C, superior vena cava: DA, descending aorta; N. lymph node. (Courtesy of Dr. Enrique Palacios, MacNeel Memorial Hospital, Berwyn, IL.)

Postoperative Evaluation Patients who survive treatment for acute AD are subject to several late complications that may lead to death or to the need for an additional surgical procedure. In the largest reported series, 29% of 527 patients, followed for 20 years after surgery, died from rupture of an aortic aneurysm

nature and characteristic location (Fig 15). A saccular aneurysm that bulges alongside the adjacent undilated aorta may also mimic AD if it has a narrow neck that is not visible.13 Accuracy High resolution CT (HRCT) has several advantages over angiography in AD. It is less invasive. Fluid and blood in the pericardial, pleural, and mediastinal spaces can be identified (Figs 7 and 9). The intimal flap is more often visible on axial images, and, since CT can demonstrate recent blood clot, an acutely thrombosed false lumen can be diagnosed (Fig 9). Although 100% accuracy has been reported for CT,7,8,%‘1,15in one series four of 76 cases with adequate examination were falsely negative.14 The overall accuracy in a number of series averaged about ~S%L~~‘~ False-negative studies have been reported in at least 10 patients; 8 had angiography, and 6 of these were positive.6*‘2~‘4~40~55An autopsied case has been reported in which three angiograms and one CT study failed to demonstrate the dissection.3g Two false positive CT studies have also been reported.13*@ The diagnosis of AD can be difficult. We have had several false negative CT and angiographic

Fig 16. Postoperative proximal (type I) aortic dissection. Asymptomatic patient with Marfan syndrome one year after grafting of ascending aorta and aortic valve replacement. The false lumen has remained widely patent. (A,Bj CT image just below aortic arch shows different rates of opacification of false lumen IF) and true lumen (Tj following a bolus injection of intravenous contrast material. The intimal flap separates the two lumens.

CT OF AORTIC

35

DISSECTION

Fig 17. Proximal (type I) aortic dissection four days postoperative. A graft (G) had been placed in the ascending aorta. The graft wall and opaque teflon buttresses are visible on scout image 1. After bolus injection there is intense enhancement of the perigraft space (H) indicating suture dehiscence (image 4). The patient was taken to surgery and there was a large, tense pseudoaneurysm surrounding the graft. The patient survived after a second surgical procedure. PA, pulmonary artery, C. cava.

or false aneurysm.56 In another study of 135 patients, 18% died within 10 years after surgery and 13% required an additional surgical procedure.4 In a more recent report, only three of 119 surgical patients followed for a mean of 4 years required additional surgery. Patients with Marfan syndrome have a much higher late complication rate than other patients.23 The three most common late complications are aneurysm or pseudoaneurysm contiguous with the dissected aorta or distal to it, progressive aortic insufficiency, and redissection or extension of the dissection.4,22,23,56 The usual surgical procedure on the aorta is a graft, with the native aorta wrapped around the repair. On follow-up angiography or CT there should be no blood flow or extravasation of contrast material between the graft and native

aorta. Suture dihiscence at either end of the graft may result in a very small collection of contrast medium adjacent to the graft that may not be significant, or may result in a large pseudoaneurysm that requires reoperation (Fig 17).57 Suture dihiscence may occur in the immediate postoperative period or years later. Chest radiographs,23 CT,44 MRI,45 and angiography42*58 have been used to follow these patients for postoperative complications (Figs 16 and 17). The least invasive and most effective methods for long-term followup are CT (Fig 16) and magnetic resonance (Fig 3). MRI will likely be the method of choice in the future. ACKNOWLEDGMENT Our thanks to Joy B. Stella preparing this manuscript.

for her invaluable

assistance

in

REFERENCES 1. Nicholls F: Observations concerning the body of His Late Majesty. Philos Tram R Sot Lond 1161;52:265-14 2. Hirst AE, Johns VJ, Kime SW: Dissecting aneurysm of the aorta: A review of 505 cases. Medicine 1958;37:217-79 3. Doroghazi RM, Slater E, Desanctis RW, et al: Long term survival of patients with treated aortic dissection. J Am Co11 Cardiol 1984;3:1026-34 4. Haverich A, Miller DC, Scott WC, Mitchell RS, et al: Acute and chronic aortic dissections. Determinants of

term outcome 1985;72(suppl):II22-1134

long

of

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Circulation

5. Godwin JD, Herfkens RL, Skioldebrand CG, et al: Evaluations of dissections and aneurysms of the thoracic aorta by conventional and dynamic CT scanning. Radiology 1980;136:125-33 6. Larde D, Belloir C, Vasile N, et al: Computed phy of aortic dissection. Radiology 1980:136:147-5

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DEMOS,

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