Clinical Features and Diagnosis of Acute Aortic Dissection

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Clinical features and diagnosis of acute aortic dissection
Authors: Warren J Manning, MD, James H Black, III, MD

Section Editors: Emile R Mohler III, MD, James Hoekstra, MD, Joseph L Mills, Sr, MD, John F Eidt, MD
Deputy Editor: Kathryn A Collins, MD, PhD, FACS
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: May 2017. | This topic last updated: Sep 14, 2016.
INTRODUCTION Aortic dissection is relatively uncommon, but it often presents acutely as a catastrophic illness with severe chest pain
and acute hemodynamic compromise. Early and accurate diagnosis and treatment are crucial for survival.
Death from aortic dissection can be related to rupture of the dissection into the pericardium precipitating cardiac tamponade, acute dissection
into the aortic valvular annulus leading to severe aortic regurgitation, obstruction of the coronary artery ostia leading to myocardial infarction,
and end-organ failure due to abdominal aortic branch vessel obstruction [1,2]. The International Registry of Acute Aortic Dissection (IRAD)
has provided a contemporary perspective from the worldwide accrual of patients into a prospective database and allowed assessment of
treatment paradigms. Despite the advances detailed in their reports, the mortality of aortic dissection remains at 25 to 30 percent [3].
The clinical manifestations and diagnosis of acute aortic dissection will be reviewed here. Medical and surgical management are discussed
separately. (See "Management of acute aortic dissection" and "Surgical and endovascular management of type B aortic dissection".)
CLASSIFICATION Aortic dissection is classified, somewhat arbitrarily, as acute or chronic based upon the duration of symptoms at the
time of presentation. During the first two weeks (acute phase), life-threatening complications due to branch involvement or aortic rupture are
more likely to occur compared with the timeframe past two weeks (chronic phase) [4,5].
Anatomic classification The two main anatomic classifications used to classify aortic dissection are the DeBakey and Daily (Stanford)
systems (figure 1) [6-9]. The Stanford system is more widely used. It classifies dissections that involve the ascending aorta as type A,
regardless of the site of the primary intimal tear, and all other dissections as type B. By comparison, the DeBakey system is based upon the
site of origin, with type 1 originating in the ascending aorta and propagating to at least the aortic arch, type 2 originating in and confined to the
ascending aorta, and type 3 originating in the descending aorta and extending distally or proximally. An alternative classification has been
proposed, the DISSECT classification system, which assesses six characteristics of dissection that communicate the most salient details
influencing the choice of treatment, particularly those that are important when considering an endovascular procedure [10].
Ascending aortic dissections are almost twice as common as descending dissections. The right lateral wall of the ascending aorta is the most
common site of aortic dissection [11]. In patients with an ascending aortic dissection, aortic arch involvement occurs in up to 30 percent [12].
Isolated abdominal aortic dissection is reported sporadically and can be due to iatrogenic, spontaneous, or traumatic mechanisms (image 1)
[13]. The infrarenal abdominal aorta is more commonly involved than the suprarenal aorta. In one review of 52 reported cases, the entry site
for spontaneous isolated abdominal aortic dissections (SIAADs) most commonly occurred between the renal arteries and inferior mesenteric
artery [14]. A concomitant abdominal aortic aneurysm was identified in 40 percent of patients and indicated the need for repair. (See
"Management of symptomatic (non-ruptured) and ruptured abdominal aortic aneurysm".)
Variants There are several variants of aortic dissection, including intimal tear without hematoma and intramural hematoma (figure 2)
[7,15,16].
Intimal tear without hematoma Intimal tear without hematoma is an uncommon variant of aortic dissection that is characterized by a
stellate or linear intimal tear associated with exposure of the underlying aortic media or adventitial layers. There is no progression or
separation of the medial layers (image 2) [16]. Blunt aortic injury with focal tear may manifest in this manner.
Aortic intramural hematoma Aortic intramural hematoma, characterized by blood in the wall of the aorta in the absence of an intimal
tear, is another variant of aortic dissection that accounts for 5 to 13 percent of patients with clinical features consistent with an aortic
dissection. The false channel is probably produced by a rupture of the vaso vasorum into the media of the aortic wall and can occur in
the absence of significant atherosclerosis or with concomitant atherosclerotic ulcer. The clinical features and management of this
disorder are discussed separately. (See "Overview of acute aortic syndromes".)
Penetrating atherosclerotic ulcer Penetrating ulceration of an atherosclerotic plaque often complicates an aortic intramural hematoma
and can also lead to aortic dissection or perforation [7]. Noninvasive imaging shows an ulcer-like projection into the hematoma, and
some have suggested that penetrating atherosclerotic ulcers are almost always seen with a type B hematoma (31 of 34 cases in one
series) [17]. (See "Overview of acute aortic syndromes", section on 'Definition and pathophysiology'.)
PATHOPHYSIOLOGY The primary event in aortic dissection is a tear in the aortic intima (image 3). Degeneration of the aortic media, or
cystic medial necrosis, is felt to be a prerequisite for the development of nontraumatic aortic dissection. Blood passes into the aortic media
through the tear, separating the intima from the surrounding media and/or adventitia, and creating a false lumen. It is uncertain whether the
initiating event is a primary rupture of the intima with secondary dissection of the media, or hemorrhage within the media and subsequent
rupture of the overlying intima [11]. (See "Overview of acute aortic syndromes".)
Fifty to 65 percent of aortic intimal tears originate in the ascending aorta within the sinotubular junction and extend to involve remaining
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portions of the thoracoabdominal aorta [3]. Approximately 20 to 30 percent of intimal tears will originate in the vicinity of the left subclavian
artery and extend into the descending thoracic and thoracoabdominal aorta [3]. The commonality of these two predominant locales for
development of the aortic tear is hypothesized to be related to shear forces (dP/dT) being highest in these regions [5,18,19].
The dissection can propagate proximally or distally to involve the aortic valve and enter the pericardial space, or branch vessels [6]. Such
propagation is responsible for many of the ischemic clinical manifestations, including aortic regurgitation (figure 3), cardiac tamponade, or
ischemia (coronary, cerebral, spinal, or visceral). Patients with involvement of the ascending aorta have imminent risk for aortic rupture. The
intimal tear with type B dissection can spiral into a cleavage plane within the media of the aorta along the posterolateral descending thoracic
aorta, leaving the celiac artery, superior mesenteric artery, and right renal artery, typically originating in the true lumen, with the left renal
artery deriving false lumen flow [5]. Variations in anatomy of the dissection are typical and underscore the critical need for proper axial
imaging. In addition, multiple communications may form between the true lumen and the false lumen.
Immediately following dissection, there is "intrinsic true lumen collapse" to a variable degree, and false lumen dilation, thus increasing the
aortic cross-sectional area [20]. The increase of the false lumen area correlates with blood pressure, the size of the entry tear into the false
lumen, the depth of the dissection plane within the media, and the percentage of aortic circumference involved. Because the outer wall of the
false lumen is thinned, it expands to generate the necessary wall tension to accommodate aortic pressure. The true lumen collapses as a
result of the pressure differential between the true and false lumens, and may be exacerbated by the intrinsic recoil of the muscular elements
within the dissection flap [21].
Malperfusion of aortic branch vessels may occur due to the extension of the dissection throughout the thoracoabdominal aorta. Malperfusion
of a vascular bed can occur in one or more branch territories simultaneously. The standard nomenclature of the mechanisms of malperfusion
of aortic branch vessels is termed "dynamic obstruction" and "static obstruction" [22]. Malperfusion syndromes may occur in 30 to 45 percent
of descending dissections and correlate with early mortality [3,23-26].
INCIDENCE AND ASSOCIATED CONDITIONS The incidence of acute aortic dissection in the general population is estimated to range
from 2.6 to 3.5 per 100,000 person-years [27-29]. Patients with acute aortic dissection tend to be 60- to 80-year-old men [3,11,30-32]. In a
review of 464 patients from the International Registry of Acute Aortic Dissection (IRAD), 65 percent were men and the mean age was 63
years [3]. Women presenting with aortic dissection were generally older than men (67 versus 60 years) [15].
There are some important differences between older adult patients and younger patients with dissections involving the ascending aorta. In an
IRAD review, 32 percent of patients were 70 years of age and were significantly more likely to have atherosclerosis, prior aortic aneurysm,
iatrogenic dissection, or intramural hematoma [33]. In a review of patients under age 40, only 34 percent had a history of hypertension and
only 1 percent had a history of atherosclerosis [34]. Marfan syndrome is present in 8.5 percent of the younger patients (mean age 55 years),
and was not seen in any older adult patient [33].
High-risk conditions High-risk conditions commonly associated with aortic dissection include the following [35-37]:
Hypertension The most important predisposing factor of acute aortic dissection is systemic hypertension [3,11,30,38]. In the IRAD
registry data, 72 percent had a history of hypertension [3]. Hypertension was more common in those with a distal (type B) dissection
compared with a type A dissection (70 versus 36 percent) [3,39].
An abrupt, transient, severe increase in blood pressure has been associated with acute aortic dissection through various mechanisms.
Crack cocaine, which may cause transient hypertension due to catecholamine release, accounted for 37 percent of dissections in a
report of an inner city population [40]. The mean duration from last cocaine use to the onset of symptoms was 12 hours. High-intensity
weight lifting or other strenuous resistance training can also cause a transient elevation in blood pressure and has been reported as an
antecedent [41]. Hypertension is also the postulated mechanism when energy drinks [42] or ergotism [43,44] have been associated with
aortic dissection. (See "Exercise in the treatment and prevention of hypertension", section on 'Exaggerated exercise-induced
hypertension' and "Evaluation and management of the cardiovascular complications of cocaine abuse".)
Genetically-mediated collagen disorders (eg, Marfan syndrome, Ehlers-Danlos syndrome, annuloaortic ectasia) (image 4) In an IRAD
review, Marfan syndrome was present in 50 percent of those under age 40, compared with only 2 percent of older patients [34]. Most
patients with Marfan syndrome and aortic dissection have a family history of dissection. There may also be an association between
Marfan syndrome and aortic dissection in the third trimester of pregnancy [45]. (See "Genetics, clinical features, and diagnosis of Marfan
syndrome and related disorders".).
Preexisting aortic aneurysm In an IRAD review, 13 percent of patients had a known aortic aneurysm prior to dissection [34]. The
ascending aorta was more often the site of origin of the dissection than the aortic arch or descending aorta. Such a history was more
common in patients under age 40 (19 percent). In a later IRAD review, known aortic aneurysm was present in 20.7 percent of patients
identified to have descending aortic dissection, and 12.7 percent of those with ascending aortic dissection [39]. (See "Clinical
manifestations and diagnosis of thoracic aortic aneurysm" and "Clinical features and diagnosis of abdominal aortic aneurysm".)
Bicuspid aortic valve In an IRAD review, 9 percent of patients under age 40 with aortic dissection had a bicuspid valve, compared with
1 percent of those over age 40 [34] and 1 percent in the general population. Aortic dissection in patients with a bicuspid valve always
involves the ascending aorta, usually with severe loss of elastic fibers in the media [46]. The predisposition to dissection may reflect a
congenital defect in the aortic wall, as enlargement of the aortic root and/or ascending aorta is frequently associated with bicuspid aortic
valves, even those that function normally, independent of their function [47,48]. (See "Clinical manifestations and diagnosis of bicuspid
aortic valve in adults".)
Aortic instrumentation or surgery Cardiac surgery or catheterization for coronary or valvular disease can be complicated by aortic
dissection [34,49,50]. Cardiac catheterization with or without coronary intervention was reported to cause 14 of 723 dissections (2
percent) in a report from the IRAD registry [51]. Ascending aortic dissection is a rare complication of coronary artery bypass grafting
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(CABG), occurring with both conventional on-pump CABG and, perhaps more often, with minimally invasive off-pump CABG [52-55]. In a
review from a single institution, ascending aortic dissection occurred in 1 of 2723 patients (0.04 percent) treated with conventional CABG
and 3 of 308 undergoing off-pump CABG (1 percent) [54]. (See "Early noncardiac complications of coronary artery bypass graft surgery",
section on 'Aortic dissection' and "Off-pump and minimally invasive direct coronary artery bypass graft surgery: Outcomes".)
Although rare, other procedures that manipulate the aorta, including carotid or other great vessel interventions and thoracic or abdominal
aortic repair (open or endovascular), can also be complicated by aortic dissection.
Aortic coarctation Aortic dissection can occur in patients with an aortic coarctation when surgery leaves behind abnormal para
coarctation aorta that has intrinsic medial faults, when balloon dilatation of native coarctation mechanically damages the inherently
abnormal para coarctation aorta. (See "Clinical manifestations and diagnosis of coarctation of the aorta".)
Turner syndrome Aortic dissection or rupture, often occurring with coarctation, is an increasingly recognized cause of death in women
with Turner syndrome. In a survey of 237 patients, at least 15 (6.3 percent) had aortic dilation: all involved the ascending aorta, 12 had
an associated risk factor such as hypertension or another cardiovascular malformation (eg, coarctation), and two had a dissection
[56,57]. (See "Clinical manifestations and diagnosis of Turner syndrome".)
Inflammatory diseases that cause a vasculitis (giant cell arteritis, Takayasu arteritis, rheumatoid arthritis, syphilitic aortitis) [58,59]. (See
"Overview of and approach to the vasculitides in adults" and "Clinical manifestations of giant cell (temporal) arteritis", section on 'Large
vessel GCA'.)
Trauma rarely causes a classic dissection, but can induce a localized tear in the region of the aortic isthmus (image 5). More commonly,
chest trauma from acute deceleration (as in a motor vehicle accident) results in aortic rupture or transection [60]. (See "Blunt thoracic
aortic injury".)
Pregnancy and delivery Pregnancy and delivery are independent risk factors for aortic dissection; however, the presence of other
conditions (eg, bicuspid aortic valve, Marfan syndrome) may compound the risk [45,61-64]. A cohort study of administrative claims data
in several states from 2005 through 2013 found a rate of aortic complications of 5.5 per million patients during pregnancy and the
postpartum period. Pregnancy was associated with a significantly increased risk of aortic dissection or rupture compared with the control
period one year later (incidence rate ratio 4.0; 95% CI 2.0-8.2) among women with and without documented connective tissue diseases
(eg, Marfan syndrome), although the risk was significantly greater in those with connective tissue diseases [62]. The authors noted that
the findings may reflect prevalent but undiagnosed or undocumented connective tissue disorders, or they may indicate that the
physiologic changes of pregnancy can cause aortic injury even in otherwise healthy women.
CLINICAL FEATURES Clinical symptoms and signs related to aortic dissection events are listed below and discussed in detail in the
linked topics.
Symptoms and signs The symptoms and signs of aortic dissection depend upon the extent of the dissection and the affected
cardiovascular structures (table 1). Pain is the most common symptom, occurring in over 90 percent of patients, most commonly in the chest
or back [39]. Although painless dissection has been reported, it is relatively uncommon (6.4 percent in one retrospective review) [65].
Patients with painless dissection were older (mean age 67 versus 62 years) and more often had ascending aortic dissection (75 versus 61
percent). A prior history of diabetes, aortic aneurysm, or cardiovascular surgery was more common in patients with painless dissection.
Presenting symptoms of syncope, heart failure, or stroke were seen more often in this group. In another review, up to 10 percent of patients
presented with neurologic symptoms, but without chest pain [66].
Hypertension is present in 70 percent of type B dissections, but only in 25 to 35 percent of type A dissections. The presence of hypotension
complicating a type B dissection is rare, seen in less than 5 percent of patients, and usually implies rupture of the aorta. By contrast,
hypotension may be present in 25 percent of dissections that involve the ascending aorta, potentially as a result of aortic valve disruption
leading to severe aortic regurgitation and/or extravasation into the pericardial space leading to cardiac tamponade [3]. Malperfusion of
brachiocephalic vessels by the dissection may falsely depress brachial cuff pressures, usually by involving the left subclavian artery origin in
the type B dissection patient.
Acute pain The most common presenting symptom is pain occurring in over 90 percent of patients, with 85 percent noting the onset to
be abrupt [3,30,39,67,68]. Typically the pain is severe, sharp/knife-like, causing the patient to seek medical attention within minutes to hours
of onset, and categorically unlike any pain experienced before. Pain can occur in isolation or be associated with syncope, a cerebrovascular
accident, acute coronary syndrome, heart failure, or other clinical symptoms or signs.
While the pain is typically described as anterior chest in location in ascending (type A) dissection, for descending (type B) dissection, the pain
was more often experienced in the back [3]. Chest pain was significantly more common in patients with type A dissections (83 versus 71
percent in type B dissections) [39], while both back pain (64 versus 47 percent) and abdominal pain (43 versus 22 percent) were significantly
more common with type B dissections [3]. The pain can radiate anywhere in the thorax or abdomen [3,11]. Unlike the classic description of
the character of pain in aortic dissection as ripping or tearing (50 percent), pain is more often described as sharp (68 percent), and less often
as migratory (19 percent) [3,39]. Older adult patients (>70 years) were significantly less likely to have an abrupt onset of pain compared with
younger patients (77 versus 89 percent) [33].
The localization of pain to the abdomen was reported by 21 percent of patients in type A dissection and 43 percent of patients in type B
dissection [3]. In such patients, a high index of suspicion for mesenteric vascular compromise is warranted [6,69-71]. (See "Overview of
intestinal ischemia in adults" and "Acute mesenteric arterial occlusion" and "Renal infarction" and "Ischemic hepatitis, hepatic infarction, and
ischemic cholangiopathy".)
Pulse deficit The presence of impaired or absent blood flow to peripheral vessels is manifest as a pulse deficit, defined as a weak or
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absent carotid, brachial, or femoral pulse resulting from the intimal flap or compression by hematoma. A considerable variation (>20 mmHg)
in systolic blood pressure may be seen when comparing the blood pressure in the arms. In International Registry of Acute Aortic Dissection
(IRAD) reviews, women are less likely to have a pulse deficit than men [15]. Compared with younger patients, older adult patients (>70 years)
were significantly less likely to have any pulse deficit (24 versus 33 percent) [33].
In those with aortic arch and/or the thoracoabdominal aorta involvement, pulse deficits are common and occur in 19 to 30 percent of patients
compared with 9 to 21 percent with a descending aortic dissection [3,39,72,73]. In the IRAD population, the involvement of the
brachiocephalic trunk was noted in 14.5 percent of patients, the left common carotid artery in 6.0 percent, the left subclavian artery in 14.5
percent, and the femoral arteries in 13.0 to 14.0 percent [3]. Patients presenting with pulse deficits more often had neurologic deficits, coma,
and hypotension. Carotid pulse deficits, not surprisingly, were strongly correlated with fatal stroke, consistent with prior observations [74].
The number of pulse deficits was also clearly associated with increased mortality. Within 24 hours of presentation, 9.4 percent of patients
with no deficits died, 15.8 percent of patients with one or two deficits died, and 35.3 percent of patients with three or more deficits died [72].
With respect to isolated lower extremity pulse deficits, mortality from lower extremity ischemia or its sequelae were uncommon [23].
Nonetheless, leg ischemia caused by acute dissection is a marker of extensive dissection and may be accompanied by other compromised
vascular territories. The clinical course of the peripheral ischemia can be quite variable, and up to one-third of this group may demonstrate
spontaneous resolution of their pulse deficits [23].
Patients with a pulse deficit have a higher rate of in-hospital complications and mortality compared with those without a pulse deficit [72]. A
rapid bedside pulse examination can provide important information in the diagnosis of acute aortic dissection and those at risk for
complications. In a previous report of patients treated during the 1990s, those with peripheral branch obstruction had a mortality rate of 23
percent compared with 16 percent for those without obstruction [24]. In contrast to the IRAD study findings, the presence of peripheral
vascular complications did not increase mortality [20]. This finding was thought to be due to a more timely diagnosis, prompt initiation of
therapy, and the recognition of the importance and appropriate treatment of peripheral vascular complications.
Heart murmur Aortic dissection that propagates proximal to the initial tear can involve the aortic valve (figure 3) [6]. A new diastolic
murmur in association with severe acute chest pain is a sign of acute aortic regurgitation. Characteristically, it is a diastolic decrescendo
murmur associated with a wide pulse pressure, hypotension, and/or heart failure. Acute aortic valve regurgitation occurs in one-half to
two-thirds of ascending dissections [3,75]. The murmur of aortic regurgitation related to aortic dissection is most commonly heard along the
right sternal border, as compared with the left sternal border for aortic regurgitation due to primary aortic valve disease. The duration of the
diastolic murmur may be quite short due to rapid ventricular filling and early equilibration of aortic and left ventricular diastolic pressures. (See
"Auscultation of cardiac murmurs in adults" and "Acute aortic regurgitation in adults".)
In one IRAD review, patients older than 70 years were significantly less likely to have a murmur of aortic regurgitation compared with younger
patients (29 versus 47 percent) [33].
Focal neurologic deficit Focal neurologic deficits are due to propagation of the dissection proximally or distal to the initial tear
involving branch arteries, or due to mass effects as the expanding aorta compresses surrounding structures [15].
Stroke or altered consciousness can be from direct extension of the dissection into the carotid arteries or diminished carotid blood flow.
Alterations of consciousness are more common in women than in men.
Horner syndrome is from compression of the superior cervical sympathetic ganglion.
Hoarseness is from vocal cord paralysis due to compression of the left recurrent laryngeal nerve.
Acute paraplegia is from spinal cord ischemia. Spinal cord ischemia from the interruption of intercostal vessels is clearly more common
with type B aortic dissections than with type A dissections, and it may occur in 2 to 3 percent of all patients [3,76].
Hypotension Syncope, hypotension, and/or shock at initial presentation are more common in patients with ascending aortic dissection,
whereas hypertension is more common in patients with descending aortic dissection [74]. Hypotension/shock may be related to rupture of the
aorta, or propagation of the dissection via the following mechanisms:
Cardiac tamponade from rupture can lead to sudden death. Tamponade occurs more often in women than in men [15]. (See "Cardiac
tamponade".)
Acute aortic valve regurgitation (figure 3). (See 'Heart murmur' above.)
Acute myocardial ischemia or myocardial infarction (MI) due to coronary occlusion. The right coronary artery is most commonly involved
and, in infrequent cases, leads to complete heart block. (See 'Electrocardiogram' below.)
Hemothorax or hemoperitoneum, and possibly exsanguination if the dissection extends through the adventitia in the thoracic or
abdominal aorta.
Syncope Syncope occurs in 5 to 10 percent of patients, and often indicates the development of cardiac tamponade or involvement
of the brachiocephalic vessels [74]. Overall, patients in the IRAD study presenting with syncope were more likely to have a type A dissection
than a type B dissection (19 versus 3 percent), and more likely to have cardiac tamponade (28 versus 8 percent). Similarly, they were more
likely to have a stroke (18 versus 4 percent) and more likely to die in the hospital (34 versus 23 percent). Although patients presenting with
syncope had a higher rate of severe complications (tamponade, stroke, death), almost half of syncope patients had none of the
aforementioned complications to explain their loss of consciousness [74].
Electrocardiogram Electrocardiography (ECG) is often obtained in the initial evaluation of patients with chest pain. Aortic dissection that
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does not involve coronary ostia can usually be distinguished from acute coronary syndrome by the nature and location of the chest pain and
the absence of ECG changes characteristic of ischemia. (See "Evaluation of the adult with chest pain in the emergency department", section
on 'Electrocardiogram'.)
However, the ECG is less helpful when dissection leads to coronary ischemia. Data from IRAD further suggest that involvement of a coronary
artery in an aortic dissection may not manifest changes in the electrocardiogram [77]. In a review of 464 patients, the ECG was normal in 31
percent, showed nonspecific ST and T wave changes in 42 percent (commonly, left ventricular hypertrophy and strain patterns associated
with hypertension), ischemic changes in 15 percent, and, among patients with an ascending aortic dissection, showed evidence of an acute
myocardial infarction in 5 percent [3].
Chest radiograph Plain chest films are also commonly obtained to help rapidly differentiate the various causes of chest pain (eg,
pneumothorax). (See "Evaluation of the adult with chest pain in the emergency department", section on 'Chest radiograph'.)
The most common abnormality seen in aortic dissection is widening of the aortic silhouette, appearing in 60 to 90 percent of cases [3,78].
The IRAD review of 464 patients found that mediastinal widening was present in 63 percent with type A dissections, while 11 percent of
patients had no abnormality on chest radiography [3]. The comparable values in patients with type B dissections were 56 and 16 percent.
Radiographic evidence of a pleural effusion was found in 19 percent of dissections; this finding is more common in women than in men (26
versus 15 percent) [15]. Other findings, which are less specific for dissection but have been described, include widening of the aortic contour,
displaced calcification, aortic kinking, and opacification of the aorticopulmonary window [78]. Hemothorax may be seen if the dissection
extends through the adventitia, with hemorrhage into the pleural space, which can lead to exsanguination.
However, because of the limited sensitivity of the chest radiograph, especially in type B dissections, additional imaging studies are obtained
in almost all patients (98 percent in data from IRAD) [3,73,78]. (See 'Cardiovascular imaging' below.)
Laboratory studies Serum markers for acute aortic dissection are emerging as a diagnostic option, particularly in screening patients in
the setting of differentiating chest pain where the cost of widespread cardiovascular imaging would be prohibitive.
D-dimer D-dimer is a degradation product of cross-linked fibrin and reflects activation of the extrinsic pathway of the coagulation
cascade by tissue factor exposed in the aortic media by the intimal tear. As such, D-dimer has emerged as a potential serum marker for
acute dissection [79]. However, as a nonspecific indicator of intravascular coagulation, D-dimer can be elevated in many conditions (table 2).
D-dimer appears to be a useful screening tool to identify patients who do not have acute aortic dissection. A widely-used cut-off is 500
ng/mL; a level below this value is highly predictive for excluding dissection [79].
The systematic review identified seven studies that used assays for plasma D-dimer to screen patients for acute aortic dissection and
included a control group [80]. For D-dimer <500 ng/mL, the pooled estimate of the sensitivity was 97 percent, specificity was 56 percent, and
negative predictive value was 96 percent. This study and others have concluded that patients with a D-dimer <500 ng/mL are not likely to
benefit from further aortic imaging [79,81-89]. However, caution should be exercised in the application of D-dimer levels as some authors
have reported up to 18 percent of patients with confirmed aortic dissection may have levels <400 ng/mL [81]. While D-dimer testing carries a
sensitivity of 90 to 95 percent, a meta-analysis suggests that its very low specificity, a lack of standardized testing protocols, and the
variability of levels from the time since onset of symptoms should limit its usage to patients at low risk for having aortic dissection but in whom
there remains a clinical diagnostic uncertainty [90].
Other experimental tests Other experimental tests include measurements of soluble elastin fragments, smooth muscle myosin heavy
chain, high-sensitivity C-reactive protein, fibrinogen, and fibrillin fragments [91-93].
A rapid 30-minute immunoassay for the serum concentration of smooth muscle myosin heavy chain has been evaluated in patients
suspected of having an aortic dissection [91,92]. The sensitivity and specificity of this assay in the first three hours were similar and possibly
superior to those of transthoracic echocardiogram, conventional computed tomography (CT), and aortography, but were lower than those of
transesophageal echocardiogram, helical CT, or magnetic resonance imaging. The utility of this test needs further evaluation.
DIAGNOSIS The diagnosis of aortic dissection may be suspected clinically based upon the presence of high-risk clinical features
(discussed above), but confirmation of the diagnosis requires cardiovascular imaging that demonstrates the dissection flap separating a false
lumen from the true lumen (image 3 and image 6). (See 'Cardiovascular imaging' below and "Management of acute aortic dissection".)
It is important to rapidly distinguish acute ascending thoracic aortic dissection, which is a cardiac surgical emergency, from descending
thoracic aortic dissection, which is managed medically in hemodynamically stable patients who do not have end-organ complications. In
general, imaging studies should not be performed until the patient can be initially stabilized. (See "Management of acute aortic dissection"
and "Surgical and endovascular management of type B aortic dissection".)
High-risk clinical features Many studies have sought to identify which of the clinical features presented above are most reliable for
predicting aortic dissection to avoid a missed or delayed diagnosis [53,94-97]. An analysis of 250 patients with acute chest and/or back pain
(128 with a dissection) found that 96 percent of acute aortic dissections could be identified based upon three clinical features [98]:
Abrupt onset of thoracic or abdominal pain with a sharp, tearing and/or ripping character
A variation in pulse (absence of a proximal extremity or carotid pulse) and/or blood pressure (>20 mmHg difference between the right
and left arm)
Mediastinal and/or aortic widening on chest radiograph
The probability of a dissection related to the presence or absence of these three were:
Isolated pulse or blood pressure differential, or any combination of the three: 83 percent
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Presence of mediastinal widening: 39 percent

Pain alone: 31 percent
All three absent: 7 percent
Certain clinical features suggest involvement of the ascending versus descending aorta.
Ascending aorta: Pain located in the chest more so than the back or abdomen [3]. Other clinical features include acute aortic valve
regurgitation, acute coronary syndrome, cardiac tamponade, hemothorax, focal neurologic deficits related to cerebrovascular ischemia,
and upper extremity pulse deficit [6,30]. As most type A dissections include a distal extent to the abdomen, descending aortic
manifestations may be included too.
Descending aorta: Pain is located in the posterior chest/upper back and may radiate to the abdomen [3]. Other clinical features include
visceral ischemia, renal insufficiency, lower extremity ischemia, and focal neurologic deficits related to spinal ischemia [6,73].
Cardiovascular imaging Our recommendations for cardiovascular imaging are generally in agreement with multidisciplinary consensus
guidelines [35,36]. Multiple imaging modalities can be used to demonstrate the dissection, including magnetic resonance (MR) angiography,
computed tomographic (CT) angiography, and multiplane transesophageal echocardiography (TEE) [99]. Each has its advantages and
disadvantages and one may be more appropriate for selected patient populations as an initial study.
CT is the most common initial choice, due to its widespread availability, particularly in the emergency department setting. More than one
study is often needed to obtain all the necessary information to fully guide treatment. In one IRAD review, patients had an average of 1.83
studies per patient [3]. The initial study was CT in 61 percent, TEE in 33 percent, aortography in 4 percent, and MR in 2 percent. The
availability of some studies may be limited, and accuracy depends upon the performance and interpretation of the test by skilled individuals,
and as such, the studies chosen may differ from institution to institution.
The imaging diagnosis of aortic dissection is based on the presence of an intimal flap separating a false lumen from a true lumen, and
associated complications [6,100-103]:
The intimal flap (image 3 and image 7 and image 8)

True and false lumen (image 9A-B)
Involvement of the ascending aorta (image 10)
The extent of dissection and the sites of entry and reentry
Thrombus in the false lumen
Branch vessel involvement
Coronary artery involvement
Aortic valve regurgitation
Pericardial effusion
Hemodynamically stable For hemodynamically stable patients, we obtain CT angiography as an initial study in patients with
suspected aortic dissection, particularly in the emergency department setting where other studies are less available. The majority of patients
with suspected acute aortic dissection should be evaluated with both chest and abdominal dynamic contrast-enhanced fine-cut CT scanning.
In comparison with other modalities, CT scanning is the least operator dependent, provides useful anatomic correlates for surgical and
endovascular therapy, and collects information for follow-up analysis and measurement. Most importantly, three-dimensional CT scan
reconstructions can aid treatment planning, and axial imaging affords the best opportunity to detect topographic relationships of the true and
false lumens and potential aortic branch compromise.
CT scanning has a reported sensitivity of 83 to 95 percent and specificity of 87 to 100 percent for the diagnosis of acute aortic dissection
[104-106]. The chief limitation of imaging is the ascending aorta, where the sensitivity may drop to <80 percent, as contrast enhancement can
be dependent on timing of the injection. As an example, a CT scan to evaluate for initially suspected pulmonary embolus as a source of chest
pain may or may not time correctly for assessment of the ascending aorta. The accuracy of CT may be substantially improved with spiral
(helical) CT and perhaps with multidetector (multislice) CT [107-110]. Spiral CT may be more accurate than MR or TEE for the detection of
aortic arch vessel involvement [107]. A potential limitation is a spiral CT artifact that can simulate an aortic dissection flap in patients if
performed without echocardiogram (ECG) gating [111-113]. Advantages of CT include ready availability at most hospitals, even on an
emergency basis, and identification of intraluminal thrombus and pericardial effusion. Two disadvantages of standard CT are that the intimal
flap is seen in less than 75 percent of cases and that the site of entry is rarely identified [114]. In addition, potentially nephrotoxic iodinated
contrast is required, and there is no capability to assess for aortic insufficiency. If the CT is equivocal, or further delineation of the dissection
is needed, MR angiography or TEE is indicated.
The diagnosis of aortic dissection by CT scanning requires the identification of two distinct lumens; the intimal flap may or may not be
demonstrated. In most cases, the true lumen may be localized by its continuity with an undissected proximal or distal segment of the aorta.
The presence of intraluminal thrombus is a good marker of the false lumen, but in patients with a concomitant degenerative aneurysm,
thrombus may be present in the true lumen. In the majority of cases, the false lumen is larger than the true lumen [106]. A compressed true
lumen is the key radiographic finding, which should substantially raise the index of suspicion for renal/visceral/lower extremity malperfusion
syndrome. Curving of the dissection flap into the true lumen is seen in 63 percent of acute type B dissections, but only 25 percent of chronic
dissections [106]. Indeed, it may be appropriate, if open surgical intervention is chosen as the revascularization procedure, to proceed
directly to surgery after CT alone in circumstances where the clinical and/or laboratory signs dictate the need for urgent revascularization, as
in evidence of bowel ischemia or vascular rupture.
For hemodynamically stable patients, MR angiography is an alternative to CT angiography, depending on availability [113,115]. Although less
commonly used, MR angiography is highly accurate for diagnosing aortic dissection. Gadolinium-enhanced MR angiography has an overall
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sensitivity and specificity to diagnose aortic dissection of 95 to 100 percent [116]. In a prospective trial of 110 patients, MR angiography had
85 percent sensitivity for identifying the site of entry [105]. MR angiography can also detect differential flow between the true and false
lumens. Additional suggestive findings include widening of the aorta with a thickened wall and thrombosis of the false lumen. The chief
advantage of MR angiography is avoiding excess radiation exposure, and it can be afforded in the long-term serial studies required in the
standard surveillance of type B dissection patients. MR is safe in adequately monitored patients with aortic dissection, and MR contrast
agents have a more favorable safety profile than iodinated contrast agents. Noncontrast MR angiography is another option. Other
advantages of MR include the ability to assess branch vessels, although it may be less sensitive than spiral CT [107], and to assess for aortic
insufficiency. The main disadvantages of MR imaging are inconvenience (patients are required to remain motionless with relatively limited
access for more than 30 minutes), and limited applicability (MR imaging cannot be performed in patients with claustrophobia, pacemakers, or
certain types of aneurysm clips or metallic ocular/auricular implants). MR is also not readily available on an emergency basis at many
institutions, and there are concerns about patient monitoring and relative patient inaccessibility during prolonged scanning. Gadolinium
administration for contrast-enhanced MR imaging in patients with moderate to severe kidney disease (particularly dialysis patients) should be
avoided. The accuracy of noncontrast MR angiography for aortic dissection has been less well defined. (See "Nephrogenic systemic
fibrosis/nephrogenic fibrosing dermopathy in advanced renal failure".)
Hemodynamically unstable For hemodynamically unstable patients, we suggest transesophageal echocardiography (TEE) as an
initial study in patients with suspected aortic dissection, wherever available. TEE is a portable procedure that yields a diagnosis within
minutes, and is easily performed in the emergency department [105]. The sensitivity of TEE has been reported to be as high as 98 percent,
and the specificity ranging from 63 to 96 percent [117,118]. The ascending aorta is typically assessed at about 130 degree orientation while
the arch and descending thoracic aorta are assessed at 0 degrees. Biplane imaging may be useful.
The advantages of TEE include generally wide availability, ease of use, and bedside capability. In addition, TEE can detect entry tear sites,
false lumen flow/thrombus, involvement of the arch or coronary arteries, degrees of aortic valvular regurgitation, and pericardial effusions.
The addition of color flow Doppler patterns may decrease false positives by recognizing differential flow velocities in the true and false
lumens that may assist in the diagnosis of malperfusion syndromes.
A disadvantage of TEE is that it requires esophageal intubation, which usually requires procedural sedation, which may have untoward
effects in hemodynamically unstable patients. TEE requires the availability of experienced operators (both physicians and technicians) to
ensure accurate results. As such, it is often not attainable on a "stat" basis in many centers. The theoretical technical limitation of TEE is the
anatomic "blind spot" in the distal ascending aorta and proximal arch secondary to the air-filled trachea and left main stem bronchus, and
inability to document dissection extension beyond the diaphragm that may be causing malperfusion of abdominal aorta branches. Despite
these shortcomings, TEE can be particularly useful in delineating acute dissection and relevant surgical pathology in the ascending aorta,
and therefore, it is chiefly applied in this territory. Moreover, in the unstable patient with a suspected acute dissection in the ascending aorta,
TEE may be performed in the operating room to expedite diagnosis and definitive therapy. In the IRAD study, TEE was employed second
most frequently (after CT) in the diagnosis and workup of an acute aortic dissection [118].
The following findings may be seen on TEE in patients with aortic dissection [50,103,105]:
Intimal dissection flaps can be identified with high spatial resolution (image 8 and movie 1). The use of M-mode echocardiography may
improve diagnostic accuracy by demonstrating a lack of relation between movement of the intimal flap and the aortic wall [119].
The true and false lumens can be identified. They may not be distinguishable without color Doppler imaging or identification of the
proximal border of the dissection. However, in some cases, the false lumen can be seen to surround the true lumen (movie 2 and movie
3). Color Doppler permits clear identification of flow within and between the true and false lumens (image 8 and movie 4). The presence
of flow does not absolutely distinguish the true lumen from the false lumen. The true lumen has an endothelial lining and is contiguous
with the aortic valve.
Thrombosis in the false lumen, pericardial effusion, concomitant aortic regurgitation, and the proximal coronary arteries can be readily
seen.
The 135 degree long axis view from TEE can define the severity and mechanism of aortic regurgitation that complicates acute type A
dissection [75]. Patients with an intrinsically normal valve who have aortic regurgitation due to a correctable aortic lesion (incomplete
leaflet closure, leaflet prolapse, or dissection flap prolapse) can undergo aortic valve repair (movie 5). By contrast, abnormalities that
cannot be repaired (eg, Marfan syndrome, bicuspid valve, aortitis) will require valve replacement. (See "Management of acute aortic
dissection".)
A less favorable alternative to TEE is transthoracic echocardiography (TTE), which can quickly identify ascending aortic dissection,
particularly coexistent aortic valve disruption/regurgitation and hemopericardium (movie 6 and movie 7) [49,105,120]. The primary
disadvantage with TTE is its inability to adequately visualize the mid- and distal ascending, transverse arch, and descending aorta, or the
presence of other complications in a substantial number of patients. Furthermore, the sensitivity and specificity of TTE are inferior to CT
angiography, MR angiography, and TEE.
Role of aortography Formerly the gold standard for the diagnosis of aortic dissection, aortography has largely yielded to CT
angiography in the initial diagnosis of aortic dissection. In the endovascular management of dissection, it is used mainly as a component of
an interventional treatment strategy. However, for patients in whom the suspicion for ascending aortic dissection is very strong but
noninvasive imaging is unavailable or inconclusive, digital subtraction aortography should be performed. Aortography involves the injection of
iodinated contrast media into the aortic lumen, permitting identification of the site of dissection, the relationship between the dissection and
the major branches of the aorta, and the communication site between the true and false lumen (image 11) [103].
Findings on aortography considered supportive of a diagnosis of aortic dissection include distortion of the normal contrast column, flow
reversal or stasis into a false channel, failure of major branches to fill, and aortic valvular regurgitation. Most contemporary diagnostic
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algorithms have deemphasized the role of aortography, especially when assessing for malperfusion syndromes. Furthermore, pressurized
contrast injections into either lumen in the presence of aortic dissection can, in fact, lead to diagnostic confusion with respect to malperfusion
syndromes by altering the hemodynamic gradients between lumens (during the hydraulically powered injections) that are causing
malperfusion. Evaluation for aortic regurgitation, and coronary angiography, when indicated (suspected ascending aortic aneurysm and prior
history or angina or myocardial infarction [MI], age >60 years of age, multiple risk factors for coronary disease) can also be performed during
the same procedure [121].
Aortography is only moderately sensitive for the diagnosis of thoracic aortic dissection [122]. In a review of 164 patients (82 had a dissection),
aortography had a sensitivity of 88 percent and a specificity of 94 percent; the positive and negative predictive values were 96 and 84
percent, respectively [104]. Lower values for sensitivity (77 percent) and accuracy (87 percent) were noted in other reports [123,124].
However, false negative results may be obtained when there is simultaneous opacification of the true and false lumen so that the intimal flap
between them is not visible, when thrombosis of the false lumen results in lack of opacification with contrast, or when there is an intramural
hematoma with noncommunicating dissection [104,123,125,126]. Also, intimal tears associated with only a minimal amount of blood in the
dissected aortic wall may not be seen with noninvasive imaging. In one study of 181 patients who underwent repair of the ascending aorta or
aortic arch, nine (5 percent) had a subtle aortic dissection that was not diagnosed preoperatively despite the use of three or more imaging
techniques [16].
DIFFERENTIAL DIAGNOSIS The differential diagnosis of acute aortic dissection includes other entities associated with acute chest or
back pain, pulse deficit and neurologic deficits, which includes both nonvascular and vascular pathologies [127]. Nonvascular pathologies
include acute coronary syndrome, pulmonary embolus, spontaneous pneumothorax, aortic regurgitation without dissection, esophageal
rupture, pericarditis, and pleuritis, among others (table 3). Artifact on echocardiography can also mimic the appearance of a dissection flap
[35]. (See "Evaluation of the adult with chest pain in the emergency department".)
Vascular pathologies include other acute aortic pathologies such as aortic intramural hematoma without dissection, aortic aneurysm, aortic
injury without dissection, peripheral artery disease, and chronic aortic dissection [128]. These may be suspected by risk factors and patient
history, but cardiovascular imaging distinguishes these from aortic dissection. In patients with new symptoms and chronic dissection, detailed
comparison with existing/prior imaging data are necessary to distinguish dissection extension from other causes of their symptoms.
Lower extremity ischemia in the absence of typical chest or back pain can also occur and can lead to a missed or delayed diagnosis [129].
The clinical features of acute extremity ischemia are discussed separately. (See "Overview of acute arterial occlusion of the extremities
(acute limb ischemia)".)
INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, The Basics and Beyond the Basics. The
Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key
questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer
short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles
are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some
medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You
can also locate patient education articles on a variety of subjects by searching on patient info and the keyword(s) of interest.)
Basics topics (see "Patient education: Aortic dissection (The Basics)")
SUMMARY AND RECOMMENDATIONS
Aortic dissection is a relatively uncommon, though catastrophic, acute illness. The inciting event in aortic dissection is a tear in the aortic
intima. Propagation of the dissection can occur proximal (retrograde) or distal (antegrade) to the initial tear, involve the aortic valve, or
branches of the thoracic and/or abdominal aorta. Propagation of the dissection (antegrade, retrograde) is responsible for clinical
manifestations that can include aortic regurgitation, cardiac tamponade, and end-organ ischemia (coronary, cerebral, spinal, or visceral,
extremity). (See 'Pathophysiology' above.)
The estimated incidence of acute aortic dissection ranges from 2.6 to 3.5 per 100,000 person-years. Risk factors for acute aortic
dissection include advancing age, male sex, systemic hypertension, preexisting aortic aneurysm, and risk factors for atherosclerosis. For
patients under age 40, these risk factors are less common, but other predisposing factors are often present, such as collagen vascular
disorders, vasculitis, bicuspid aortic valve, aortic coarctation, Turner syndrome, prior aortic valve surgery, instrumentation, trauma, high
intensity weight lifting or other exercise, and cocaine use. (See 'Incidence and associated conditions' above.)
Aortic dissection is classified using two anatomic systems. The more commonly used system (Stanford) classifies dissections that
involve the ascending aorta as type A, regardless of the site of the primary intimal tear, and all other dissections as type B. Ascending
aortic dissections are almost twice as common as descending dissections. Isolated abdominal aortic dissection can also occur. Several
anatomic variants of aortic dissection are described, including intimal tear without hematoma and aortic intramural hematoma. These
variants are felt to be precursors to aortic dissection. (See 'Pathophysiology' above.)
Routine blood tests are generally nondiagnostic in aortic dissection. However, D-dimer may become a useful screening tool in the setting
of chest pain where the cost of widespread imaging would be prohibitive. A D-dimer <500 ng/mL may indicate a subset of patients who
are not likely to benefit from aortic imaging. D-dimer levels may be most appropriate for patients with a low risk for aortic dissection, but
in whom there remains a clinical diagnostic uncertainty. (See 'D-dimer' above.)
Acute aortic dissection typically presents with anterior chest pain in ascending aortic dissection or severe, sharp, or "tearing" posterior
chest or back pain when the dissection progresses distal to the left subclavian artery. Pain can be an isolated symptom or associated
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with syncope, symptoms of stroke, myocardial infarction (MI), heart failure, or other clinical signs of end-organ ischemia (splanchnic
ischemia, renal insufficiency, extremity ischemia, spinal cord ischemia). Hypertension upon initial clinical presentation is more common
with distal type B dissection than with type A dissection. (See 'Clinical features' above.)
A diagnosis of acute aortic dissection depends upon demonstration of the dissection on imaging studies, which defines the extent of
aortic involvement, and identifies sites of entry and reentry, branch vessel involvement, aortic insufficiency, and pericardial effusion. No
one study is capable of obtaining all the information that is needed to evaluate aortic dissection, and thus, a combination of studies is
usually obtained. (See 'Diagnosis' above and 'Cardiovascular imaging' above.)
The initial imaging study of choice depends upon the hemodynamic status of the patient and institutional resources. It is important to
rapidly distinguish acute ascending thoracic aortic dissection, which is a cardiac surgical emergency, from descending thoracic aortic
dissection, which is managed medically in hemodynamically stable patients without end-organ complications.
Computed tomographic (CT) angiography is generally used as the initial screening study in hemodynamically stable patients with
suspected aortic dissection because of its widespread availability and speed of image acquisition, particularly for those presenting to
the emergency department in a setting where transesophageal echocardiography (TEE) and magnetic resonance (MR) angiography
may be unavailable, especially after hours. If CT is equivocal, or further delineation of the dissection is needed, TEE or MR
angiography is indicated. Digital subtraction aortography is indicated when noninvasive tests are unavailable or inconclusive when
there is a strong suspicion for ascending aortic dissection.
For patients with chest pain suspected of having acute aortic dissection who are hemodynamically unstable, we suggest multiplanar
TEE at the bedside or in the emergency department (or operating room) to establish the diagnosis and evaluate the location of the
dissection.
MR imaging is usually preferred for those who are hemodynamically stable or have chronic aortic dissection, but is time consuming,
often not available on an urgent basis, and places the patient away from ready care. (See 'Diagnosis' above and 'Cardiovascular
imaging' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
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79. Suzuki T, Distante A, Zizza A, et al. Diagnosis of acute aortic dissection by D-dimer: the International Registry of Acute Aortic Dissection
Substudy on Biomarkers (IRAD-Bio) experience. Circulation 2009; 119:2702.
80. Shimony A, Filion KB, Mottillo S, et al. Meta-analysis of usefulness of d-dimer to diagnose acute aortic dissection. Am J Cardiol 2011;
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81. Paparella D, Malvindi PG, Scrascia G, et al. D-dimers are not always elevated in patients with acute aortic dissection. J Cardiovasc
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82. Asha SE, Miers JW. A Systematic Review and Meta-analysis of D-dimer as a Rule-out Test for Suspected Acute Aortic Dissection. Ann
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83. Sbarouni E, Georgiadou P, Marathias A, et al. D-dimer and BNP levels in acute aortic dissection. Int J Cardiol 2007; 122:170.
84. Wiegand J, Koller M, Bingisser R. Does a negative D-dimer test rule out aortic dissection? Swiss Med Wkly 2007; 137:462.
85. Ohlmann P, Faure A, Morel O, et al. Diagnostic and prognostic value of circulating D-Dimers in patients with acute aortic dissection. Crit
Care Med 2006; 34:1358.
86. Hazui H, Fukumoto H, Negoro N, et al. Simple and useful tests for discriminating between acute aortic dissection of the ascending aorta
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87. Akutsu K, Sato N, Yamamoto T, et al. A rapid bedside D-dimer assay (cardiac D-dimer) for screening of clinically suspected acute aortic
dissection. Circ J 2005; 69:397.
88. Eggebrecht H, Naber CK, Bruch C, et al. Value of plasma fibrin D-dimers for detection of acute aortic dissection. J Am Coll Cardiol
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89. Weber T, Hgler S, Auer J, et al. D-dimer in acute aortic dissection. Chest 2003; 123:1375.
90. Marill KA. Serum D-dimer is a sensitive test for the detection of acute aortic dissection: a pooled meta-analysis. J Emerg Med 2008;
34:367.
91. Suzuki T, Katoh H, Watanabe M, et al. Novel biochemical diagnostic method for aortic dissection. Results of a prospective study using
an immunoassay of smooth muscle myosin heavy chain. Circulation 1996; 93:1244.
92. Suzuki T, Katoh H, Tsuchio Y, et al. Diagnostic implications of elevated levels of smooth-muscle myosin heavy-chain protein in acute
aortic dissection. The smooth muscle myosin heavy chain study. Ann Intern Med 2000; 133:537.
93. Marshall LM, Carlson EJ, O'Malley J, et al. Thoracic aortic aneurysm frequency and dissection are associated with fibrillin-1 fragment
concentrations in circulation. Circ Res 2013; 113:1159.
94. Rogers AM, Hermann LK, Booher AM, et al. Sensitivity of the aortic dissection detection risk score, a novel guideline-based tool for
identification of acute aortic dissection at initial presentation: results from the international registry of acute aortic dissection. Circulation
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95. Sattiraju S, Missov E. Delayed presentation of acute aortic syndrome. Lancet 2014; 383:2238.
96. Harris KM, Strauss CE, Eagle KA, et al. Correlates of delayed recognition and treatment of acute type A aortic dissection: the
International Registry of Acute Aortic Dissection (IRAD). Circulation 2011; 124:1911.
97. Kimura N, Ohnuma T, Itoh S, et al. Utility of the Penn classification in predicting outcomes of surgery for acute type a aortic dissection.
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98. von Kodolitsch Y, Schwartz AG, Nienaber CA. Clinical prediction of acute aortic dissection. Arch Intern Med 2000; 160:2977.
99. Kienzl D, Prosch H, Tpker M, Herold C. Imaging of non-cardiac, non-traumatic causes of acute chest pain. Eur J Radiol 2012;
81:3669.
100. Sueyoshi E, Nagayama H, Hayashida T, et al. Comparison of outcome in aortic dissection with single false lumen versus multiple false
lumens: CT assessment. Radiology 2013; 267:368.
101. Moon MC, Greenberg RK, Morales JP, et al. Computed tomography-based anatomic characterization of proximal aortic dissection with
consideration for endovascular candidacy. J Vasc Surg 2011; 53:942.
102. Jaussaud N, Chitsaz S, Meadows A, et al. Acute type A aortic dissection intimal tears by 64-slice computed tomography: a role for
endovascular stent-grafting? J Cardiovasc Surg (Torino) 2013; 54:373.
103. Cigarroa JE, Isselbacher EM, DeSanctis RW, Eagle KA. Diagnostic imaging in the evaluation of suspected aortic dissection. Old
standards and new directions. N Engl J Med 1993; 328:35.
104. Erbel R, Engberding R, Daniel W, et al. Echocardiography in diagnosis of aortic dissection. Lancet 1989; 1:457.
105. Nienaber CA, von Kodolitsch Y, Nicolas V, et al. The diagnosis of thoracic aortic dissection by noninvasive imaging procedures. N Engl
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106. LePage MA, Quint LE, Sonnad SS, et al. Aortic dissection: CT features that distinguish true lumen from false lumen. AJR Am J
Roentgenol 2001; 177:207.
107. Sommer T, Fehske W, Holzknecht N, et al. Aortic dissection: a comparative study of diagnosis with spiral CT, multiplanar
transesophageal echocardiography, and MR imaging. Radiology 1996; 199:347.
108. Sebasti C, Pallisa E, Quiroga S, et al. Aortic dissection: diagnosis and follow-up with helical CT. Radiographics 1999; 19:45.
109. Hamada S, Takamiya M, Kimura K, et al. Type A aortic dissection: evaluation with ultrafast CT. Radiology 1992; 183:155.
110. Hayter RG, Rhea JT, Small A, et al. Suspected aortic dissection and other aortic disorders: multi-detector row CT in 373 cases in the
emergency setting. Radiology 2006; 238:841.
111. Loubeyre P, Angelie E, Grozel F, et al. Spiral CT artifact that simulates aortic dissection: image reconstruction with use of 180 degrees
and 360 degrees linear-interpolation algorithms. Radiology 1997; 205:153.
112. Schertler T, Glcker T, Wildermuth S, et al. Comparison of retrospectively ECG-gated and nongated MDCT of the chest in an
emergency setting regarding workflow, image quality, and diagnostic certainty. Emerg Radiol 2005; 12:19.
113. Freeman LA, Young PM, Foley TA, et al. CT and MRI assessment of the aortic root and ascending aorta. AJR Am J Roentgenol 2013;
200:W581.
114. Vasile N, Mathieu D, Keita K, et al. Computed tomography of thoracic aortic dissection: accuracy and pitfalls. J Comput Assist Tomogr
1986; 10:211.
115. Clough RE, Waltham M, Giese D, et al. A new imaging method for assessment of aortic dissection using four-dimensional phase
contrast magnetic resonance imaging. J Vasc Surg 2012; 55:914.
116. Gebker R, Gomaa O, Schnackenburg B, et al. Comparison of different MRI techniques for the assessment of thoracic aortic pathology:
3D contrast enhanced MR angiography, turbo spin echo and balanced steady state free precession. Int J Cardiovasc Imaging 2007;
23:747.
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117. Moore AG, Eagle KA, Bruckman D, et al. Choice of computed tomography, transesophageal echocardiography, magnetic resonance
imaging, and aortography in acute aortic dissection: International Registry of Acute Aortic Dissection (IRAD). Am J Cardiol 2002;
89:1235.
118. Hartnell G, Costello P. The diagnosis of thoracic aortic dissection by noninvasive imaging procedures. N Engl J Med 1993; 328:1637;
author reply 1638.
119. Evangelista A, Garcia-del-Castillo H, Gonzalez-Alujas T, et al. Diagnosis of ascending aortic dissection by transesophageal
echocardiography: utility of M-mode in recognizing artifacts. J Am Coll Cardiol 1996; 27:102.
120. Roudaut RP, Billes MA, Gosse P, et al. Accuracy of M-mode and two-dimensional echocardiography in the diagnosis of aortic
dissection: an experience with 128 cases. Clin Cardiol 1988; 11:553.
121. Penn MS, Smedira N, Lytle B, Brener SJ. Does coronary angiography before emergency aortic surgery affect in-hospital mortality? J
Am Coll Cardiol 2000; 35:889.
122. Rizzo RJ, Aranki SF, Aklog L, et al. Rapid noninvasive diagnosis and surgical repair of acute ascending aortic dissection. Improved
survival with less angiography. J Thorac Cardiovasc Surg 1994; 108:567.
123. Bansal RC, Chandrasekaran K, Ayala K, Smith DC. Frequency and explanation of false negative diagnosis of aortic dissection by
aortography and transesophageal echocardiography. J Am Coll Cardiol 1995; 25:1393.
124. White RD, Lipton MJ, Higgins CB, et al. Noninvasive evaluation of suspected thoracic aortic disease by contrast-enhanced computed
tomography. Am J Cardiol 1986; 57:282.
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280:225.
126. Earnest F 4th, Muhm JR, Sheedy PF 2nd. Roentgenographic findings in thoracic aortic dissection. Mayo Clin Proc 1979; 54:43.
127. Erbel R, Alfonso F, Boileau C, et al. Diagnosis and management of aortic dissection. Eur Heart J 2001; 22:1642.
128. Steuer J, Bjrck M, Mayer D, et al. Distinction between acute and chronic type B aortic dissection: is there a sub-acute phase? Eur J
Vasc Endovasc Surg 2013; 45:627.
129. Pacifico L, Spodick D. ILEAD--ischemia of the lower extremities due to aortic dissection: the isolated presentation. Clin Cardiol 1999;
22:353.
Topic 8190 Version 23.0
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GRAPHICS
Classification of aortic dissection
In the DeBakey classification of aortic dissection:

Type I involves the ascending aorta, arch, and descending thoracic aorta and may progress
to involve the abdominal aorta.
Type II is confined to the ascending aorta.
Type IIIa involves the descending thoracic aorta distal to the left subclavian artery and
proximal to the celiac artery.
Type IIIb dissection involves the thoracic and abdominal aorta distal to the left subclavian
artery.
In the Stanford classification of aortic dissection:
Type A involves the ascending aorta and may progress to involve the arch and
thoracoabdominal aorta.
Type B involves the descending thoracic or thoracoabdominal aorta distal to the left
subclavian artery without involvement of ascending aorta.
Graphic 100115 Version 4.0
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Focal aortic dissection on CT scan
An axial CT scan through the upper abdomen shows a focal dissection (arrowhead) and a small mural hematoma (arrow). Small bilateral pleural
effusions are present (asterisks). Image B is a magnified view and shows focal dissection (arrowhead) and the mural hematoma (arrow).
CT: computed tomography.
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Acute aortic syndromes
Class I Classic dissection with separation of intima/media and dual lumens; there is a flap
between true and false aneurysm and clot in false lumen.
Class II Intramural hematoma with separation of intima/media but no intraluminal tear or
flap on imaging.
Class III Limited intimal tear without hematoma and eccentric bulge at tear site (limited
dissection).
Class IV Atherosclerotic ulcer penetrating to adventitia with surrounding hematoma that is
usually subadventitial.
Class V Iatrogenic or traumatic dissection (eg, due to a cardiac catheterization).
Modified from:
1. Lahey Clinic, Burlington, MA.
2. Svensson LG, Lalsib JB, Eisenhauer AC, et al. Intimal tear without hematoma: an important
variant of aortic dissection that can elude current imaging techniques. Circulation 1999;
99:1331.
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Diagnosis and treatment of focal aortic dissection using CTA
CTA in the transverse plane through the mid thorax (A) shows a focal dissection of the aorta (arrow). Image B is a
magnified view and shows a curvilinear accumulation of extraluminal contrast in the wall of the aorta (arrow). Image C
is a sagittal reconstruction and shows a short focal dissection of the descending thoracic aorta (arrow). Image D is a
magnified view showing localized dissection (arrow). Image E is a reconstruction of the aorta showing a stent in the
descending thoracic aorta (arrow).
CTA: computed tomography angiography.
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Aortic dissection on noninvasive imaging
Representative transesophageal echocardiograms (TEE) (panels A and B) and

computed tomograms (CT) (panels C and D) of a section of the descending
aorta in distal aortic dissection. Panels A and C are acute studies, while B and D
are from follow-up evaluation. Both TEE and CT scan show persistence of the
intimal flap forming the true lumen (TL) and a markedly dilated false lumen (FL)
with the development of thrombi.
From Song, JK, Kang, DH, Lim, TH, et al. Different remodeling of descending thoracic
aorta after acute event in aortic intramural hemorrage versus aortic dissection. Am J
Cardiol 1999; 83:937 with permission from Excerpta Medica Inc.
http://www.elsevier.com/locate/jacc
http://www.sciencedirect.com
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Proximal aortic dissection
Mechanisms of aortic regurgitation in ascending aortic dissection may include:

(A) Dilation of the aortic root
(B) Asymmetric cusp coaptation
(C) Disruption of aortic annulus
Original figure modified for this publication. Isselbacher EM, Eagle KA, Desanctis RW. Diseases of
the aorta. In: Braunwalds Heart Disease: A Textbook of Cardiovascular Medicine, 5th ed,
Mendelsohn ME (Ed), Philadelphia: Saunders, 1997. Illustration used with the permission of
Elsevier Inc. All rights reserved.
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Aortic root aneurysm in Marfan syndrome on chest film
This aortogram in a young patient with Marfan syndrome demonstrates

significant dilation of the aortic root (white arrows). There is also opacification of
the left ventricle as a result of aortic regurgitation (black arrow).
Courtesy of Jonathan Kruskal, MD.
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Aortogram showing aortic rupture with pseudoaneurysm
The aortogram, obtained following administration of contrast material into the

aortic root, demonstrates a focal pseudoaneurysm (arrow) arising from the
proximal descending aorta immediately distal to the origin of the left subclavian
artery (small arrow). This traumatic tear of the aorta occurred during a motor
vehicle accident.
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Presentations of aortic dissection based on affected structures
Clinical findings Artery or structure involved
Aortic insufficiency or heart failure Aortic valve
Myocardial infarction Coronary artery (often right)
Cardiac tamponade Pericardium
Hemothorax Thorax
Horner syndrome (ptosis, miosis, anhidrosis) Superior cervical sympathetic ganglion
Stroke or syncope Brachiocephalic, common carotid, or left subclavian arteries
Upper extremity pulselessness, hypotension pain Subclavian artery
Paraplegia Intercostal arteries (give off spinal and vertebral arteries)
Back or flank pain; renal failure Renal artery
Abdominal pain; mesenteric ischemia Celiac or mesenteric arteries
Lower extremity pain, pulselessness, weakness Common iliac artery
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Disorders associated with increased plasma levels of fibrin D-dimer
Arterial thromboembolic disease
Myocardial infarction
Stroke
Acute limb ischemia
Atrial fibrillation
Intracardiac thrombus
Venous thromboembolic disease
Deep vein thrombosis
Pulmonary embolism
Disseminated intravascular coagulation
Preeclampsia and eclampsia
Abnormal fibrinolysis; use of thrombolytic agents
Cardiovascular disease, congestive failure
Severe infection/sepsis/inflammation
Surgery/trauma (eg, tissue ischemia, necrosis)
Systemic inflammatory response syndrome
Vasoocclusive episode of sickle cell disease
Severe liver disease (decreased clearance)
Malignancy
Renal disease
Nephrotic syndrome (eg, renal vein thrombosis)
Acute renal failure
Chronic renal failure and underlying cardiovascular disease
Normal pregnancy
Venous malformations
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Aortic dissection noncontrast CT
In this noncontrast CT scan, calcification is appreciated in the middle of the aortic lumen. Displacement of calcification may be an
indicator of a dissection flap of an aortic dissection.
CT: computed tomography.
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Aortic dissection on magnetic resonance imaging
Transverse (axial) spin-echo CMR in a patient with an aortic dissection at the

level of the aortic arch. The true lumen (TL), false lumen (FL), and intimal flap
can be easily identified. The trachea and superior vena cava (SVC) are also
seen.
CMR: cardiovascular magnetic resonance.
Courtesy of Warren Manning, MD.
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Transesophageal echocardiogram of descending aortic dissection
Aortic dissection is characterized by the formation of an "intimal flap" seen as a hyperechoic line extending
across the vessel delimiting two distinct lumens (A). Color flow Doppler (B) depicts higher (orange) blood flow
velocity and intraluminal velocity in the inferior of the two lumens, but does not provide definitive information
regarding which is the true lumen and false lumen.
Courtesy of W Manning, MD.
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Thoracic aortic dissection on computed tomography
Transverse plane through ascending (AA) and descending (DA) thoracic aorta
showing the intimal flap (arrows) and both lumens of a type A aortic dissection.
One cannot distinguish between the true and false lumens based on this view
alone.
Courtesy of Vassilios Raptopoulos, MD.
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Thoracic aortic dissection on reconstructed computed

tomography
Sagittal plane reconstruction of transverse and descending thoracic aorta

showing the true (TL) and false (FL) lumens of the same patient as the previous
CT.
Courtesy of Vassilios Raptopoulos, MD.
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Electron beam computed tomography scan of aortic

dissection
Single electron beam computed tomography scan of the ascending and

descending aorta showing a clear "flap" in the ascending aorta. This finding is
consistent with a type A aortic dissection.
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Aortogram showing descending thoracic aortic

dissection
This aortogram demonstrates dissection of the descending thoracic aorta,

arising immediately distal to the origin of the left subclavian artery. An oblique
lucency is noted within the lumen of the aorta, which is a diagnostic feature
(arrows).
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Differentiation of life-threatening causes of chest pain
Additional
Historical Examination Chest Additional
Diagnosis Electrocardiogram important
features findings radiograph tests
information
Acute Nonspecific ST segment elevations, Nonspecific Troponin Assume

coronary Substernal/left-sided May detect Q waves, new left bundle May show evidence and/or CK-MB symptoms of
syndrome chest pressure or signs of HF branch block are of HF elevations ACS within days
tightness is common evidence of AMI diagnose AMI or a few weeks
Onset is gradual Single ECG is not Single set of of PCI or CABG
sensitive for ACS biomarkers is is from an
Pain radiating to
not sufficiently occluded artery
shoulders or pain with Prominent R waves with
sensitive to rule or graft
exertion increases ST segment depressions
relative risk in V 1 and V 2 strongly out AMI
"Atypical" suggests posterior AMI

symptoms (eg,
dyspnea, weakness)
more common in
older adults, women,
diabetics
Older adults can
present with dyspnea,
weakness, syncope,
or MS alone
Aortic Sudden onset of Absent upper Ischemic changes in 15 Wide mediastinum Can mimic
dissection sharp, tearing, or extremity or percent or loss of normal many diseases
ripping pain carotid pulse is Nonspecific ST and T aortic knob contour is depending on
Maximal severity at suggestive changes in 30 percent common (up to 76 branch arteries
onset Discrepancy in percent) involved (eg,
systolic BP >20 10 percent have AMI, stroke)
Most often begins in
chest, can begin in mmHg between normal CXR
back right and left
upper extremity
Can mimic stroke,
is suggestive
ACS, mesenteric
ischemia, kidney Up to 30
stone percent with
neurologic
findings
Findings vary
with arteries
affected
Pulmonary Many possible No finding is Usually abnormal but Great majority are A
embolism presentations, sensitive or nonspecific normal high-sensitivity
including pleuritic specific Signs of right heart May show D-dimer is
pain and painless Extremity exam strain suggestive (eg, atelectasis, elevated useful to rule
dyspnea generally normal RAD, RBBB, RAE) hemidiaphragm, out PE only
Often sudden onset pleural effusion when negative
Lung exam
in low-risk
Dyspnea often generally
patients
dominant feature nonspecific; focal
wheezing may be
present;
tachypnea is
common
Tension Often sudden onset Ipsilateral Demonstrates air in

pneumothorax Initial pain often diminished or pleural space
sharp and pleuritic absent breath
sounds
Dyspnea often
dominant feature Subcutaneous
emphysema is
uncommon
Pericardial Pain from Severe Decreased voltage and May reveal enlarged Ultrasound
tamponade pericarditis is most tamponade electrical alternans can heart reveals
often sharp anterior creates appear with significant pericardial
chest pain made obstructive shock effusions effusion with
worse by inspiration and causes Diffuse PR segment tamponade
or lying supine and jugular venous depressions and/or ST
relieved by sitting distension, pulsus segment elevations can
forward paradoxus appear with acute
Dyspnea is common Pericardial pericarditis
effusion can
cause friction rub
Mediastinitis Forceful vomiting Ill-appearing; Large majority have

(esophageal often precedes shock; fever some abnormality:
rupture) esophageal rupture May hear pneumomediastinum,
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Recent upper (Hamman's) pleural effusion,

endoscopy or crunch over pneumothorax
instrumentation mediastinum
increases risk of
perforation
Odontogenic
infection is possible
cause
Coexistent
respiratory and
gastrointestinal
complaints may occur
MS: altered mental status; ACS: acute coronary syndrome; AMI: acute myocardial infarction; BP: blood pressure; CABG: coronary artery bypass graft;
CK-MB: creatine kinase-MB; CXR: chest radiograph; ECG: electrocardiogram; HF: heart failure; PCI: percutaneous coronary intervention; PE: pulmonary
embolism; RAD: right axis deviation; RAE: right atrial enlargement; RBBB: right bundle branch block.
32 of 33 6/8/17, 2:43 PM
Contributor Disclosures
Warren J Manning, MD Patent Holder: Samsung Electronics [MRI]. Equity Ownership/Stock Options (Spouse): General Electric [Cardiac
imaging]; Pfizer [Anticoagulants]. James H Black, III, MD Nothing to disclose Emile R Mohler III, MD Grant/Research/Clinical Trial Support:
NIH, Pluristem and Celgene [PAD (Mesenchymal stem cells)]. Patent Holder: University of Pennsylvania [Cardiovascular (Vascular health
profile blood test)]. Equity Ownership/Stock Options: Cytovas [Cardiovascular biomarker (Vascular health profile blood test)]. James
Hoekstra, MD Consultant/Advisory Boards: AstraZeneca [ACS (Ticagrelor)]; Janssen [ACS (Rivaroxaban)]. Joseph L Mills, Sr,
MD Grant/Research/Clinical Trial Support: Cesca Therapeutics [Critical limb ischemia (Hepatocyte growth factor)]; Voyager Trial [Peripheral
artery disease (Rivoxaraban)]. Consultant/Advisory Boards: AnGes [Critical limb ischemia (Hepatocyte growth factor)]; AstraZeneca
[Peripheral artery disease (ticagrelor)]. Other Financial Interest: Elsevier; Rutherford [Vascular surgery (Rutherford and Comprehensive
Vascular and Endovascular Surgery textbooks)]. John F Eidt, MD Nothing to disclose Kathryn A Collins, MD, PhD, FACS Nothing to
disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a
multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content
is required of all authors and must conform to UpToDate standards of evidence.
Conflict of interest policy
33 of 33 6/8/17, 2:43 PM

Clinical Features and Diagnosis of Acute Aortic Dissection

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Clinical features and diagnosis of acute aortic dissection - UpToDate https://www.uptodate.com/contents/clinical-features-and-diagnosis-of-...

Official reprint from UpToDate

Clinical features and diagnosis of acute aortic dissection

Authors: Warren J Manning, MD, James H Black, III, MD

Horner syndrome is from compression of the superior cervical sympathetic ganglion.

Presence of mediastinal widening: 39 percent

The intimal flap (image 3 and image 7 and image 8)

Basics topics (see "Patient education: Aortic dissection (The Basics)")

SUMMARY AND RECOMMENDATIONS

Use of UpToDate is subject to the Subscription and License Agreement.

Topic 8190 Version 23.0

Classification of aortic dissection

In the DeBakey classification of aortic dissection:

Graphic 100115 Version 4.0

Focal aortic dissection on CT scan

CT: computed tomography.

Graphic 101579 Version 2.0

Acute aortic syndromes

Graphic 62132 Version 6.0

Diagnosis and treatment of focal aortic dissection using CTA

CTA: computed tomography angiography.

Graphic 101393 Version 1.0

Aortic dissection on noninvasive imaging

Representative transesophageal echocardiograms (TEE) (panels A and B) and

Proximal aortic dissection

Mechanisms of aortic regurgitation in ascending aortic dissection may include:

Graphic 101679 Version 1.0

Aortic root aneurysm in Marfan syndrome on chest film

This aortogram in a young patient with Marfan syndrome demonstrates

Courtesy of Jonathan Kruskal, MD.

Graphic 66051 Version 4.0

Aortogram showing aortic rupture with pseudoaneurysm

The aortogram, obtained following administration of contrast material into the

Courtesy of Jonathan Kruskal, MD.

Graphic 73280 Version 4.0

Presentations of aortic dissection based on affected structures

Clinical findings Artery or structure involved

Aortic insufficiency or heart failure Aortic valve

Myocardial infarction Coronary artery (often right)

Cardiac tamponade Pericardium

Horner syndrome (ptosis, miosis, anhidrosis) Superior cervical sympathetic ganglion

Stroke or syncope Brachiocephalic, common carotid, or left subclavian arteries

Upper extremity pulselessness, hypotension pain Subclavian artery

Paraplegia Intercostal arteries (give off spinal and vertebral arteries)

Back or flank pain; renal failure Renal artery

Abdominal pain; mesenteric ischemia Celiac or mesenteric arteries

Lower extremity pain, pulselessness, weakness Common iliac artery

Graphic 77441 Version 4.0

Disorders associated with increased plasma levels of fibrin D-dimer

Arterial thromboembolic disease

Acute limb ischemia

Venous thromboembolic disease

Deep vein thrombosis

Disseminated intravascular coagulation

Preeclampsia and eclampsia

Abnormal fibrinolysis; use of thrombolytic agents

Cardiovascular disease, congestive failure

Surgery/trauma (eg, tissue ischemia, necrosis)

Systemic inflammatory response syndrome

Vasoocclusive episode of sickle cell disease

Severe liver disease (decreased clearance)

Nephrotic syndrome (eg, renal vein thrombosis)

Acute renal failure

Chronic renal failure and underlying cardiovascular disease