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).
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Clinical features and diagnosis of acute aortic dissection

Topic Outline
SUMMARY & RECOMMENDATIONS
INTRODUCTION
CLASSIFICATION
o Anatomic classification
o Variants
PATHOPHYSIOLOGY
INCIDENCE AND ASSOCIATED CONDITIONS
o High-risk conditions
CLINICAL FEATURES
o Symptoms and signs
- Acute pain
- Pulse deficit
- Heart murmur
- Focal neurologic deficit
 - Hypotension
Syncope
o Electrocardiogram
o Chest radiograph
o Laboratory studies
- D-dimer
- Other experimental tests
DIAGNOSIS
o High-risk clinical features
o Cardiovascular imaging
- Hemodynamically stable
- Hemodynamically unstable
- Role of aortography
DIFFERENTIAL DIAGNOSIS
INFORMATION FOR PATIENTS
SUMMARY AND RECOMMENDATIONS
REFERENCES

GRAPHICS View All

DIAGNOSTIC IMAGES
o - CT of focal aortic dissection
o - CTA showing focal aortic dissection
o - Aortic dissection on noninvasive imaging
o - Aortic root aneurysm in Marfan syndrome on chest film
o - Aortogram showing aortic rupture with pseudoaneurysm
o - Aortic dissection noncontrast CT
o - Aortic dissection on magnetic resonance imaging
o - TEE descending aortic dissection
o - Thoracic aortic dissection on computed tomography
o - Thoracic aortic dissection on reconstructed computed tomography
o - Electron beam computed tomography scan of aortic dissection
o - Aortogram showing descending thoracic aortic dissection
FIGURES
o - Classification of aortic dissection
o - Acute aortic syndromes
o - Proximal aortic dissection
MOVIES
o - Aortic dissection transesophageal echocardiogram
o - Mobile aortic dissection flap on TEE
o - Dissection of the descending aorta on TEE
o - Color flow doppler of aortic dissection
o - Dissection of the ascending aorta on TEE
o - Abdominal aortic dissection
o - Ascending aortic dissection
TABLES
o - Aortic dissection anatomy based clinical findings
o - Causes elevated D-dimer
o - Chest pain differentiation
RELATED TOPICS
Acute aortic regurgitation in adults
Acute mesenteric arterial occlusion
Auscultation of cardiac murmurs in adults
Blunt thoracic aortic injury
Cardiac tamponade
Clinical features and diagnosis of abdominal aortic aneurysm
Clinical manifestations and diagnosis of Turner syndrome
Clinical manifestations and diagnosis of bicuspid aortic valve in adults
Clinical manifestations and diagnosis of coarctation of the aorta
Clinical manifestations and diagnosis of thoracic aortic aneurysm
Clinical manifestations of giant cell (temporal) arteritis
Early noncardiac complications of coronary artery bypass graft surgery
Evaluation and management of the cardiovascular complications of cocaine
abuse
Evaluation of the adult with chest pain in the emergency department
Exercise in the treatment and prevention of hypertension
Genetics, clinical features, and diagnosis of Marfan syndrome and related
disorders
Ischemic hepatitis, hepatic infarction, and ischemic cholangiopathy
Management of acute aortic dissection
Management of symptomatic (non-ruptured) and ruptured abdominal aortic
aneurysm
Nephrogenic systemic fibrosis/nephrogenic fibrosing dermopathy in advanced
renal failure
Off-pump and minimally invasive direct coronary artery bypass graft surgery:
Outcomes
Overview of acute aortic syndromes
Overview of acute arterial occlusion of the extremities (acute limb ischemia)
Overview of and approach to the vasculitides in adults
Overview of intestinal ischemia in adults
Patient education: Aortic dissection (The Basics)
Renal infarction
Surgical and endovascular management of type B aortic dissection

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

Contributor Disclosures
All topics are updated as new evidence becomes available and our peer review process
is complete.
Literature review current through: Aug 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 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 (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 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 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

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 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 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 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.)

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Management of acute aortic dissection

Topic Outline
SUMMARY & RECOMMENDATIONS
INTRODUCTION
ACUTE MEDICAL MANAGEMENT
TYPE AND ETIOLOGY OF DISSECTION
o Extent and classification
o Etiology
ASCENDING (TYPE A) AORTIC DISSECTION
o Efficacy of intervention
o Medical risk assessment
- Prognostic factors
o Extent of open repair
o Role for endovascular repair
DESCENDING (TYPE B) AORTIC DISSECTION
o Efficacy of medical management
o Intervention
- Endovascular repair
- Open repair
LONG-TERM MANAGEMENT
o Anti-impulse therapy
 o Identifying associated genetic conditions
o Serial imaging
COMPLICATIONS
o Recurrent dissection
o Reintervention for endograft complications
o Reoperation
MORTALITY
INFORMATION FOR PATIENTS
SUMMARY AND RECOMMENDATIONS
REFERENCES

GRAPHICS View All

FIGURES
o - Classification of aortic dissection
o - Endovascular repair of acute type B aortic dissection
TABLES
o - Acute aortic dissection - Rapid overview
o - Antihypertensive therapy for acute aortic syndromes in adults

RELATED TOPICS
Clinical features and diagnosis of acute aortic dissection
Endoleak following endovascular aortic repair
Management of Marfan syndrome and related disorders
Management of thoracic aortic aneurysm in adults
Overview of acute aortic syndromes
Overview of open surgical repair of the thoracic aorta
Pathogenesis, clinical features, and diagnosis of contrast-induced nephropathy
Patient education: Aortic dissection (The Basics)
Patient education: Thoracic aortic aneurysm (The Basics)
Surgical and endovascular management of type B aortic dissection
Transesophageal echocardiography in the evaluation of aortic valve disease

Management of acute aortic dissection

Authors:
James H Black, III, MD
Warren J Manning, MD
Section Editors:
Emile R Mohler III, MD
Gabriel S Aldea, MD
Edward Verrier, MD
Deputy Editor:
Kathryn A Collins, MD, PhD, FACS

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process
is complete.
Literature review current through: Aug 2017. | This topic last updated: Jan 09, 2017.

INTRODUCTION Thoracic aortic dissection is usually suspected clinically from the

history and physical examination when a patient presents with severe, sharp, or
"tearing" anterior chest pain (in ascending aortic dissection) or posterior chest or back
pain (arch or descending aortic dissection). This diagnosis can be easily overlooked
among patients with acute chest pain, and a high index of suspicion is needed to obtain
a timely diagnosis such that appropriate initial therapy can be instituted promptly.
Advances in imaging and better awareness have improved the diagnosis, which is
confirmed using advanced cardiovascular imaging.

The DeBakey and the Stanford (Daily) systems are used to classify aortic dissection
(figure 1) [1,2]. The Stanford system, which is more widely used, classifies dissections
that involve the ascending aorta as type A, regardless of the site of the primary intimal
tear; all other dissections are classified as type B.

The goals of early management of aortic dissection are to control pain and limit the
extent of the dissection using anti-impulse therapy, which typically involves
administration of beta blockers. Timing of intervention differs for ascending (type A)
and descending (type B) thoracic aortic dissection, and thus, early determination of the
extent of dissection is important.

The management of acute aortic dissection will be reviewed here. The recommendations
are generally in agreement with multidisciplinary cardiovascular guidelines [3-5]. The
clinical evaluation and diagnosis of aortic dissection are reviewed separately.
Management of other acute aortic syndromes is discussed separately. (See "Clinical
features and diagnosis of acute aortic dissection" and "Overview of acute aortic
syndromes" and "Overview of acute aortic syndromes", section on 'Definition and
pathophysiology'.)

ACUTE MEDICAL MANAGEMENT Acute medical management of acute aortic

syndromes including aortic dissection involves controlling pain, and providing anti-
impulse therapy in the form of blood pressure lowering and decreasing the velocity of
left ventricular contraction, to decrease aortic shear stress and minimize the tendency
for the dissection to propagate (table 1). Medications and dosing used in acute aortic
dissection are similar to other acute aortic syndromes and are reviewed separately (table
2). (See "Overview of acute aortic syndromes", section on 'Acute medical
management'.)

TYPE AND ETIOLOGY OF DISSECTION Determining the location of the aortic

dissection and its etiology are important, as these impact management. Acute type A
aortic dissection is a surgical emergency. Acute type B aortic dissection typically does
not require urgent surgery unless the patient develops complications (eg, end-organ
malperfusion, refractory pain, rapidly expanding false lumen, impending or frank
rupture). Acute medical therapies should not interfere with timely transfer to the
operating room for those in whom immediate surgery is indicated. An experienced
cardiovascular surgeon should be involved early in the course to discuss any decision
for surgery and its timing, which must be individualized, taking into account the
patient's comorbidities (eg, prior stroke, renal failure, hypertension, coronary heart
disease), age, and patient and family wishes. (See "Surgical and endovascular
management of type B aortic dissection", section on 'Indications for intervention'.)

Extent and classification The diagnosis is confirmed and the extent of the dissection
is determined using advanced cardiovascular imaging. Diagnostic evaluation should be
accomplished as promptly as possible. For patients who are hemodynamically unstable,
bedside transesophageal echocardiography (TEE) can be used with high sensitivity [6].
In stable patients, computed tomographic (CT) angiography is more frequently chosen
for the reasons discussed elsewhere. (See "Clinical features and diagnosis of acute aortic
dissection", section on 'Cardiovascular imaging'.)

The DeBakey and the Stanford (Daily) systems are used to classify aortic dissection
[1,2]. The Stanford system, which is more widely used, classifies dissections that
involve the ascending aorta as type A, regardless of the site of the primary intimal tear
(figure 1); all other dissections are classified as type B. By comparison, the DeBakey
system is based on the site of origin with type I originating in the ascending aorta and
propagating to at least the aortic arch, type II originating in and confined to the
ascending aorta, and type III originating in the descending aorta and extending distally
or proximally. (See "Overview of acute aortic syndromes", section on 'Classification'.)

Etiology The etiology of the dissection also has a bearing on management and, in
particular, the nature of aortic repair, when indicated, for descending thoracic aortic
dissection. In general, patients with idiopathic (sporadic) descending thoracic and
abdominal aortic dissection can be managed with endovascular techniques, whereas an
open surgical approach is preferred for those with genetically medicated dissection due
to the likelihood of further aortic degeneration. (See "Clinical features and diagnosis of
acute aortic dissection", section on 'Incidence and associated conditions' and 'Ascending
(type A) aortic dissection' below and 'Descending (type B) aortic dissection' below.)

High-risk medical conditions for aortic dissection are listed below and discussed in
more detail separately (see "Clinical features and diagnosis of acute aortic dissection",
section on 'Incidence and associated conditions'):

Hypertension (abrupt, transient severe increase)

Genetically mediated aortic disease

Syndromic: Marfan syndrome, Loeys-Dietz syndrome (LDS), Vascular Ehlers-Danlos

syndrome, Turner syndrome, osteoarthritis syndrome

Nonsyndromic: Familial aortic aneurysm/dissection, bicuspid aortic valve, aortic

coarctation

Sporadic aortic disease including preexisting thoracic aortic aneurysm (TAA) and
abdominal aortic aneurysm (AAA)

Inflammatory conditions

Aortic instrumentation, trauma, or surgery

ASCENDING (TYPE A) AORTIC DISSECTION Acute type A aortic dissection is
a surgical emergency since these patients are at high risk for a life-threatening
complication such as aortic regurgitation, cardiac tamponade, stroke, frank rupture, and
myocardial infarction with mortality rates as high as 1 to 2 percent per hour early after
symptom onset without surgical intervention [7].

The only reason to avoid surgical intervention in any patient with documented type A
dissection is the presence of significant comorbidities that impact survival to one year or
less such as with very advanced age and frailty, advanced malignancy, dementia, or
patient/family wishes. Even in patients with malperfusion syndromes, survival is better
with surgical intervention, although prognosis is significantly worse when these risk
factors are present. Hemorrhagic stroke is a relative contraindication to urgent surgical
intervention.

Efficacy of intervention Operative mortality for acute type A aortic dissection at

experienced centers ranges from 7 to 36 percent, which is well below the more than 50
percent mortality with medical therapy [8-17]. (See 'Extent of open repair' below.)

The survival benefits of surgery were illustrated in an International Registry of Acute

Aortic Dissection (IRAD) review of 547 patients with a type A dissection [10]. Eighty
percent of patients were treated surgically. The main cited reasons for medical therapy
were comorbid conditions, advanced age (mean of 80 years), and patient refusal. The in-
hospital mortality rates were 27 and 56 percent for surgical and medical therapy,
respectively, which is a difference that was due in part to increased comorbidity in
medically treated patients. Not surprisingly, the patients who died had a higher rate of
in-hospital complications, including neurologic deficits, coronary or mesenteric
ischemia, acute renal failure, and limb ischemia. In a separate series of 487 patients, a
similar in-hospital mortality with surgical therapy (22 percent) was noted [18].

Even the presence of acute myocardial infarction, which may be due to the dissection
involving a coronary ostium (particularly the right coronary artery), should not entirely
exclude the option of rapid surgical intervention. However, patients with a stroke in
progress are at increased risk for hemorrhagic cerebral infarction due to intraoperative
heparinization. Thus, hemorrhagic stroke is a relative contraindication to urgent surgical
intervention, as are major comorbidities. (See 'Prognostic factors' below.)

In one of the IRAD studies, patients with acute type A dissection who were older than
69 years of age were less likely to be treated surgically compared with younger patients
(64 versus 86 percent) [19]. However, older age alone should not preclude surgery
[11,19]. In the registry report, although in-hospital mortality was significantly higher in
older patients compared with younger patients (38 versus 23 percent), it was lower in
older patients treated surgically compared with medical management [19]. Thus,
surgery should be considered in older patients, even some octogenarians with an
otherwise good prognosis and few comorbidities [19]. Women were also less likely to
be treated surgically (71 versus 87 percent) [20]. As with older patients, women have a
higher in-hospital mortality with surgical treatment than men (32 versus 22 percent), but
they have a lower mortality compared with medical therapy (32 versus 54 percent).

Medical risk assessment In addition to the imaging necessary to confirm the

diagnosis of type A aortic dissection, other studies may be useful to evaluate the patient
for concomitant coronary artery disease, particularly the right coronary artery, or aortic
valve disease prior to urgent surgical repair of the ascending aorta. (See "Clinical
features and diagnosis of acute aortic dissection", section on 'Diagnosis'.)

Older patients with acute aortic dissection may have a significant prevalence of
coronary artery disease, some have suggested that coronary angiography should be
performed prior to surgery so that bypass surgery on critical stenosis can be performed
while the patient is under cardiopulmonary bypass. There has also been concern that the
presence of undiagnosed critical coronary stenoses may make weaning from
cardiopulmonary bypass more difficult and can increase the risk of perioperative
myocardial infarction or death. We do not advocate preoperative coronary angiography,
since the resulting delay of surgery for type A aortic dissection increases the risk of
cardiac tamponade or aortic rupture, and engaging the native coronary arteries may be
technically difficult due to the dissection. Intraoperative transesophageal
echocardiography (TEE) may identify regional wall motion abnormalities that would
need to be considered and addressed. Moreover, type A aortic dissection that is
compressing the coronary artery ostia may require bypass as part of the initial treatment.

The role of percutaneous coronary angiography was evaluated in a study that

retrospectively analyzed the outcome of 122 patients who underwent emergency aortic
surgery, primarily for a type A aortic dissection [21]. There was no difference in the in-
hospital mortality between those who did or did not undergo coronary angiography (22
versus 16 percent), including those who had a prior myocardial infarction, which was
the only predictor of in-hospital mortality. Coronary angiography had no impact on the
incidence of coronary artery bypass grafting (17 versus 25 percent), three-quarters of
which were performed because of coronary artery dissection, not atherosclerotic
disease. These observations suggest limited value from coronary angiography and
support our recommendation of proceeding to surgery as rapidly as possible [21].

In addition to its important role in the diagnosis of aortic dissection, TEE can define the
severity and mechanism of aortic regurgitation that can complicate acute type A aortic
dissection [22]. (See "Transesophageal echocardiography in the evaluation of aortic
valve disease".)

Prognostic factors In a review of 464 patients from an IRAD study who presented
with aortic dissection, 72 percent of those with a type A dissection were treated
surgically [8]. Reasons for medical therapy included advanced age, comorbidity, patient
refusal, or death prior to planned surgery. Poor prognostic factors in this study and
others included [8,10,12-14,16,18,19,21,23-25]:

Age over 70 years

Abrupt onset of chest pain

Hypotension, shock, or tamponade at presentation

Renal failure at presentation and before surgery

Pulse deficit
Abnormal electrocardiogram, particularly ST segment elevation

Prior myocardial infarction

Previous aortic valve replacement

Renal and/or visceral ischemia

Underlying pulmonary disease

Preoperative neurologic impairment

The first six factors were the most important predictors of in-hospital mortality in the
IRAD review [10]. Using a predictive score that incorporated these parameters, patients
could be identified with subsequent in-hospital mortality rates that ranged from 2 to
over 80 percent. However, age alone is not reason to withhold surgical treatment in a
previously active patient.

Extent of open repair Surgical treatment involves:

Excision of the intimal tear

Obliteration of entry into the false lumen proximally

Reconstitution of the aorta with interposition of a synthetic vascular graft

Repair or replacement of the aortic valve

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 often undergo successful aortic valve repair. Abnormalities that cannot be
repaired (eg, Marfan aortic root dilation, bicuspid valve, aortitis) may require valve
replacement [26]. An aggressive surgical approach, including a full aortic root or
hemiarch replacement when the aortic valve, sinuses, or arch are involved, may not be
associated with an increased operative risk [27,28]. (See "Overview of open surgical
repair of the thoracic aorta", section on 'Ascending aorta' and "Overview of open
surgical repair of the thoracic aorta", section on 'Aortic arch'.)

Role for endovascular repair A possible alternative to surgery in patients with type A
dissection who have ischemic complications is endovascular stent-grafting. There is
only a limited experience in patients with acute type A dissections. Further study is
required to determine the role for this approach in such patients.

A hybrid approach to the repair of type A aortic dissection, sometimes referred to as the
"frozen elephant trunk repair," uses an open approach to surgically repair the ascending
aorta, while using a stent-graft to manage the descending aorta. Several case series have
compared this technique with conventional open repair [29-31]. In one series, the false
lumen was completely obliterated in 14 of 15 patients within three months [32]. In
another, a triple-branched stent-graft was placed into the three arch vessels and
descending aorta in 30 patients with acute type A dissection [33]. The procedure was
technically successful in all patients, and aortic cross-clamp and lower body ischemic
times were 84 and 31 minutes, respectively, which is generally much lower compared
with conventional open surgical treatment.

Although initial repair of the dissection may result in resolution of peripheral ischemia,
stenting and/or balloon fenestration of the dissecting membrane may be needed for
patients with mesenteric, renal, or peripheral ischemia after the initial repair [6,34,35].
(See "Surgical and endovascular management of type B aortic dissection", section on
'Fenestration of septum' and "Surgical and endovascular management of type B aortic
dissection", section on 'Stenting branch obstruction'.)

DESCENDING (TYPE B) AORTIC DISSECTION Type B dissection is generally

managed medically initially, with surgical intervention reserved for those who develop
complications related to the dissection [9,36,37]. However, there is an increasing
interest to consider endovascular treatment of type B aortic dissection preemptively
before the onset of malperfusion, which has the potential to reduce the incidence of late
aortic expansion [38-42]. (See "Surgical and endovascular management of type B aortic
dissection", section on 'Indications for intervention'.)

Efficacy of medical management Based upon historical observational data and a

randomized trial, we suggest initial medical management for patients with
uncomplicated type B aortic dissection. Medical management includes long-term blood
pressure and imaging surveillance. In a series of 384 patients with type B dissections
from IRAD, 73 percent were managed medically; in-hospital mortality for these patients
was 10 percent [43].

Some clinicians have suggested that endovascular intervention in patients with acute
dissection, but without malperfusion or other complications, may improve long-term
outcomes by favorably influencing the relationships of the true and false lumen and
obliterating anatomy that would otherwise contribute to late morbidity and mortality
[38,44,45]. However, the overall results of these studies support a complication-specific
approach to type B dissection as the best treatment paradigm.

One randomized trial compared endovascular with conventional medical management

for uncomplicated type B aortic dissection. The INvestigation of STEnt grafts in
patients with Aortic Dissection (INSTEAD) trial randomly assigned 140 patients who
were clinically stable and free of malperfusion syndrome at the time of treatment
(median of 12 days from randomization to stent-graft insertion) to continued medical
therapy with a goal blood pressure of 120/80 mmHg, or to medical therapy and
endovascular stent-grafting [38]. At two-year follow-up, there were no significant
differences between the endovascular and medical groups for overall survival (89 versus
96 percent). The study assumed a 30 percent risk of death after type B dissection in a
two-year time frame; thus, the study showed that medical therapy was quite effective
and was associated with a low incidence of death. It is interesting to note that favorable
aortic remodeling was seen in 91.3 percent of the endovascular group compared with
only 19.4 percent of the medically treated patients; however, this did not translate into
clinical benefit. In the five-year follow-up (INSTEAD-XL), endovascular treatment was
associated with favorable aorta-specific mortality compared with optimal medical
management alone [46].
Another trial similarly randomly assigned 61 patients to best medical therapy or best
medical therapy plus endovascular stent-grafting [47]. At one-year follow-up, the
combined endpoint of incomplete/no false lumen thrombosis, aortic dilation, or aortic
rupture was significantly less for those who were treated with stent-grafts (per protocol
results). Technical failures, loss to follow-up, and crossovers from the best medical
therapy group limited the analysis.

The reported long-term survival rate with medical therapy is approximately 60 to 80

percent at four to five years [9,48-50], and approximately 40 to 45 percent at 10 years
[48,49]. Survival is best for patients with noncommunicating and retrograde dissections
[51]. Despite fair survival among patients treated medically, spontaneous healing of the
dissection, characterized by disappearance of the false lumen due to complete
thrombosis, is uncommon [36,51,52]. Continued flow through the false lumen (patent
false lumen), which occurs with either partial thrombosis or no significant thrombosis,
has been postulated to prevent healing. The relationship between long-term prognosis
and the degree of patency of the false lumen was evaluated in 201 hospital survivors of
type B acute aortic dissection who were enrolled in IRAD [52]. Complete false lumen
patency or partial thrombosis was present in 57 and 34 percent of patients, respectively.
The mean three-year mortality rate was significantly worse in patients with partial
thrombosis compared with those with complete patency (32 versus 14 percent). With
longer-term follow-up of five years, the risk of all-cause mortality was again not
significant for endovascular versus medical treatment (11.1 versus 19.3 percent).
However, aorta-specific mortality (6.9 versus 19.3 percent) and progression (27 versus
46.1 percent) were significantly lower for endovascular compared with optimal medical
treatment alone [46].

Intervention Intervention (surgical or endovascular) for descending thoracic aortic

dissection is generally reserved for patients who develop complications including
occlusion of a major aortic branch leading to end-organ ischemia (ie, malperfusion),
persistent severe hypertension or chest pain, propagation of the dissection (as may be
manifested by persistent or recurrent pain), aneurysmal expansion, expanding
hematoma, or rupture [6,53,54]. Aortic dissection frequently causes life-threatening
ischemia of distal organs, and the mortality associated with such complications can
exceed 60 percent.

Endovascular repair Endovascular stent-grafting has been used as a less invasive

alternative to open surgery for the management of type B aortic dissection [6]. The
stent-graft is positioned to cover the intimal flap to seal the entry site of the dissection,
resulting in thrombosis of the false lumen (figure 2). (See "Surgical and endovascular
management of type B aortic dissection", section on 'Endovascular repair' and "Surgical
and endovascular management of type B aortic dissection", section on 'Coverage of
entry tear'.)

In an IRAD series of 384 type B dissections, 46 (12 percent) were managed with
endovascular stent-grafting [43]. The technique was reserved for patients who had
undergone at least eight weeks of medical management. Only three (6.5 percent) died
during the initial hospitalization. Stent-grafting has been evaluated for acute and, in
some cases, life-threatening dissections, but the outcomes are not as good [34,55,56].
One report evaluated 19 patients with an acute dissection (15 with type B) and an
indication for surgery [55]. Complete thrombosis of the false lumen was achieved in 79
percent, and revascularization with relief of ischemic symptoms occurred in 76 percent
of obstructed aortic branch sites. The 30-day mortality rate was 16 percent, and
morbidity was 21 percent (small bowel and renal infarction and lower extremity
gangrene). Among patients who survived this period, there were no deaths or instances
of aneurysm or aortic rupture during the subsequent 13-month follow-up period.
Longer-term follow-up was described in a series of 49 patients with acute and chronic
aortic dissection who were treated with stent-grafts [32]. Serial computed tomography
(CT) studies in the 34 patients with type B aortic dissection showed that, at two years,
total occlusion of the false lumen was achieved with acute dissection in 76 percent of
patients.

To overcome the small number of patients in most published series, a meta-analysis was
performed of 39 studies involving a total of 609 patients who underwent stent-graft
placement for a type B dissection [56]. The following findings were noted:

Procedure success was achieved in 98 percent of patients.

Major complications occurred in 11.1 percent; neurologic complications, the most

serious, occurred in 2.9 percent, mostly periprocedural stroke and paraplegia (1.9 and
0.8 percent, respectively). The major complication rate was significantly higher for
acute compared with chronic dissection (21.7 versus 9.1 percent). Minor complications
occurred in 2.5 percent. The rate of complications compared favorably with previously
reported surgical series. The rate was higher in later studies, which may reflect inclusion
of higher-risk patients with increasing experience with the procedure.

The false lumen was not abolished in approximately 25 percent of patients, and at a
mean follow-up of 19 months, aortic rupture occurred in 2.3 percent.

The in-hospital mortality rate was 5.2 percent. Thirty-day mortality was 5.3 percent
and was significantly higher for acute compared with chronic dissection (9.8 versus 3.2
percent). Kaplan-Meier analysis revealed overall survival rates of 90 percent at one year
and 89 percent at two years.

Outcomes were much better in centers that had performed more than 20 endovascular
procedures compared with fewer. This included significantly lower rates of overall
complications (7.7 versus 20.9 percent), neurologic complications (1.0 versus 5.7
percent), and 30-day mortality (3.2 versus 8.5 percent).

Although initial repair of the dissection often results in resolution of peripheral

ischemia, stenting and/or balloon fenestration of the dissecting membrane may be
noninvasive alternatives for patients with mesenteric, renal, or peripheral ischemia after
the initial repair [6,34,35]. (See "Surgical and endovascular management of type B
aortic dissection", section on 'Fenestration of septum' and "Surgical and endovascular
management of type B aortic dissection", section on 'Stenting branch obstruction'.)

Open repair Although rarely necessary for type B complicated aortic dissection,
given the advances in thoracic aortic stent-graft designs (eg, fenestrated devices) and
use of debranching procedures, open surgical repair may be needed only for those
whose anatomy will not support an endovascular stent-graft and for patients with high-
risk genetically mediated conditions [26]. Because patients treated surgically are
primarily those with a complicated course, it is not surprising that short-term mortality
for these patients is much higher compared with those managed with medical therapy.
In data from IRAD, in-hospital mortality for surgical patients was 32 percent compared
with 10 percent for those treated medically [43]. Two independent predictors for
surgical mortality were identified: age greater than 69 years and hypotension or shock
on admission [57]. (See "Surgical and endovascular management of type B aortic
dissection", section on 'Open surgery'.)

Although short-term outcomes are better for medically versus surgically treated patients
with type B dissection [9,48,50], long-term outcomes may be similar [9,48]. This was
illustrated in a report of 142 patients, 111 (78 percent) of whom were treated medically
[48]. There was a trend toward lower mortality with medical therapy at one year (15
versus 33 percent), but the difference tended to diminish over time. Both groups had
similar survival at 5 and 10 years (60 and 35 percent). (See 'Long-term management'
below.)

LONG-TERM MANAGEMENT There are three main management issues in

patients who have survived the initial dissection: ongoing anti-impulse therapy, in the
form of blood pressure lowering, to minimize aortic wall shear stress; evaluation for
high-risk clinical conditions; serial imaging to detect signs of dissection progression, re-
dissection, or aneurysm formation; and reoperation when indicated.

Anti-impulse therapy Once heart rate control has been achieved and the patient is
tolerating an oral diet, intravenous beta blocker (or other antihypertensive) therapy can
be switched to an oral route. All patients should be maintained on lifelong therapy to
reduce systemic blood pressure and the rate of rise in systolic pressure, both of which
will minimize aortic wall stress [6]. Although not evaluated in controlled trials, we
suggest a target blood pressure of less than 120/80 mmHg [6]. Combination
antihypertensive drug therapy is usually required.

Though unproven, avoidance of strenuous physical activity that would lead to a spike in
blood pressure is also recommended as another method to minimize aortic shear stress.
(See "Management of Marfan syndrome and related disorders", section on 'Restriction
of strenuous activity'.)

Identifying associated genetic conditions Similarly to thoracic aortic aneurysm,

patients with thoracic aortic dissection should be evaluated for possible underlying
genetic or familial disorders known to be related, which may increase their individual
risk of progression or complications. (See "Clinical features and diagnosis of acute
aortic dissection", section on 'Incidence and associated conditions' and "Management of
thoracic aortic aneurysm in adults", section on 'Identifying associated genetic
conditions'.)

Serial imaging We generally perform a baseline thoracic magnetic resonance (MR)

or computed tomographic (CT) angiography prior to discharge, with follow-up
examinations at 3, 6, and 12 months, and annually thereafter, even if the patient remains
asymptomatic (and presuming the patient is a candidate for an intervention) [6,36]. (See
'Reintervention for endograft complications' below and 'Reoperation' below.)

The following abnormalities can be detected on serial imaging:

Extension or recurrence of the dissection

Aneurysm formation

Leakage at surgical anastomotic or stent-graft component overlap sites

MR angiography is as accurate as transesophageal echocardiography (TEE), and

because it is noninvasive, it is more acceptable for serial studies. MR angiography does
not expose patients to iodinated contrast and ionizing radiation, which are important
factors for younger patients who will likely have many years of serial monitoring. CT
angiography is an alternative, but it exposes the patient to considerable ionizing
radiation and requires iodinated contrast, which may cause nephrotoxicity. (See
"Pathogenesis, clinical features, and diagnosis of contrast-induced nephropathy".)

Alternating CT and MR angiography is a reasonable option for patients with good renal
function. Noncontrast MR is an alternative for patients with impaired renal function.
Transthoracic echocardiography is not considered a monitoring alternative, but it may
be necessary to monitor ongoing valvular dysfunction.

COMPLICATIONS

Recurrent dissection In an International Registry of Acute Aortic Dissection (IRAD)

study that identified 204 of 3624 patients with recurrent aortic dissection, patients with
recurrent aortic dissection were more likely to have Marfan syndrome (21.5 versus 3.1
percent) but not bicuspid aortic valve (3.6 versus 3.2 percent) [58]. Recurrent dissection
is likely to increase the risk for rupture, given the inherent weakness of the now twice-
dissected aorta. Early intervention may be warranted, especially if the aortic diameter
has increased with serial imaging.

Reintervention for endograft complications Although perioperative outcomes are

improved compared with open surgery, complications related to the endograft
placement such as endoleak or device migration may indicate the need for
reintervention, which occurs in up to one-third of patients. (See "Endoleak following
endovascular aortic repair", section on 'Endoleak management after TEVAR'.)

Reoperation Repeat surgery is required in up to one-half of patients at 10-year

follow-up, usually because of extension or recurrence of dissection at the previous site
of intervention, localized aneurysm formation remote from the site of repair, graft
dehiscence or infection, or aortic regurgitation [13,14,36,51,59,60]. Higher reoperation
rates generally reflect surgery among those with Marfan syndrome or other genetically
mediated conditions [36]. (See "Management of Marfan syndrome and related
disorders".)

The occurrence of a residual aortic dissection requiring subsequent surgical repair was
evaluated in a report of 58 patients who were discharged from the hospital and then
followed with serial magnetic resonance (MR) scans [60]. Residual distal dissection
was present in 45 (78 percent). The yearly aortic growth rate of this segment was 0.37
cm overall and significantly higher at 0.56 cm in the absence of thrombus in the false
lumen. During a seven-year follow-up, 16 patients (28 percent) underwent reoperation
because of progressive dilation of the untreated aortic segment. Residual dissection was
present in all but one, and 13 had no thrombosis in the false lumen.

Late aneurysm formation and adverse outcomes, including death, are related to the
initial diameter of the false lumen in the upper thoracic aorta. This was illustrated in a
study of 100 patients (51 with type I and 49 with type III) who survived initial
hospitalization for aortic dissection in whom contrast-enhanced computed tomography
(CT) scan was performed during the acute phase [61]. The following findings were
noted at a mean CT follow-up of 31 months and a mean clinical follow-up of 53
months:

Aneurysm (diameter greater than 59 mm) formation occurred in 15 (28 percent) of the
53 patients, most often in the upper thoracic descending aorta.

Patients with an initial false lumen diameter of >21 mm in the upper thoracic aorta,
compared with those with a smaller diameter, were significantly more likely to develop
late aneurysm formation (42 versus 5 percent) or to die.

In another study, the natural history of the distal aorta was evaluated in 89 surgical
survivors of type A dissection. Serial CT angiography identified a median expansion
rate of approximately 1 mm/year. Male gender, an initial descending aorta diameter of
greater than 4 cm, or an initial diameter of less than 4 cm with a patent false lumen were
identified as predictive of more rapid descending aorta expansion [62]. The overall risk
of reoperation was 16 percent at 10 years.

MORTALITY The 10-year actuarial survival rate of patients with an acute aortic
dissection who leave the hospital has ranged from 30 to 88 percent; survival appears
similar for both type A and type B dissections [9,13-15,18,48,49,59]. This may be
explained by the fact that adverse events, such as recurrent dissection or complications
of aneurysm formation in the descending aorta, occur in both type A and type B
dissection (DeBakey type I) patients [63]. Survival is also impacted by preexisting
medical comorbidities such as ongoing smoking, hypertension, and coronary and
peripheral artery disease.

Long-term survival after surgical repair of type A dissections at one and three years was
96 and 91 percent, respectively, in an IRAD report of 303 patients with type A
dissection [64]. In a separate study, causes of death in 31 of 380 survivors of an initial
type A dissection were stroke (12 patients), aortic reoperation for re-dissection or
progressive dilatation of the false lumen (seven patients), malignancy (five patients),
myocardial infarction (four patients), and heart failure (three patients) [18].

Longer-term follow-up was provided in a series of 208 patients presenting between

1978 and 1995 [15]. Patient survival at 5 and 10 years was 68 and 52 percent,
respectively; residual distal dissected aorta did not affect late survival and had a low risk
for aneurysmal change and reoperation. Whether improvements in surgical and medical
care have led to better long-term outcomes over time is not known.

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)" and "Patient
education: Thoracic aortic aneurysm (The Basics)")

SUMMARY AND RECOMMENDATIONS

Aortic dissection is classified using two anatomic systems. The Stanford system is
more widely used and classifies dissections that involve the ascending aorta as type A,
regardless of the site of the primary intimal tear (figure 1); all other dissections are
classified as type B. By comparison, the DeBakey system is based on the site of origin
with type I originating in the ascending aorta and propagating to at least the aortic arch,
type II originating in and confined to the ascending aorta, and type III originating in the
descending aorta and extending distally or proximally. (See 'Extent and classification'
above.)

Medical treatment of acute aortic dissection includes pain control and anti-impulse
therapy to reduce the rate of progression, which should be initiated for all patients
(unless hypotension is present) but should not interfere with the timely transfer to the
operating room for those with indications for immediate aortic repair. Intravenous beta
blockers (eg, propranolol, labetalol) are typically used as initial anti-impulse therapy.
Blood pressure should be maintained at as low a level in this range as can be achieved
without compromising mentation or urine output. Intravenous sodium nitroprusside can
be added if the systolic blood pressure remains above 100 mmHg. Nitroprusside should
not be used without beta blockade, since vasodilation induces reflex activation of the
sympathetic nervous system, leading to enhanced ventricular contraction and aortic
shear stress. Direct vasodilators, such as hydralazine, should be avoided since they
increase aortic wall shear stress. (See "Overview of acute aortic syndromes", section on
'Acute medical management'.)

Acute type A aortic dissection is a surgical emergency since these patients are at high
risk for early life-threatening complications such acute aortic regurgitation, cardiac
tamponade, and myocardial infarction. Hemorrhagic stroke is a relative contraindication
to urgent surgical intervention. When the aortic valve, sinuses, or arch are involved, the
surgical approach involves a full root or hemiarch replacement. Hypothermic
circulatory arrest has been used in repairs involving the aortic arch. A hybrid approach
to the repair of type A aortic dissection, sometimes referred to as the "frozen elephant
trunk repair," uses an open approach to surgically repair the ascending aorta while using
a thoracic endograft to manage the descending aorta. (See 'Ascending (type A) aortic
dissection' above.)
For patients who are hemodynamically stable with uncomplicated type B aortic
dissection, we suggest initial medial therapy, rather than intervention (open surgery or
endovascular treatment) (Grade 2B). Indications for intervention for type B dissection
include occlusion of a major aortic branch leading to end-organ ischemia, persistent
severe hypertension or pain, propagation of the dissection (as may be manifested by
persistent or recurrent pain), aneurysm expansion, and aortic rupture. Acute distal
dissections in patients with Marfan syndrome may also be best treated with surgery.
(See 'Descending (type B) aortic dissection' above and "Surgical and endovascular
management of type B aortic dissection", section on 'Indications for intervention'.)

Repeat surgery is required in up to one-half of patients at 10-year follow-up, usually

because of extension or recurrence of dissection at the previous site of intervention,
localized aneurysm formation remote from the site of repair, graft dehiscence or
infection, or aortic regurgitation. The rate of secondary intervention following thoracic
stent-grafting due to endoleak or device migration is also high (up to 25 percent) and
depends on the duration of follow-up. (See 'Complications' above.)

Following treatment of aortic dissection (medical or surgical), the patients should be

maintained on anti-impulse therapy to minimize aortic wall stress with a target blood
pressure of less than 120/80 mmHg. Predischarge advanced vascular imaging using
magnetic resonance (MR) or computed tomographic (CT) angiography should be
performed with follow-up examinations at 3, 6, and 12 months, and annually thereafter
to detect signs of dissection progression, re-dissection, or aneurysm formation (even if
the patient remains asymptomatic). We prefer thoracic MR for younger patients, but
chest CT scanning is an alternative; however, CT exposes the patient to ongoing
radiation and requires iodinated contrast. Alternating chest CT and thoracic MRI is a
reasonable option. (See 'Long-term management' above.)

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