Management of acute aortic dissection - UpToDate 17/07/17 9:11 p.m.

Official reprint from UpToDate

www.uptodate.com 2017 UpToDate

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

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jun 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. Medications and dosing used in acute aortic dissection are similar to
other acute aortic syndromes and are reviewed separately. (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-

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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

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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.

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(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

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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'.)

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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 years' 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

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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.

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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'.)

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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 years' 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

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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

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medical care have led to better long-term outcomes over time is not known.

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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.)

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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 years' 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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GRAPHICS

Classification of aortic dissection

In the DeBakey classification of aortic dissection:

Type I involves the ascending aorta, arch, and descending thoracic aorta and may
progress to involve the abdominal aorta.
Type II is confined to the ascending aorta.
Type IIIa involves the descending thoracic aorta distal to the left subclavian artery and
proximal to the celiac artery.
Type IIIb dissection involves the thoracic and abdominal aorta distal to the left
subclavian artery.
In the Stanford classification of aortic dissection:
Type A involves the ascending aorta and may progress to involve the arch and
thoracoabdominal aorta.
Type B involves the descending thoracic or thoracoabdominal aorta distal to the left
subclavian artery without involvement of ascending aorta.

Graphic 100115 Version 4.0

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Endovascular repair of acute type B aortic dissection

For endovascular repair descending (type B) aortic dissection, the stent-graft is positioned
to cover the tear, while avoiding obstructing flow to the left subclavian artery.

Graphic 106801 Version 1.0

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