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Acute Aortic syndrome: Current Understandings Chapter | 44 487
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MANAGEMENT OF PENETRATING AORTIC ULCER AND DIFFERENTIATION FROM
ULCERLIKE PROJECTIONS
The differentiation of PAU and ulcerlike projection (ULP) is difficult, as the natural course of both entities have been underreported because of confusion in its definition and characterization. However, correct characterization should be sought as
PAU and ULP carry different clinical implications and management. According to the European consensus, PAU is considered a primary cause of AAS and should be identified on the first diagnostic study preceding development of IMH or dissection [55]. The presence of irregularities of the intima with calcified ulcer edges suggests PAU over ULP, and a localized
hematoma may be present surrounding a PAU.
ULP on the other hand is considered an evolution of IMH, which develops days to weeks after an acute IMH (Fig. 44.6).
It is characterized as a localized focal dissection with a small intimal flap in a background of IMH. Accurate diagnostic
differentiation of both entities can be difficult as the evolution of disease morphology may be rapid and patients may not
present at onset of symptoms; hence, the time frame of occurrence of AAS may not be accurate. PAU with localized hematoma is similar to pseudoaneurysms and has a higher risk of rupture when compared with ULP with IMH or localized dissection. Symptomatic PAU, with hematoma or periaortic hemorrhage, should be treated with TEVAR or surgery. Mortality
rate of open surgery is 15.9%, whereas that of TEVAR is 7.2%. There is no consensus on the management of nonruptured,
uncomplicated PAU because of lack of data on the natural course of disease. Studies show 5-year survival of PAU to be 65%
and that mid- to long-term prognosis is heavily influenced by comorbidities that are common and significant in patients
with PAU as most have concomitant neurologic and cardiac diseases [56,57]. The consensus is that treatment should be
considered in PAUs if they show mean growth > 5 mm/year or mean aortic diameter > 55 mm, after thorough assessment of
operative risks and availability of access vessels in the case of TEVAR planning.
ULP on the other hand develops in around 20%–60% of type B IMH and is defined as a localized blood-filled
pouch protruding into the hematoma of the aortic wall with an intimal communication more than 3 mm. TEVAR is an
accepted indication if ULP develops in an IMH, but its prognostic significance is still unclear as some studies show
it runs a benign course, whereas others show it is related to increased risk of aortic-related complications and death.
Depth of ULP seems to be prognostically significant, but no definite cut-off values are validated for treatment decisions.
According to the European consensus, ULP depth of >10 mm warrants close follow-up and depth >15 mm could be a
trigger for operative treatment.
CONCLUSION
Recent reports show an inverse relationship between hospital/surgeon volume and operative mortality in patients with aortic
dissection. Studies have shown that early outcomes from centers with a dedicated aortic surgery team are better for patients
with type A aortic dissection. With increasing and deeper understanding of the complexity of acute aortic syndrome, the
FIGURE 44.6 Evolution from intramural hematoma (A) to ulcerlike projection (B) in a patient after 2-week follow-up computed tomography scan.
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importance of forming dedicated aortic teams consisting of physicians, interventional radiologists specializing in aortic
stenting, aortic surgeons, and vascular surgeons to provide state-of-the-art care for patients cannot be understated. With the
fast expanding growth of evidence in the field of aortic disease, sound and appropriate management of patients with acute
aortic syndrome will require multidisciplinary expert input across specialties.
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[39] Song JK. Update in acute aortic syndrome: intramural hematoma and incomplete dissection as new disease entities. J Cardiol 2014;64:153–61.
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Ann Thorac Surg 2008;86(2):453–6.
[41] Park KH, Lim C, Choi JH, et al. Prevalence of aortic intimal defect in surgically treated acute type A intramural hematoma. Ann Thorac Surg
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[42] Kitai T, Kaji S, Yamamuro A, et al. Detection of intimal defect by 64-row multidetector computed tomography in patients with acute aortic intramu-
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[45] von Kodolitsch Y, Csosz SK, Koschyk DH, et al. Intramural hematoma of the aorta: predictors of progression to dissection and rupture. Circulation
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[46] Evangelista A, Mukherjee D, Mehta RH, et al. Acute intra mural hematoma of the aorta. A mystery in evolution 2005;111:1063–70.
[47] Song JK, Kim HS, Song JM, et al. Outcomes of medically treated patients with aortic intramural hematoma. Am J Med 2002;113:181–7.
[48] Moizumi Y, Komatsu T, Motoyoshi N, Tabayashi K. Management of patients with intramural hematoma involving the ascending aorta. J Thorac
Cardiovasc Surg 2002;124:91.
[49] Tittle SL, Lynch RJ, Cole PE, et al. Midterm follow-up of penetrating ulcer and intramural hematoma of the aorta. J Thorac Cardiovasc Surg
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[50] Kaji S, Akasaka T, Katayama M, et al. Long-term prognosis of patients with type B aortic intramural hematoma. Circulation 2003;108:9.
[51] Sueyoshi E, Sakamoto I, Fukuda M, et al. Long-term outcome of type B aortic intramural hematoma: comparison with classic aortic dissection
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[53] Troxler M, Mavor AI, Homer-Vanniasinkam S. Penetrating atherosclerotic ulcers of the aorta. Br J Surg 2001;88:1169–77.
[54] Cho KR, Stanson AW, Potter DD, et al. Penetrating athero-sclerotic ulcer of the descending thoracic aorta and arch. J Thorac Cardiovasc Surg
2004;127:1393–401.
[55] Evangelista A, Czerny M, Nienaber C, et al. Interdisciplinary expert consensus on management of type B intramural hematoma and penetrating
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[56] Gottardi R, Zimpfer D, Funovics M, Schoder M, Lammer J, Wolner E, et al. Mid-term results after endovascular stent-graft placement due to pen-
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[57] Geisbüsch P, Kotelis D, Weber TF, Hyhlik-Dürr A, Kauczor HU, Böckler D. Early and midterm results after endovascular stent graft repair of pen-
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FURTHER READING
[1] Nishigami K, Tsuchiya T, Shono H, et al. Disappearance of aortic intramural hematoma and its significance to the prognosis. Circulation
2000;102(Suppl. 3):243–7.
Chapter 45
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Surgical Treatment of Acute Aortic
Syndrome
Nora Goebel, Adrian Ursulescu, Alina Stan, Magdalena Rufa, Ulrich F.W. Franke
Robert Bosch Hospital, Stuttgart, Germany
Chapter Outline
Introduction 491
Definition 491
Classification 491
Epidemiology 493
Diagnostics 493
Surgical Treatment 493
General Principles 493
Aortic Dissection 493
Stanford Type A Classic Aortic Dissection 493
Stanford Type B Classic Aortic Dissection 495
Iatrogenic Classic Aortic Dissection 497
Intramural Hematoma 497
Penetrating Aortic Ulcer 497
Aortic Pseudoaneurysm, Contained Rupture of Aortic
Aneurysm, Traumatic Aortic Injury 497
Follow-Up 498
References 498
INTRODUCTION
Definition
Acute aortic syndrome (AAS) is the generic term comprising several emergency conditions with similar underlying pathol-
ogies leading to a breakdown of intimal and media integrity. All common pathologies are blood entering the media either
from the inside by intimal tear or by rupture of external vasa vasorum. Acute is defined as within 14 days of onset of symptoms [1].
Classification
There are several classifications with the Stanford and DeBakey anatomical classifications as the most common used (see
Fig. 45.1). First, the Stanford classification as the most decisive for surgical treatment. It discriminates upon proximal
extent between the following:
l Type A involving the ascending aorta and
l Type B affecting the descending aorta distal of the left subclavian artery, irrespective of entry site or distal extent [2]
Second, the DeBakey classification denominates three types:
l Type I starting in the ascending aorta and proceeding to the whole thoracic aorta;
l Type II with extent limited to the ascending aorta;
l Type III limited to the descending aorta equivalent to Stanford type B [3].
Third, AAS can be classified upon morphology and pathologic mechanism as first described by Svensson. Five entities
are specified (see Fig. 45.2):
1. Classic aortic dissection (AoD) with true and false lumen, with or without reentry;
2. Intramural hematoma (IMH);
3. Limited intimal tear with excentric bulge;
New Approaches to Aortic Diseases from Valve to Abdominal Bifurcation. http://dx.doi.org/10.1016/B978-0-12-809979-7.00045-6
Copyright © 2018 Elsevier Inc. All rights reserved.
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FIGURE 45.1 Stanford and DeBakey classification of aortic dissection: 1. Stanford type A, DeBakey type I; 2. Stanford type A, DeBakey type II; 3.
Stanford type B, DeBakey type III.
FIGURE 45.2 Svensson classification of acute aortic syndrome: 1. Classic aortic dissection (AoD) with true and false lumen; 2. Intramural hematoma; 3.
Limited intimal tear with excentric bulge; 4. Plaque rupture/penetrating aortic ulcer; 5. Iatrogenic or traumatic AoD.
4. Plaque rupture/penetrating aortic ulcer (PAU);
5. Iatrogenic or traumatic AoD [4].
Fourth, orientated on the pattern of malperfusion estimating the risk of mortality, the Penn classification for type A AoD
was introduced:
l Penn class Aa—no ischemia (absence of ischemia);
l Penn class Ab—localized ischemia (branch vessel malperfusion producing clinical organ ischemia);
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l Penn class Ac—generalized ischemia (circulatory collapse, with or without cardiac involvement);
l Penn class Ab&c—combined ischemia [5].
Epidemiology
Epidemiological data of AAS are scarce mainly due to high fatal potential of the disease and misdiagnosis. For AoD, with
about 70% the most common entity within the AAS, the incidence is estimated at 3–6/100,000 persons/year with a higher
incidence in men and patients at higher age [6–8]. Mortality rate is high with estimated 50% within the first 48 hours [1,9].
For IMH and PAU, even less data are available, but prognosis seems to be similar to classic AoD [10]. The main acquired
risk factors are arterial hypertension, atherosclerosis, and diabetes type 2. In younger patients, often a congenital (familial
thoracic aortic aneurysm and dissection) or connective tissue disease (Marfan, Ehlers–Danlos, Loeys–Dietz syndrome) is
found as underlying predisposing pathology [8,11].
Diagnostics
The diagnosis of AAS is commonly secured with imaging techniques like echocardiography, computed tomography (CT),
or magnet resonance imaging (MRI). In the emergency setting, verification of a dissecting membrane in the ascending aorta
by echocardiography (transthoracic or transesophageal) can be sufficient to indicate emergent operation. In cross-sectional
imaging, whenever possible an electrocardiogram-triggered CT should be undertaken, otherwise artifacts can mimic a dissecting membrane leading to misdiagnosis and unnecessary operation.
SURGICAL TREATMENT
General Principles
Initial management of all patients presenting with AAS includes analgesia for pain relief and blood pressure control
for reduction of aortic wall shear stress or hemodynamic stabilization, respectively [12]. Indication for surgery versus
endovascular, hybrid, or medical therapy alone depends on clinical presentation, pathology, and diagnostic findings. The
aim of surgical treatment is the exclusion of the entry, saving cardiopulmonary stability, and treatment or prevention of
complications. The most frequent complications are aortic rupture, aortic valve regurgitation, with or without congestive
heart failure culminating in cardiogenic shock as well as myocardial infarction, pleural effusions/pulmonary complications, and malperfusion resulting in neurological symptoms (central and peripheral), mesenterial or limb ischemia, or
acute kidney injury.
Aortic Dissection
Treatment of acute AoD is mainly orientated on the proximal extent according to the Stanford classification (see Fig. 45.1).
In type A AoD, usually emergent surgery is indicated, whereas in type B dissection has become the domain of conservative
and endovascular therapy. The aortic arch, lying in between classifications of type A (ascending aorta) and type B (distal of
left subclavian artery) historically, is counted among Stanford type A due to the fatality of potential cerebral malperfusion
and the high risk of proximal progression of dissection. Yet current data suggest a differentiated approach to aortic arch socalled non-A–non-B dissection as conservative therapy has shown to be noninferior to surgery in recent but small studies
[13]. This is supported by data from the International Registry of Acute Aortic Dissection, which stated no difference in
short-term mortality between type B AoD with or without aortic arch involvement [14].
Stanford Type A Classic Aortic Dissection
Operative Strategy
Acute AoD type A is usually treated as an emergency condition requiring immediate surgery. Standard is a classical sur-
gical and “proximal first” approach, i.e., repair of the proximal entry site, which is usually located in the aortic root or
ascending aorta. For DeBakey type I dissection, malperfusion has shown to carry a high risk of mortality. That is why the
hybrid-operating room concept was developed where the patient is treated by a multidisciplinary team in a hybrid operation room. In the case of hemodynamic-stable DeBakey type I dissection with visceral or peripheral malperfusion, first the
descending/abdominal aorta is treated endovascularly as so-called “distal first” approach before repair of the proximal aorta
is undertaken in a second step [15].
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Monitoring, Access, Cannulation
As acute disease and interventions on the thoracic aorta carry a high risk of morbidity and mortality and are undertaken
under general anesthesia extended monitoring is recommended: central venous line, radial and femoral arterial lines for
detection of potential malperfusion of true lumen, transesophageal echocardiography for valve and left ventricular function evaluation as well as detection of dissecting membrane and false lumen thrombosis, five-lead electrocardiogram, and
neuro-monitoring for aortic arch interventions, e.g., by near-infrared spectroscopy.
Access to heart, aortic root, ascending aorta, and aortic arch up to beginning of descending aorta is best gained via
median sternotomy. For better exposition of the aortic arch, the skin incision can be extended upward to the jugulum. Under
stable hemodynamic conditions, even a minimally invasive approach with partial upper sternotomy is possible.
Establishment of cardiopulmonary bypass is mandatory. For cannulation, several options come into consideration.
Venous drainage is achieved using a two-stage cannula either inserted via right atrium into the vena cava inferior or via femoral vein and pushed forward in a retrograde manner placing the tip into the vena cava superior. Femoral venous cannulation
can be performed open and percutaneously, the latter preferable to avoid groin wound complications. Arterial cannulation
can be done central or peripheral. The difficulty in central cannulation is to place the cannula safely into the true lumen to
avoid devastating complications. If Seldinger technique is applied transechocardiographically, control is mandatory to guide
cannulation into the true lumen. In cases where the true lumen cannot be securely identified with echocardiography, an alternative cannulation strategy should be employed. The recommended way of cannulation is under direct vision: after blood
volume is emptied via venous drainage into the heart–lung machine, the patient is brought in Trendelenburg position and
transverse ascending aortic transection is performed to secure aortic true lumen cannulation and ligation. Because of the risk
of aortic rupture before safe cannulation, peripheral arterial cannulation has gained popularity over the last years. Although
the femoral common artery was preferred over the last decade, now a shift to the axillary artery can be observed and is also
recommended in current guidelines [1]. This is mainly based not only on the concerns about retrograde arterial perfusion
with the risk of retrograde dissection, embolization, and thus stroke, but also because the antegrade fashion of axillary artery
perfusion allows for antegrade cerebral perfusion during circulatory arrest in aortic arch repair via the same cannula.
Circulatory Arrest, Cooling, Organoprotection
The management of temperature and circulatory arrest has evolved over the years. Although deep hypothermia ensured
a sufficient organoprotection during circulatory arrest, it has shown to be associated with severe coagulopathy during
rewarming. Therefore, a trend is seen toward only mild-to-moderate hypothermia with comparable results regarding outcomes, stroke, or spinal cord injury. To reach a sufficient organoprotection, complete cooling is recommended before
aortic cross-clamping. As with moderate temperatures, brain protection could be limited; selective antegrade perfusion
uni- or bilaterally has been established after retrograde cerebral perfusion strategies did not show any significant impact.
Nowadays, concepts of visceral perfusion (e.g., Foley catheter) and aortic arch surgery with a beating heart are described to
minimize the risk of perioperative malperfusion and heart failure due to prolonged cross-clamp times [16,17].
Surgical Treatment of Aortic Root
The majority of type A dissections affect the aortic root +/− aortic valve. In case of a destroyed valve, the choice of a
biological versus mechanical valve substitute follows the same principles as in elective aortic valve surgery [18,19]. With
a growing expertise in aortic valve-sparing surgery even in the acute setting of AoD, more aortic valves can be preserved
by reimplantation technique into a polyester graft with good medium-term results [20]. Prerequisite are intact and mobile
valve cusps without retraction. This is the case in aortic regurgitation due to annulus dilatation with otherwise intact valve
cusps. Diseased aortic wall tissue should be resected. For reimplantation, a polyester tube graft, alternatively with already
preformed sinuses of Valsalva, is used. Surgical glue (gelatin–resorcin–formaldehyde, glutaraldehyde) to adhere dissected
aortic wall layers is not applied any more, as it has been shown to induce inflammation and tissue necrosis with the risk
of subsequent rupture. In case of sole dissection or dilatation of the noncoronary sinus resection and supracommissural,
ascending aortic replacement with replacement of the noncoronary sinus can be sufficient.
Surgical Treatment of Ascending, Arch, Descending Aorta
The major principle of aortic surgery in type A dissection is the exclusion of the entry tear, which is mostly found in
the aortic root, the sino-tubular junction, and ascending aorta. In DeBakey type II dissection, all diseased tissue can
and should be resected and replaced by a polyester tube graft [1,12]. To which extent reentries in DeBakey type I
dissection should be excluded still remains unclear as a more aggressive approach with extended surgery leads to prolonged cardiopulmonary bypass time and higher risk of morbidity and mortality. Otherwise, a conservative approach
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FIGURE 45.3 Proximal aortic arch replacement/open anastomosis.
with short operation times but leaving a large portion of dissected aorta in place bears the risk of subsequent distal
dissection, dilatation, and therefore reoperation or reintervention. Consensus is at least an open aortic arch inspection to detect and resect arch lesions under circulatory arrest [1]. In case of arch reentries, these should be resected to
minimize the risk of subsequent dissection of the supra-aortic vessels. Depending on the site of lesion and reentry a
proximal, hemi-, or total arch replacement might be required with supra-aortic vessel reimplantation as island or separately (see Figs. 45.3 and 45.4). For extensive aortic repair, the frozen elephant trunk (FET) technique has evolved
in recent years. This is a hybrid prosthesis combining a polyester tube graft portion for aortic arch replacement and
a covered stent graft for antegrade deployment into the descending aorta to cover reentries and establish true lumen
expansion over the descending aorta (see Fig. 45.5). The aim is to provide aortic remodeling and long-term durability with reduction of the need for reoperation or reintervention. As extended aortic surgery can include higher rates
of perioperative mortality, stroke and spinal cord injury indication must be well considered and applying the FET in
acute dissection is recommended only for experienced centers [21].
Stanford Type B Classic Aortic Dissection
Treatment of acute Stanford type B dissection depends on the presence of complications and is therefore differentiated into
umcomplicated and complicated entity.
FIGURE 45.4 Hemiarch replacement with brachiocephalic trunk and left carotid artery reimplantation as island.
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FIGURE 45.5 Hybrid aortic repair with frozen elephant trunk technique, reimplantation of supra-aortic vessels as island.
FIGURE 45.6 Thoracic endovascular aortic repair zone 3 and zone 2 with left subclavian artery sacrifice.
Uncomplicated Type B Dissection
In uncomplicated type B dissection conservative, i.e., medical management is the therapy of choice [1,12]. To detect possibly the progression or complication of dissection substantially elevating the risk of mortality, subsequent imaging (MRI,
CT) is recommended. The fact that long-term prognosis can be improved by early interventional therapy with TEVAR
(thoracic endovascular aortic repair) is under investigation, but it still has to be proved [22].
Complicated Type B Dissection
In the case of persistent pain or hypertension despite medical therapy, contained rupture, rapid progression, or malperfusion
type B AoD is classified “complicated” and should be treated more aggressively. TEVAR is the first-line therapy recommended to cover the entry tear, decompress the false lumen, and restore true lumen perfusion (see Fig. 45.6) [1,12]. Sacrifice
of the left subclavian artery can be necessary to create a sufficient proximal landing zone and sealing to avoid an endoleak
(see Fig. 45.6). TEVAR is possible even more proximal in the aortic arch when supra-aortic vessels are debranched and/or
bypassed (see Fig. 45.7). If an endovascular therapy is not possible, e.g., for anatomical reasons, open descending aortic
surgery is recommended but affected with an elevated risk of mortality, stroke, and spinal cord injury. Surgical access is
gained via left thoracotomy and often a two-cavity surgery (thoracic and abdominal) is necessary. Resection and replacement of the diseased aorta are carried out with polyester tube graft; optional is the reimplantation of intercostal artery (supplying the great radicular artery of Adamkiewicz) to reduce the risk of spinal cord injury, hypothermic circulatory arrest for
proximal aortic repair, or application of the FET technique in the case of aortic arch involvement.
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FIGURE 45.7 Thoracic endovascular aortic repair zone 1 with debranching of left carotid artery and left carotid-subclavian bypass.
For the treatment of visceral malperfusion, fenestration of the abdominal dissecting membrane can be considered,
endovascular or open, to allow for an equal perfusion of true and false lumen-deriving branch vessels without aortic
replacement [23].
Iatrogenic Classic Aortic Dissection
Management of iatrogenic AoD is dependent on the site (Stanford type) of dissection, the extent, and possible complications. Iatrogenic dissection during cardiac surgery mostly emanates from the site of aortic cannulation or cross-clamping.
Emergent surgical repair follows the same principles as the surgical treatment of type A AoD (see above, Section 4.2.1.5).
Catheter-induced AoD is a rare complication and can occur during coronary catheterization or interventional trans-aortic
procedures. Uncomplicated coronary dissection affecting the aortic root can safely be treated by overstenting the entry and
conservative management with close control [24]. In case of complications such as aortic regurgitation, pericardial effusion, or coronary malperfusion emergent aortic root surgery is indicated. Catheter-induced AoD at the site of aortic arch
or descending aorta can be treated conservatively in the case of local restriction but must be addressed by endovascular or
surgical treatment when causing complications such as malperfusion or showing fast progression.
Intramural Hematoma
IMH, defined as bleeding into the media layer of the aortic wall without an intimal tear, has been shown to have a similar
prognosis in terms of mortality as AoD and is therefore classified and treated in the same way according to the Stanford type
A versus type B classification [10]. In patients deemed at high operative risk even in type A IMH, a conservative therapy is
reasonable provided that the risk of progression from IMH to AoD is low and close surveillance is warranted. Risk factors
for progression comprise a maximum aortic diameter >50 mm and an aortic wall thickness >11 mm [25,26]. Actually, in
the Eastern world, good results are seen with a primary conservative approach and timely operation in case of progression.
Penetrating Aortic Ulcer
PAU is treated according to the Stanford classification: type A with emergent surgical resection and prosthesis interposition and type B conservative or with endovascular covering stent graft in case of complications. For localized lesion in the
ascending aorta, in recent years, endovascular therapy with a short stent graft is described but restricted to individual cases
due to technical challenges such as length differences of inner and outer curve with the risk of endoleak.
Aortic Pseudoaneurysm, Contained Rupture of Aortic Aneurysm, Traumatic Aortic Injury
Aortic pseudoaneurysm and aneurysm with or without contained rupture can affect every part of the aorta. In contrast,
traumatic aortic injury mostly occurs in deceleration trauma in the region of ligamentum arteriosum insertion, but complete aortic arch rupture is also described. According to previous pathologies, emergent surgical repair is recommended in
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