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exposure to the tremendous burden of severe or uncontrolled hypertension [2]. The most common site of dissection is the
first few centimeters of the ascending aorta, with 90% occurring within 10 cm of the aortic valve. The second most common
site is just distal to the left subclavian artery [3]. Between 5% and 10% of dissections do not have an obvious intimal tear.
The descending aorta is the location of most late clinical events after any dissection of the aorta. Intramural hematomas
and penetrating atherosclerotic ulcers, both affect thoracoabdominal aorta, resulting in aortic dissection or rupture [4]. The
entry tear at the ulceration may be thicker and less mobile compared to the intimomedial flap seen in the classical aortic
dissection.
ETIOLOGY AND NATURAL HISTORY
Hypertension is the most common risk factor and present in up to 70% of cases [5]. The other causes are generalized
atherosclerosis, smoking, connective tissue disorders, and inflammatory diseases of the aorta (Table 29.1). Data from the
International Registry of Aortic Dissection (IRAD) revealed the average age for aortic dissection to be 63.1 years, with TAD
slightly older (66.3 vs. 61.2 years) [1].
Genetic traits are linked to acute aortic syndromes and are usually autosomal dominant and affect patients at younger
age. These result in altered connective tissue (Marfan syndrome, Turner syndrome, Type IV Ehlers–Danlos syndrome) and
smooth muscle, or pathological cell signaling (Loeys–Dietz syndrome). In Marfan syndrome and Loeys–Dietz syndrome,
mutations are either located in fibrillin gene (FBN1) or TFG-β receptor-2 (TGFBR2) gene. SMAD3 locus frame shift
causes familial thoracic dissection [6].
The short-term prognosis for patients with type TAAD is better than those with type A and the medical management of
TAAD is associated with less mortality compared to the open surgical repair (OSR) approach. Overall, 89% of patients with
TAAD survive to hospital discharge, although the in-hospital survival rates were as low as 29% for the highest risk group,
64% for the intermediate, and 97% for the lowest risk group [1,7]. Aortic rupture, shock, and malperfusion are the most
important in-hospital risks leading to poor outcome in up to 20% of these patients [1,8]. Of survivors, 80% will develop
aneurysmal dilatation of the FL, requiring OSR in one-third of the cases [8,9]. The long-term prognosis for patients with
type TAAD is not impressive. Data from IRAD indicated about one out of four patients with TAAD died at the 3-year mark
regardless of the mode of therapy. The 3-year rates of survival were 77.6%, 82.8%, and 76.2% for patients treated medically, surgically, and with endovascular therapy, respectively [7].
TABLE 29.1 Contributing Factors for Thoracoabdominal
Aortic Dissection (TAAD)
l
Long-term arterial hypertension
l
Advanced age
l
Dyslipidemia
l
Smoking
l
Connective tissue disorders
i. Marfan’s syndrome
ii. Loeys–Dietz’s syndrome
iii. Ehlers–Danlos syndrome
iv. Coarctation
l
Vascular inflammation
i. Giant cell arteritis
ii. Takayasu arteritis
iii. Behcet’s disease
l
Deceleration trauma
l
Iatrogenic factors
iv. Catheter intervention
v. Graft anastomosis
vi. Patch aortoplasty
vii. Side clamping, cross-clamping, or aortotomy
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CLASSIFICATION
The DeBakey classification was the first to be proposed in 1965 based on the extent of the dissection process along the aorta
[10]. Three main types were recognized: types I and II affect the ascending aorta; type III, distal dissection, begins distal
to the left subclavian artery, sparing the proximal arch and ascending aorta. DeBakey’s prescience in distinguishing types
IIIa (down to or ending above the visceral segment) and IIIb (extending downward to involve the abdominal aorta and iliac
arteries) has proved to be extremely valuable in the current century because of the substantial impact on the prognosis and
long-term results after thoracic endovascular repair (TEVAR). The simpler Stanford Classification has also become well
established and describes only two types of AD: type A, which signifies the involvement of the ascending aorta; type B, in
which the ascending aorta is not affected [2,11].
TAAD can also be classified according to the time since onset of the symptoms: acute (within 2 weeks), subacute
(from 2 to 8 weeks), and chronic (beyond 8 weeks). European Society of Cardiology Task Force on Aortic Dissection
has suggested a comprehensive etiological classification (Table 29.2) [8]. It can also be divided into uncomplicated
and complicated diseases. Complicated dissection consists of one or more of the following manifestations: rupture,
imminent rupture, branch vessel involvement with malperfusion syndrome or persistent or worsening thoracic pain,
drug-resistant hypertension, and FL aneurysm formation [12]. Moreover, Crawford et al. divided chronic type B dissections into different categories (Table 29.3) [13].
CLINICAL PRESENTATION
Insights into the clinical presentation of patients are gained from the International Registry of Acute Aortic dissection
(IRAD) [1]. A prototypical patient with acute aortic dissection will be a man in his fifth to seventh decade of life, whose
medical history is significant for hypertension; patients younger than 40 years may report a history of Marfan syndrome,
bicuspid aortic valve, Ehlers–Danlos syndrome, Loeys–Dietz syndrome or aortic valve surgery. The most common chief
complaint is the sudden onset of severe chest pain or back pain. Patients with TAAD and a history of back or abdominal
pain more commonly described it as sharp, and, less commonly, ripping or tearing associated with anxiety and listlessness. Those without pain are usually found to have chronic TAAD. The classical migratory pain is described in one-fifth
of the patients and often helps in localizing the anatomical site of dissection. In addition to the chest/back/abdominal pain,
patients may present with nonspecific symptoms of dyspnea, diaphoresis, bloody diarrhea, nausea, and vomiting, which
may be the prodrome of the ominous malperfusion syndrome. The clinical manifestation of the malperfusion syndrome
TABLE 29.2 European Society of Cardiology Classification [8]
Class 1: Classical aortic dissection
Class 2: Intramural hematoma/hemorrhage
Class 3: Subtle–discrete aortic dissection
Class 4: Plague rupture/ulceration
Class 5: Traumatic/iatrogenic aortic dissection
TABLE 29.3 Crawford’s Classification of Thoracoabdominal Aortic
Dissection [13]
Type 1: The dissection involving the descending aorta up to the origin of the
renal arteries.
Type 2: The descending aorta is dissected over its entire length and the
abdominal aorta up to the iliac arteries is involved.
Type 3: The dissection starts at the level of the mid-third of the descending
aorta and involves the entire abdominal aorta.
Type 4: The whole abdominal below the diaphragm is involved.
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depends on the anatomy of the affected vessels. There may be a complain of painful, plegic, pulseless, and cool extremities
if the brachiocephalic, left subclavian arteries, distal aorta, iliac arteries are compromised. A dramatic paraplegia or quadriplegia is observed when the intercostal/segmental arteries are obstructed, resulting in reduced blood flow in the anterior
spinal arteries and ischemic spinal cord. Abdominal pain and decreased urine output are a common malperfusion syndrome
resulting from compromised celiac trunk, superior mesenteric, inferior mesenteric, renal arteries causing (frequently fatal)
acute bowel ischemia, and decreased renal blood flow and glomerular filtration. Rupture of aorta results in hemothorax
or hematemesis because of aorto-esophageal fistula or massive hemoptysis because of aorto-bronchial fistula. Sometimes,
the FL expands causing aneurysmal dilation of the aorta, which can present with symptoms and signs of compression of
adjacent structures like dysphagia, hoarseness of voice, Ortner’s syndrome, Horner’s syndrome.
The physical examination may not be sufficiently sensitive. It may reveal tachycardia, usually accompanied by hypertension. The finding of pulse deficits, blood pressure difference of at least 20 mmHg, and motor and sensory deficits raise
the likelihood of diagnosis. In patients with hypotension, presence of jugular venous distension or pulsus paradoxus indicate cardiac tamponade.
DIAGNOSIS
A very low threshold of clinical suspicion is vital for timely diagnosis and proper management. X-ray of the chest is not
very specific and may sometimes show widening of aortic contour, displaced calcification, kinking of aorta, or opacification of aorto-pulmonary window. Data from the 2002 IRAD show that computed tomography angiography (CTA) is used
in 63% of cases of suspected AAD, followed by transesophageal echocardiography (TEE) in 32%, aortography 4%, and
magnetic resonance angiography (MRA) in 1% [14]. A triple rule out study by CT (electrocardiography-gated) is the most
widely used imaging mortality to differentiate between aortic dissection, pneumothorax, pulmonary embolism, and acute
coronary syndrome in patients with nonspecific acute chest pain.
CTA is widely available and relatively rapid, provides visualization of the entire aorta down to iliac arteries, and delineates the involvement of side branches. It is usually the first choice for imaging in the workup of TAAD. Disadvantages
with CTA include the requirement that patients be transported to the CTA suite, the use of potentially nephrotoxic contrast,
and the inability to assess aortic insufficiency. Overall, CTA of the chest is the preferred first diagnostic imaging method in
hemodynamically stable patients. The choice for a second imaging study includes MRA or TEE, depending on clinical condition and local environment. MRA is highly accurate and does not require the use of a contrast dye. However, it requires
patients to be in MRA suite for an extended period of time. Other issues such as claustrophobia, the use of ventilator, and
patient’s use of metal devices (pacemakers, aneurysmal clips) may further complicate its routine use [14]. TEE is a viable
alternative in patients who are critically ill and/or hemodynamically unstable. Failure of aforementioned modalities to
diagnose TAAD should prompt shifting of the patient to hybrid operating room and use of intravascular ultrasound (IVUS)
and/or aortography [15]. IVUS has 100% sensitivity and specificity during endovascular diagnosis and treatment of TAAD.
It is also a critical modality for endovascular treatment options [16].
BIOMARKERS
The Holy Grail in the workup of TAAD is an inexpensive bedside blood test with sufficient sensitivity. Out of many biomarkers evaluated in the last decade, the following deserve special mention.
D-dimer
Plasma D-dimer, a degradation product of cross-linked fibrin, has emerged as a promising diagnostic marker with high
sensitivity for exclusion of acute aortic dissection. The rise in D-dimer is thought to result from the thrombogenicity of the
FL in acute aortic dissection. As such, D-dimer values are expected to be lower with a thrombosed FL, shorter dissection
lengths, and those of younger age [17]. In an earlier pooled analysis by Sodeck, a D-dimer < 0.1 μg/mL is thought to exclude
all acute aortic dissection (sensitivity of 100%) [18].
Smooth Muscle Myosin Heavy Chain
Smooth muscle myosin heavy chain, a major component of the smooth muscle in the aortic medial layer, rises and peaks
at the initial phase of dissection. In a pilot study, the assay (>2.5 μg/L) had a sensitivity of 90.9% and specificity of 98% in
detecting acute aortic dissection compared to healthy volunteers [19]. It is normal in acute coronary syndrome.
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Matrix Metalloproteinase 9
This biomarker is raised in acute dissection within the first hour and an increased concentration is seen up till 2 months. It
could be used not only for rapid detection but also for long-term follow-up [20].
Elastin Degradation Products
Elastin lamellar disruption is a major pathological feature in acute aortic dissection and elastin degradation products are
released into circulation at the time of presentation, which remains elevated for up to 72 h of presentation.
Transforming Growth Factor-Beta (TGF-β)
TGF-β may be surrogate biomarker for assessment aortic expansion after dissection and could be used to predict the risk
of rupture and the need for repair. Findings that inhibitors of renin–angiotensin system can act directly on dysregulation of
TGF-β to affect aortic remodeling have led to new possibilities for the treatment [21,22].
MANAGEMENT
Optimal Medical Treatment (OMT)
Patients with uncomplicated TAAD should be treated with OMT. At present, there is no evidence of advantage with TEVAR
or OSR. Medical therapy is also administered to surgical patients preoperatively, intraoperatively, and postoperatively to
prevent progression or recurrence of dissection. Pain should be treated with appropriate analgesics (e.g., morphine). Heart
rate and hypertension should be aggressively controlled with B-blockers [23]. B-blockers are the firstline drugs because
they control the maximal force of left ventricular contraction (dP/dt max) in addition to controlling heart rate and blood
pressure. This helps reduce further dissection, branch-vessel malperfusion, and weakening of the aortic wall. B-blockers
and in combination angiotensin-converting enzyme inhibitors are considered the current treatment of choice. Common
B-blockers include labetalol, esmolol, metoprolol, and atenolol. Labetalol, with both alpha and B blocking properties, is
the first line of treatment. Targeted heart rate and systolic blood pressure should be <60 beats/min and <100 mmHg, respectively. In patients with potential intolerance to B-blockers (e.g., asthma, heart failure), a test dose of a short acting B-blocker
such as esmolol should be tried [8]. If B-blockers cannot be used, calcium channel blockers (e.g., nicardipine, clevidipine, or diltiazem) might be alternatives to control blood pressure in these patients. Hydralazine and sodium nitroprusside
increase the maximal force of left ventricular contraction (dP/dt max) and cause reflex tachycardia and should not be used
without pretreatment with B-blocker (Table 29.4).
TABLE 29.4 Antiimpulsive and Antihypertensive Drugs
Name Mechanism Dose
Labetalol Nonselective beta-1, 2 blocker. Selective alpha-1 blocker Load: 20 mg IV
Esmolol Cardioselective beta-1 blocker Load: 500 μg/IV
Nicardipine Calcium channel blocker Drip: 5 mg/h
Diltiazem Calcium channel blocker Load: 0.25 mg/kg over 2–5 min
Enalaprilat Angiotensin converting enzyme inhibitor 0.625–1.25 mg IV 6 h
Nitroprusside Direct arteriolar vasodilator Begin at 0.3 μg/kg/min IV
Nitroglycerine Vascular smooth muscle relaxation 5–200 μg/min IV
Drip: 2 mg/min IV
Drip: 50 μg/kg/min IV
Increase by increments of 50 μg/min
Drop: 5 mg/h
Max dose: 5 mg 6 h
Max dose 10 μg/kg/min
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TABLE 29.5 Therapeutic Strategies for Thoracoabdominal Aortic
Dissection (TAAD)
Open Surgical Repair
l
TAAD with retrograde extension into the ascending aorta
l
Dissection in fibrilinopathies (e.g., Marfan syndrome, Ehlers–Danlos syndrome)
l
Rupture or impending rupture
l
Progression with vital organ compromise
Open Medical Therapy
l
Uncomplicated chronic TAAD
Thoracic Endovascular Repair
l
Recurrent pain
l
Malperfusion syndrome
l
Refractory hypertension
l
Critical aortic diameter (≥55 mm)
l
Total aortic diameter increase (>4 mm)
l
New onset of periaortic hematoma/hemothorax
l
TAAD with retrograde extension into the ascending aorta
l
Hybrid procedure for extended type A aortic dissection
Medical therapy provides good early term results in uncomplicated dissection, with 85% of patients surviving the initial
acute phase. The 30-day mortality rate is 10% for uncomplicated patients versus 30% for those with complicated dissection
[24]. Long-term results are poor, however, with a 50% mortality at 5 years and a high incidence of aneurysm formation
(25%) at 4 years [25].
Open Surgical Repair (OSR)
OSR represents a valid therapeutic option in cases of TAAD complicated by retrograde extension into the ascending aorta,
Marfan syndrome, rupture, and progression with compromise of vital organs (Table 29.5). OSR is associated with a high
incidence of paraplegia, prolonged hospital stay, and pulmonary complications [12].
Thoracic Endovascular Aortic Repair
TEVAR is the new frontier for the treatment of TAAD. The rationale for this therapy is to obliterate the entry tear and
depressurize and shrink the FL and restore normal thoracicoabdominal aortic anatomy. TEVAR promotes thrombosis of the
FL and, in so doing, mitigate aneurysm development. Compared to OSR, reports of this technique detail lower morbidity
and mortality rates, especially for complications correlated to spinal cord ischemia [26].
TEVAR is the treatment of modality of choice in complicated TAAD (Table 29.5) meaning persisting or recurrent pain,
uncontrolled hypertension despite full medication, malperfusion (ischemia that involves the viscera, kidneys, spinal cord,
or lower extremities) and evidence of aortic rupture (hemothorax, increasing periaortic and mediastinal hematoma) [27].
INSTEAD-XL (Investigation of Stent grafts in Aortic Dissection with extended length of follow-up) demonstrates that
TEVAR in addition to OMT is associated with improved 5-year aorta-specific survival and delayed disease progression. In
stable TAAD with suitable anatomy, preemptive TEVAR should be considered to improve late outcome [28].
CONCLUSION
Diseases of the aorta are one of the most feared conditions encountered by the physicians. TAAD is uncommon but potentially catastrophic if gets complicated. Acute uncomplicated TAAD is less lethal and better managed by OMT with close
surveillance and TEVAR in case of complications. Clinical outcome and mortality rates of OMT for uncomplicated TAAD
have improved considerably. However, preemptive TEVAR in subacute phase has shown promise to prevent complications.
TEVAR has added an entirely new dimension to manage complicated TAAD. Biomarkers will probably be used in future to
select high-risk patients who may need TEVAR. Because of high morbidity and mortality with OSR, it is likely that TEVAR
will supplant OSR in the near future and pronounce a total paradigm shift in the management of TAAD.
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[5] Baguet JP, Chavanon O, Sessa C, et al. European Society of Hypertension scientific newsletter: hypertension and aortic diseases. J Hypertens
2012;30:440–3.
[6] Regalado ES, Guo DC, Villamizar C, et al. For the NHLBI GO Exome Sequencing Project. Exome sequencing identifies SMAD3 mutations as a
cause of familial thoracic aortic aneurysm and dissection with intracranial and other arterial aneurysms. Circ Res 2011;109:680–6.
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[9] Fann JI, Smith JA, Miller DC, et al. Surgical management of aortic dissection during a 30-year period. Circulation 1995;92(Suppl. 9):II113–21.
[10] DeBakey ME, Henly WS, Cooley DA, et al. Surgical management of dissecting aneurysms of the aorta. J Thorac Cardiovasc Surg 1965;49:130–49.
[11] Daily PO, Trueblood HW, Stinson EB, et al. Management of acute aortic dissections. Ann Thorac Surg 1970;10:237–47.
[12] Fanelli F, Dake MD. Standard of practice for the endovascular treatment of thoracic aortic aneurysms and type B dissections. Cardiovasc Intervent
Radiol 2009;32:849–60.
[13] Fuster V, Halperin JL. Aortic dissection: a medical perspective. J Cardiac Surg 1994;9:713–28.
[14] Moore AG, Eagle KA, Bruckman D, et al. Choice of computed tomography, transesophageal echocardiography, magnetic resonance imaging, and
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[15] Khoynezhad A, Donayre CE, Kopchok GE, et al. Use of intravascular ultrasound in endovascular stenting of traumatic rupture of the descending
thoracic aorta. Cardiothoracic Surgical Network (CTSNet) [serial on the internet] June 2006. [cited July 22, 2008]. Available from: http://www.
ctsnet.org/sections/clinicalresources/clinicalcases/article-12.html.
[16] Khoynezhad A, Donayre CE, Kopchok GE, et al. Mid-term results of endovascular treatment of complicated acute type B aortic dissection. J Thorac
Cardiovasc Surg 2008;136:424–30.
[17] Hazui H, Nishimoto M, Hoshiga M, et al. Young adult patients with short dissection length and thrombosed false lumen without ulcer-like projec-
tions are liable to have false-negative results of D-dimer testing for acute aortic dissection based on a study of 113 cases. Circ J 2006;70:1598–601.
[18] Sodeck G, Domanovits H, Schillinger M, et al. D-dimer in ruling out acute aortic dissection: a systematic review and prospective cohort study. Eur
Heart J 2007;28:3067–75.
[19] Suzuki T, Katoh H, Tsuchio Y, et al. Diagnostic implications of elevated levels of smooth-muscle myosin heavy-chain protein in acute aortic dissec-
tion. The smooth muscle myosin heavy chain study. Ann Intern Med 2000;133:537–41.
[20] Wen D, Zhou XL, Li JJ, et al. Biomarkers in aortic dissection. Clin Chin Acta 2011;412:688–95.
[21] Matt P, Schenhoff F, Habashi J, et al. Circulating transforming growth factor-beta in Marfan’s syndrome. Circulation 2009;120:526–32.
[22] Brooke BS, Habashi JP, Judge DP, et al. Angiotensin II blockade and aortic root dilatation in Marfain’s syndrome. N Engl J Med 2008;358:2787–95.
[23] Khoynezhad A, Plestis KA. Managing emergency hypertension in aortic dissection and aortic aneurysm surgery. J Card Surg 2006;21(Suppl.
1):S3–7.
[24] Winnerkvist A, Lockowandt U, Rasmussen E, et al. A prospective study of medically treated acute type B aortic dissection. Eur J Vasc Endovasc
Surg 2006;32:349–55.
[25] Nienaber CA, Zanetti S, Barbieri B, et al. INvestigation of STEnt grafts in patients with type B Aortic Dissection: design of the INSTEAD trial—a
prospective, multicenter European randomized trial. Am Heart J 2005;149:592–9.
[26] Fattori R, Nienaber CA, Rousseau H, et al. Results of endovascular repair of the thoracic aorta with the Talent thoracic stent-graft: the Talent thoracic
retrospective registry. J Thorac Cardiovasc Surg 2006;132:332–9.
[27] Szeto WY, McGarvey M, Pochettino A, et al. Results of a new surgical paradigm: endovascular repair for acute complicated type B aortic dissection.
Ann Thorac Surg 2008;86:87–93.
[28] Nienaber CA, Kische S, Rousseau H, et al. For the INSTEAD-XL trial. Endovascular repair of type B aortic dissection: long-term results of the
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Chapter 30
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Open Repair of Thoracic and
Thoracoabdominal Aortic Aneurysms
Christopher Lau, Mario Gaudino, Leonard N. Girardi
New York Presbyterian/Weill Cornell Medical Center, New York, NY, United States
Chapter Outline
Introduction 347
Intraoperative Techniques 348
Exposure 348
Proximal Control 348
Surgical Technique 348
Renal-Visceral Segment 349
Extent of Repair 349
Spinal Cord Protection 350
Methods for Augmenting Spinal Blood Flow 350
Methods to Reduce Spinal Cord Metabolism 351
Methods for Monitoring the Spinal Cord 352
Renal–Visceral Protection 352
Postoperative Management 353
Special Situations 353
Conclusion 354
References 354
INTRODUCTION
To this day, descending thoracic aortic aneurysms (DTA) and thoracoabdominal aortic aneurysms (TAAA) continue to
present a formidable challenges for both the patients and the surgeons. Without surgery, up to 80% of thoracic aneurysms will rupture within the patients’ lifetime and the 5-year survival of untreated thoracic aortic aneurysms is on
the order of 10%–20% [1] as the natural history of thoracic aneurysms is continued growth, dissection, and rupture.
The mainstay of treatment in the current era is surgical therapy, which can be associated with an unavoidable degree
of morbidity and mortality. Contemporary surgical techniques and methods for end-organ protection have mitigated
much of the risk but the procedure remains a complicated endeavor requiring active participation by all parties
involved, including the surgeons, anesthesiologists, perfusionists, and nursing staff.
Traditionally, open surgical repair has been the method of choice for repairing TAAA. Historically, open TAAA
repair was a highly morbid procedure, as evidenced by Cooley and DeBakey’s original series with a 26% mortality
within the first month and significant morbidity [2]. Crawford’s pioneering techniques involving intra-aortic anastomoses and patch reimplantation of the visceral vessels helped usher aortic surgeons into the modern era of TAAA
repair. His technique more closely resembles modern TAAA repair. In his original series of 23 patients, he had only
one death [3]. Since then, the development of end-organ preservation techniques such as partial bypass, circulatory
arrest, renal perfusion, visceral perfusion, and methods for spinal cord protection have significantly reduced the morbidity and mortality associated with open surgery. Contemporary results of open repair of DTA and TAAA are listed
in Table 30.1.
The success of a TAAA program is dependent on a multitude of factors. There is no question that the surgeon’s
technical skill and expertise is a major factor but a successful program relies on contributions from many supporting
services as well. Anesthesiologists, perfusionists, and critical care physicians and nurses all play essential roles in
managing TAAA patients in the perioperative period. A nationwide study comparing the results of low versus high
volume surgeons showed that higher volume surgeons achieve a significantly lower mortality (25.6% vs. 11.0%;
P < .001). Higher volume hospitals also have significantly lower mortality (27.4% vs. 15.0%; P < .001) [9]. Higher
volume allows for familiarity with the various skills and techniques that we describe below, which the surgeon and
team must be accustomed to.
New Approaches to Aortic Diseases from Valve to Abdominal Bifurcation. http://dx.doi.org/10.1016/B978-0-12-809979-7.00030-4
Copyright © 2018 Elsevier Inc. All rights reserved.
347
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TABLE 30.1 Contemporary Results of Open Repair of Thoracoabdominal Aneurysms
Author, Reference Number of Patients Mortality Paraplegia and Paraparesis Renal Failure
Svennson [4] 1509 8.3 15.5 17.8
Safi [5] 1004 14 3.6 NA
Acher [6] 637 2.7 5.5 2.6
Girardi [7] 675 5.6 2.8 5.2
Coselli [8] 3309 7.5 5.3 7.6
INTRAOPERATIVE TECHNIQUES
Exposure
The routine position for thoracoabdominal aneurysm surgery is the right lateral decubitus position with arms extended
at 90 degrees to the body and hips rotated posteriorly 45 degrees. This allows for excellent exposure to the thoracic and
abdominal cavities. For DTA, a lateral thoracotomy is performed, most commonly in the fifth intercostal space. The adjacent rib is shingled posteriorly and the costal margin can be divided as necessary depending upon the degree of exposure
required. For TAAA, a thoracoabdominal incision is created by extending the thoracotomy into a paramedian abdominal
incision. A medial visceral rotation is performed and the diaphragm is divided by a circumferential incision to fully expose
the aorta. After clearing the periaortic tissues, the left renal artery is visualized and it serves as a critical landmark for identifying visceral branches and the extent of aorta that will need to be replaced.
Proximal Control
Proximal control of the aorta must be obtained in a nonaneurysmal segment. For extent I and II aneurysms, the pulmonary
artery is dissected off of the underside of the aortic arch and the arch is freed circumferentially either distal to the left
subclavian artery or between the left carotid and subclavian arteries. The left recurrent laryngeal nerve should be identified
and preserved if possible. Cross-clamping the arch is a safe technique but it is associated with a significantly higher rate
of recurrent nerve palsy (33% vs. 4.9%) [10]. Working more proximally in the arch requires additional manipulation that
leads to increased stretching of the recurrent nerve. This can lead to a palsy that often resolves with time. Those that do not
resolve may require vocal cord medialization.
Patients who have had prior total arch replacements with an elephant trunk procedure do not require dissection
around the aortic arch. In these cases, the trunk is identified in the proximal descending thoracic aorta by epiaortic
ultrasound. A longitudinal incision is made in the aorta over the graft without a clamp in place. There is often a layer of
thrombus between the graft and the aortic wall that helps decrease bleeding from the aortotomy. The trunk is grasped
manually with the fingers and pulled out of the aorta. It is then clamped directly for proximal control [11].
Surgical Technique
Several surgical techniques are available for repairing TAAA. Our preferred technique for routine atherosclerotic aneurysms that can be repaired with a relatively short cross-clamp time is the clamp-and-sew technique. This technique is the
simplest to apply and requires no circulatory assistive devices. However, the surgeon must be confident that the procedure
can be completed in a reasonable amount of time. The cross-clamp time should not exceed 30–35 min to avoid spinal and
end-organ ischemia. After the cross-clamp is applied, the aorta is opened longitudinally for the length of the aneurysmal
segment but not resected. A Dacron graft is used to reconstruct the aorta using an inlay technique. Visceral vessels and
intercostal arteries are anastomosed to an opening in the side of the Dacron graft using an inclusion technique. The aortic
wall is then wrapped around the graft.
Partial bypass (left-heart bypass) can provide additional safe cross-clamp time for more complicated cases that
require more extensive reconstruction. Partial bypass also offloads the heart in patients who have compromised cardiac
function or aortic valve insufficiency. The circuit for partial bypass includes a venous cannula that is placed into the
left atrium via the left inferior pulmonary vein and an aortic cannula that is placed in either the left femoral artery or
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the distal thoracic aorta. In cases of chronic aortic dissection, the aortic cannula can be placed in either the true or false
lumen as long as adequate flow can be achieved. Fenestrations in the intimal flap allow perfusion of both lumens. The
proximal cross-clamp is placed near the arch and a distal cross-clamp is placed in the mid-descending thoracic aorta.
Partial bypass is initiated with flows of 3 L/min. This placement allows the lower intercostal arteries, abdominal viscera,
and lower extremities to be perfused while performing the proximal anastomosis. After the proximal anastomosis is
completed, partial bypass is discontinued and the distal cross-clamp is removed. Then the necessary intercostal arteries
and visceral vessels can be reimplanted and the distal anastomosis completed.
Occasionally, the aneurysm extends proximally into the aortic arch, obviating the possibility of placing a proximal
cross-clamp. In such situations, deep hypothermic circulatory arrest (DHCA) may be the most prudent option. This
allows for an open anastomosis without the need for cross-clamping. The repair can be extended proximally into a
reverse hemiarch repair. Full cardiopulmonary bypass is initiated via the femoral vessels and the body is cooled to 18°C.
The proximal anastomosis is created under circulatory arrest and then cardiopulmonary bypass is resumed via either the
femoral vessels or a side branch of the aortic graft. The remainder of the reconstruction is performed in the usual manner
while rewarming the patient.
Kouchoukos et al. have used circulatory arrest as a primary strategy for TAAA repair. However, the technique
increases operative time due to the need for cooling/rewarming. Prolonged bypass time and hypothermia can increase
coagulopathy and bleeding but the benefits of the technique include the protective qualities of hypothermia. Because the
entire body is cooled and metabolism is lowered significantly, this offers spinal cord protection as well as protection for
visceral organs [12].
In patients who have an ascending or arch aneurysm that is currently not in need of repair but may need repair via a sternotomy in the future, a reverse elephant trunk can be pre-emptively placed. Similar to a standard elephant trunk technique,
the graft used when repairing a DTA or TAAA can be inverted upon itself, leaving a double layer of graft in the descending
aorta. When surgery is indicated for the ascending or arch aneurysm, under circulatory arrest, the inverted segment of graft
can be pulled out from the descending aorta and used for the arch reconstruction. With this technique, the need to perform
a distal anastomosis deep within the chest is avoided and circulatory arrest time is significantly shortened [13].
Renal-Visceral Segment
Reimplantation of the visceral arteries can be performed in a variety of ways. When the visceral segment is very dilated,
identification of the ostia of the visceral branches can be difficult. The sac is often filled with thrombus that must be
removed before clearly identifying the ostia. The left renal artery is an excellent landmark that can be found externally prior
to cross-clamping. Once the aorta is opened, the ostia of the celiac, superior mesenteric, right renal, and any accessory renal
arteries are identified by correlating location with the preoperative computed tomography scan. For extent I aneurysms,
the visceral vessels can often be beveled into the distal anastomosis, eliminating as much aorta as possible. For aneurysms
that extend lower, a separate anastomosis is necessary. If the visceral branches are in close proximity to each other, a single
patch can often be used to reimplant all four visceral branches. If a single patch will leave too much native aorta in this segment, reimplanting the left renal artery as a separate graft can rectify this problem. In patients with large aneurysms whose
visceral branches are spread wide apart, premade multibranch grafts are commercially available to individually reimplant
each visceral artery. Patients with Marfan syndrome or other connective tissue disorders may be at higher risk for continued
aneurysmal dilatation of any aorta that is left in place. They may benefit from branched reconstruction because separate
reimplantation of the visceral arteries will minimize the chance of a patch aneurysm in the future. This technique also offers
excellent patency rates of 98% and 97% at 1 and 5 years, respectively [14].
Extent of Repair
In general, only the aneurysmal segments of aorta are replaced and relatively normal caliber aorta is spared. Although
replacing more aorta may decrease the risk of reoperation due to progression of disease, doing this is not without consequences. A more extensive aortic replacement is likely to require sacrificing more intercostal arteries and the risk of
spinal cord injury (SCI) is concordantly increased. Risk of other major complications also increases as the extent of aortic
replacement increases, with extent II TAAA repair having the highest rate of SCI, mortality, and other major morbidity
(Table 30.2) [8]. A conservative approach to the amount of aorta to replace is well-justified by the low rate of reoperation
that is seen (3% at 5 years in our series).
In the minority of patients who eventually do require reoperation, they may ultimately have an extent of aortic replacement
equivalent to a single-stage extent II TAAA repair. However, a less extensive repair at the initial operation may still be justified
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TABLE 30.2 Major Adverse Events by Aneurysm Extent
Aneurysm Extent I II III IV
Operative mortality 5.9 9.5 8.8 5.4
Stroke 3.6 4.3 1.4 1.5
Permanent spinal cord injury 3.4 8 7 2.4
Renal failure requiring dialysis 4.9 9.6 7.9 7.6
Myocardial infarction 1.3 1.2 1.5 0.9
Tracheostomy 8.1 12.3 7 4.5
in these patients. A staged approach may allow collateral circulation to develop, which may help reduce the risk of paraplegia
compared to a single-stage complete repair. Etz and Griepp had an SCI rate of 15% in single-stage extent II repairs and zero
in patients with a staged extent I followed later by extent III or IV repair [15].
SPINAL CORD PROTECTION
Ischemic SCI is one of the most devastating complications of TAAA surgery. Paraplegia in and of itself is quite physically debilitating but postoperative paraplegia/paraparesis is also associated with significantly decreased survival
rates [4].
The risk of SCI is intimately related to the extent of the thoracoabdominal aorta that must be replaced, with complete
extent II TAAA repairs having significantly higher rates of SCI than shorter segment repairs such as limited DTA repairs or
extent IV TAAA repairs. In the largest single-center experience of TAAA repair with 3309 patients by Coselli, the overall
SCI rate was 9.6% with 5.4% having permanent deficits and 4.4% having temporary deficits. The extent II group had an
SCI rate of 13.9% compared to 7.8% in extent I, 10.8% in extent III, and only 4% in extent IV repairs [8]. More extensive
repairs require longer operative and cross-clamp times and sacrifice more intercostal and lumbar arteries. Both of these
contribute significantly to the ischemic insult to the spinal cord.
Various techniques have been implemented to attempt to decrease SCI rates with varying success. The primary goals in
spinal cord protection are to maximize spinal collateral blood flow and to decrease the metabolic demand and metabolic
injury. Despite extensive research and combined use of multiple different protective adjuncts, no method has been found
to be completely effective in preventing SCI. Ischemic time plays a major role, and a risk model can be created by plotting
the risk of SCI on a curve against ischemic time. Adjunctive measures may shift this curve and decrease the risk of SCI for
a given ischemic time but they cannot eliminate the risk. Multiple techniques are available to augment spinal blood flow,
decrease the metabolism, or monitor the spinal cord function. Most centers will use some combination of the adjunctive
measures detailed below.
Methods for Augmenting Spinal Blood Flow
Lumbar cerebrospinal fluid (CSF) drainage has proven to be an effective method for decreasing SCI rates. The catheter is
placed in either the L2/L3 or L3/L4 interspace. Ideally, it is placed preoperatively but in emergent cases, it can be placed
postoperatively. Aortic cross-clamping causes an increase in CSF pressure [16]. Spinal perfusion pressure (mean arterial
pressure (MAP)–CSF pressure) is maximized by reducing the CSF pressure to less than 12 mmHg. This is most easily
done by draining CSF intermittently. A maximum of 25 mL is drained off every hour. More aggressive drainage can lead
to brain stem herniation. Several retrospective studies have suggested a benefit with CSF drainage, and the findings were
confirmed by a large, well-controlled, randomized study of 145 patients undergoing extent I or II TAAA repairs, in which
the rate of SCI was 2.6% in the CSF drain group and 13% in the control group (P = .03) [17]. The CSF drain is typically left
in place for 48–72 h postoperatively. It is then clamped and the patient is monitored for neurologic changes prior to removing the catheter. However, the risk of SCI remains even after the drain is removed, although at a lower rate. CSF drainage
can also be used to treat patients with delayed postoperative paraplegia. Neurologic deficits can often be reversed with
expedient replacement of the CSF drain, hemodynamic optimization, and aggressive physical therapy [18]. We routinely
place CSF drains in all patients undergoing DTA or TAAA repair as the benefits far outweigh the risks of placing the drain.
Complications are rare, with the most common being postdural puncture headaches. These can often be managed with
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