A A To Raco Abdominal

Management of Thoracoabdominal
Aortic Aneurysms
Thoracoabdominal aortic aneurysms (TAAAs) involve dilatation of the
descending thoracic aorta into the abdomen. The aneurysms may extend
from the left subclavian artery to the iliac arteries. The most common
etiology is from spontaneous degeneration of the aortic wall adventitia,
but other causes of accelerated or secondary dilatation of the aortic wall
include spontaneous aortic dissection, infection, trauma, and disorders of
connective tissue, such as Marfan’s, Turner’s, and Ehlers-Danlos syn-
dromes. Because nondegenerative etiologies form a very small percentage
(less than 5%) of all TAAAs, this review concentrates on the management
of degenerative TAAAs. This notwithstanding, the treatments of nonde-
generative TAAAs are all quite similar. We also exclude in this article the
management of aneurysms that involve the ascending aorta or the aortic
arch since the management of these aneurysms is significantly different
from that of TAAA.
One difficulty in describing the management of true TAAAs is that most
authors report their combined experience with TAAAs and isolated
thoracic aortic aneurysms (TAAs), or aneurysms that do not extend into
the abdomen as one. In this review, we have attempted to minimize
references to isolated TAAs whenever possible, because they can gener-
ally be treated with simple tube grafts (open or endovascular), and
because they involve shorter segments of aorta. Repair of these TAAAs
is associated with a lower complication rate than aneurysms that are
thoracoabdominal in nature. In the cases where the reference includes, or
is limited to, TAA, we identify them as such, or if possible, report the
findings limited to the data available referring specifically to TAAAs.
The treatment of TAAAs is heralded by very morbid complications in
up to two thirds of patients,1 all of which are associated with a prolonged
length of stay and high mortality rates.2 This fact is true regardless of
whether the TAAA repair technique used is open, endovascular, or a
hybrid of the 2. Therefore, we believe it is a worthwhile endeavor to first
review the etiology of these shared complications and how to avoid them,
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before discussing the techniques and outcomes of modern TAAA repair.
In this manner, we hope to allow the reader to better understand why so
many variations exist in the treatment of TAAAs, and perhaps how to
select 1 technique over the other in different clinical scenarios.
Epidemiology and Classiﬁcation
When considering all aneurysms of the thoracic aorta, ascending aortic
aneurysms are the most common (40%), while TAAAs only account for
10%.3 In the United States, fewer than 1000 TAAAs are repaired
annually,4 compared with almost 100,000 infrarenal abdominal aortic
aneurysms (AAAs).5 This large disparity impairs our ability to develop
the “ideal” surgical technique, or even improve the management of
TAAAs. The surgical TAAA literature is therefore mostly populated by
the anecdotal experience of a few high-volume surgeons, who often
produce results that are not reproducible by others.
Population studies have documented approximately 5.9 to 10.4 new
TAAs per 100,000 person-years with nearly equal incidence in the sexes
(males, 44%).3,6-8 The mean age at diagnosis is 63 to 65 years for men
and 75 to 77 years for women.2,5 A study of deaths associated with TAA
captured by the Swedish National Bureau of Statistics and Swedish
hospital records found that almost three quarters of TAA ruptures
occurred in women, mostly aged 70 to 84 years.6 This dramatic difference
in gender-associated rupture rates does not correlate with the incidence of
TAAAs reported from single-center reports of treated TAAAs. Surgical
series consistently report a slightly higher incidence of TAAA ruptures in
male patients (approximately 60%). This difference may be because these
series only include patients arriving and treated at their hospital,9-11
whereas the Swedish study included all ruptures in the country— dead or
alive. Similarly, another population-based study from Mayo Clinic also
found that older women accounted for 51% of all degenerative thoracic
aneurysms and most of the ruptures.12 Therefore, it is possible that the
rupture rate is truly higher in women, and as such, a lower percentage of
them make it to a medical institution.
Almost one quarter of patients with any thoracic aortic aneurysm will
also have concomitant AAAs.3 Thus, whole-body aortic imaging should
be considered for screening for both types of aneurysms when either is
identified. This is most relevant in contemporary practice because AAAs
are commonly diagnosed serendipitously and treated by multiple medical
specialties (especially in the endovascular era). TAAA patients may have
multiple abdominal endovascular procedures without recognizing or
managing large TAAAs (Fig 1). Not evaluating the patient completely
Curr Probl Surg, February 2011 71
FIG 1. Common cardiovascular complexities in patients with TAAA. Untreated thoracoabdominal
aortic aneurysm (white arrows) in a patient with a previous infrarenal endovascular abdominal aortic
aneurysm graft (bifurcated endograft identified by short black arrows), a low thoracic aortic
endograft, and a superior mesenteric artery stent (identified by upper and lower long black arrows,
respectively). Sternotomy wires are also visible after previous coronary artery bypass procedure.
and missing more extensive aneurysm disease may lead to poor surgical
planning and erroneous surgical risk stratification.
Aortic aneurysm morphology is often referred to as “saccular” or
“fusiform” and these findings may change the management, although no
prospective natural history data exist. Most TAAAs are fusiform aneu-
rysms (ie, diffuse, irregular shape), which are thought to be due to a
chronic, continuous dilatation of the aorta involving the whole circum-
ference of the aorta. In contrast, saccular aneurysms often represent an
eccentric or focal dilatation of the aorta that may have been preceded by
local trauma or plaque rupture. The shape of an aneurysm can change the
management or direct further care because as many as 93% of mycotic
aortic aneurysms are saccular.13
Saccular thoracic aneurysms also include “penetrating aortic ulcers” or
“ulcerlike projections” and appear as focal areas of the aorta that are
aneurysmal. Although rarely extensive enough to be “true” TAAAs, since
the advent of endovascular repair, more and more asymptomatic aneu-
FIG 2. Crawford classification of TAAAs. The Crawford classification is determined by the relationship
of the aneurysm to the left subclavian artery, the diaphragm, and whether it extends into the
abdominal visceral branches. Type I TAAAs start at the left subclavian artery and end before the
visceral branches. Type II TAAAs start at the left subclavian artery and involve all the visceral and renal
branches of the abdominal aorta. Type III TAAAs involve the distal half of the thoracic aorta and
include the visceral and renal arteries. Type IV TAAAs begin below the diaphragm and involves the
visceral and renal arteries.16 (Color version of figure is available online.)
rysms are treated with endografts. This occurs even though some report
that these aneurysms have a low risk of spontaneous rupture, or in some
cases may even resolve.14 In contrast, symptomatic penetrating ulcers
carry a higher risk of death and benefit from treatment even if other
complex aortic or cardiac procedures are necessary.15
Crawford and Coselli described the original classification of TAAAs
into 4 types according to the extent of the aneurysm starting from the left
subclavian artery, and the risk of complications (particularly paraplegia)
associated with the repair. They also correlated the extent of the
aneurysms to the surgical approach required to repair them (Fig 2).16 A
FIG 3. Type I thoracoabdominal aortic aneurysm. Patient with both an ascending thoracic aortic
aneurysm as well as a Crawford type I thoracoabdominal aortic aneurysm starting distal to the left
subclavian artery and ending before the distal thoracic aorta. (Color version of figure is available
online.)
Crawford type I TAAA involves most of the descending thoracic aorta

from the left subclavian artery up to the abdominal visceral vessels,
excluding the renal arteries (Fig 3). A Crawford type II TAAA is the most
extensive aneurysm. It starts at the origin of the left subclavian artery and
continues into the abdominal aorta and up to the iliac arteries (Fig 4).
Because Crawford type I and II TAAAs involve most of the descending
aorta, they have the highest incidence of paraplegia with repair. Crawford
type III TAAAs involve the distal half of the thoracic aorta and the
visceral and renal arteries. Type IV TAAAs are limited to the abdominal
aorta below the diaphragm, and involve all the visceral and renal arteries
(Fig 5). Most TAAAs are Crawford classification type IV (52%), and in
descending order of incidence include type II (23%) ⬎ type III (15%) ⬎
type I (9%).8
Risk Factors for Developing a TAAA
There is little information published about the risk factors for TAAA
outside of retrospective observations obtained from small surgical case
series that tend to be combined with data that include isolated TAAs. In
general, most of the risk factors common to patients with AAAs are
reported with degenerative TAAAs, including smoking, hypertension,
FIG 4. Aneurysmal degeneration of an aortic dissection. Spontaneous aortic dissection extending
from the ascending aorta (previously repaired) to the abdominal aorta, with subsequent aneurysmal
degeneration resulting in a Crawford type II TAAA. The arrow indicates the interface between the true
and false lumens. (Color version of figure is available online.)
chronic obstructive pulmonary disease (COPD), and atherosclerotic

disease of the coronary and peripheral arteries. However, AAAs and
TAAAs are not the same because they do not have the same incidence,
gender distribution, or outcomes, regardless of these shared risk factors
(Table 1).3,17-19
An evaluation of the prevalence of coronary artery disease (CAD) in
patients with aortic aneurysms supports that AAAs and aneurysms of the
thoracic aorta (TAA and TAAA) are indeed quite different. There is an
overall prevalence of silent CAD of 63% in all aneurysms; however, 76%
of patients with AAAs have CAD, whereas it is only found in 30% of
patients with a TAAA. This is surprising when both of these patient
populations have similar exposure to smoking and incidence of hyperlip-
FIG 5. Crawford type IV TAAA. Three-dimensional, color reconstruction of a Crawford type IV TAAA
involving the distal thoracic aorta, extending through the entire visceral plate, and ending at the aortic
bifurcation. Color key for the online version: red, blood flow; white, calcifications of the aortic wall;
yellow, thrombus within the aorta. (Color version of figure is available online.)
idemia.20 Ito and colleagues reported similar findings in the 343 consec-
utive patients with aneurysms. There were 211 patients with AAAs and
132 with a thoracic aortic aneurysm (TAA and TAAA). They also found
that patients with AAAs had a significantly higher likelihood of concom-
itant CAD (odds ratio [OR]: 4), but also diabetes (OR: 2) and COPD (OR:
2). Meanwhile, those with any TAAA or TAA were more likely to have
a higher body mass index (OR: 9), hypertension, and stroke (OR: 3 for
TABLE 1. Risk factors for the incidence of TAAs compared with AAA
Relative risk or incidence in TAA
Risk factor in TAA when compared with AAA20,21
Smoking Lower
Hypertension Higher
Coronary and peripheral artery disease Lower
Chronic obstructive pulmonary disease Lower
Previous thoracic aortic dissection —
Connective tissue disorders (especially Marfan’s Higher
and Ehlers-Danlos type IV)
Trauma —
Elevated body mass index Higher
Stroke Higher
Male gender Lower
Table identifying and comparing the shared risk factors for developing thoracic aortic
aneurysms (all types) and AAA.
AAA, abdominal aortic aneurysm; —, unknown.
each).21 The Yale University Thoracic Aneurysm Database also revealed

that in 721 patients with aneurysms of the thoracic aorta (13% were
TAAAs and 72% were of the ascending aorta), the incidence of CAD was
only 27%.22 These data support the contention that although aortic
aneurysm formation seems to share the same risk factors as other
arteriopathies, aneurysms are more likely to occur in the abdominal aorta
than the thoracic aorta, and that AAAs and TAAAs do not have the same
etiology.
Although most TAAAs are degenerative, up to 20% are eventual
sequelae of chronic aortic dissection that becomes aneurysmal.23
Patients with chronic aortic dissection develop aneurysmal dilatation
of the outer wall of the false lumen and eventually need aortic repair
up to 40% of the time. The most consistently demonstrated risk factor
shown to accelerate the progression of dissections to aneurysm and
rupture is poorly managed hypertension—particularly diastolic blood
pressure greater than 100 mm Hg.24,25
Other causes of aneurysm formation of the thoracic aorta include
genetic abnormalities of the aortic wall (notably Marfan’s, Loeys-
Dietz,26 and Ehlers-Danlos syndromes) and inflammatory vascular
diseases, such as giant cell arteritis.27 Although they do form TAAAs,
most of the aneurysms associated with these syndromes involve the
ascending aorta and any extension into the descending aorta is usually
secondary to aortic dissection rather than primary aortic degenera-
tion28-30 (Fig 6).
FIG 6. Typical etiology of TAAAs in patients with Marfan’s syndrome. Patient with Marfan’s syndrome
with a history of an aortic dissection that extended from the aortic root to the left external iliac artery.
Twelve years after his ascending aorta and arch were repaired with Bentall and elephant trunk
procedures, the descending aortic dissection degenerated to a Crawford type II TAAA involving the
entire aorta.
Risk Factors for TAAA Rupture and Death

Unfortunately, because TAAAs are relatively rare and usually asymp-
tomatic, there are little data on their natural history and rupture risk. Most
of the data available involves patients who are either denied surgical
repair due to coexisting medical conditions that shorten their overall
survival or is collected retrospectively from patients who rupture.
Additionally, many reports mix in patients with acute and chronic aortic
dissections, which have different expansion rates and etiology. These
combined limitations severely cripple our ability to gain accurate prog-
nostic data that can be used to counsel patients, although some risk factors
seem to be consistent (Table 2).
TABLE 2. Risk factors for TAAA rupture
Size ⬎5 cm
Each increase in size ⬎1 cm
Chronic obstructive pulmonary disease
Aortic dissection as the etiology
Pain
Uncontrolled hypertension (especially diastolic)
Age
Female gender
Aneurysm diameter increase greater than expected (2 mm/year)
Initial reports from the 1970s by Pressler and McNamara documented

that approximately 40% of patients who did not undergo surgical repair
died of TAAA rupture, whereas one third of patients died of other
cardiovascular complications. The mean survival was less than 3 years.
During their extended observation period, more than 90% of the patients’
aneurysms ruptured, and 68% of ruptures occurred more than a month
after the diagnosis.31,32 Crawford’s report on 110 untreated thoracic and
TAAAs from 1984 to 1993 revealed that the overall mortality of isolated
TAA was 65%, while that of TAAAs was 87%. Regarding the causes of
death, 42% and 58%, respectively, were due to ruptured aneurysms. The
most common cause of nonoperative management was poor anesthetic
risk (15 cases), age greater than 70 years (20 cases), and small aneurysms
(21 cases). The mean time to rupture was 1300 days (3.6 years).33 Similar
findings published by Davies and colleagues found that the median
survival among patients with untreated TAAAs calculated to be 3.3 years.
Patients with a 6.0 cm TAAA have a 5-year survival of 54%, yielding a
3.7% per year risk for rupture, and risk of death of 12% per year.22
The Scottish National Thoraco-abdominal Aneurysm Service evaluated
89 patients with TAAAs that were treated nonoperatively due to high risk
for open repair. They included 3 patients that did not have true TAAAs
(TAAs and suprarenal AAAs). The authors found an approximately 60%
survival at 1 year and reported a mean survival of only 24 months.
Nevertheless, they did not find a statistical difference in rupture rate nor
mortality in relation to the size of the aneurysms (dividing them into
groups of less than or greater than 6 cm). The survival of patients with
aneurysms less than 6 cm at 1 year was 71%, compared with those with
aneurysms greater than or equal to 6 cm, which was 60% (not statistically
significant). This was true even though almost half the total mortality
(47%) was classified as secondary to aneurysm rupture. The next most
common etiologies for death were found to be ischemic heart disease
(12%), malignancies (12%), and pulmonary disease (10%).8 This is
inconsistent with all other series, which always document a difference in
rupture rate relative to the TAAA diameter. Most reports find that TAAA
diameter greater than 5 cm is a major risk factor for rupture and death, and
the larger the TAAA, the greater the risks. The lack of difference in the
Scottish series may be related to the rather small sample size, by mixing
lower risk aneurysms in the study groups, and that the authors stated that
“the UK has a low rate of post-mortem examinations,”8 which may have
erroneously misclassified “nonaneurysm” deaths.
There is almost a doubling of the rupture risk for every 1 cm greater
than 5 cm of the descending thoracic aorta, and a 1.5 times increase in the
risk of rupture with every 1 cm growth of the abdominal aortic component
of the TAAA.34 The risk of death from rupture for untreated TAAAs
within 2 years of diagnosis (larger than 5.6 cm) is approximately 25%,
while another 25% will die from other causes. These findings are similar
to those reported from the Mayo Clinic, which found a 14% rupture rate
for untreated TAAAs and accounted for 24% of all deaths over a 4-year
follow-up period.35 These numbers are important when planning to
perform TAAA repair (whether open or endovascular), since patients who
are high risk for repair should have a predicted survival greater than 25%
at 2 to 4 years from other causes to benefit from repair.
The Yale University prospective database of more than 1600 TAAs and
dissections over 10 years revealed that an aneurysmal thoracic aorta
grows 0.10 cm per year on average (0.07 cm for the ascending aorta, and
0.19 cm for the descending aorta). In addition, when the aorta reaches 6
cm, the yearly rates of rupture, dissection, death, or a combination of all
3 is 4%, 4%, 11%, and 14%, respectively.36 Meanwhile, the growth rate
for a TAAA secondary to dissection can be as high as 0.28 cm per year,
highlighting the reason aortic dissections most often require surgical
repair and why this disease is different from degenerative TAAAs.37 In
another study of a mixed group of 165 patients with chronic descending
aortic (type B) dissections and degenerative TAAAs that were followed
nonoperatively, almost 20% ruptured. Once ruptured, their mortality was
close to 90% of patients with chronic type B dissections and 75% of
patients with degenerative aneurysms. Risk factors identified for rupture
included age, COPD, and pain. Ruptured aneurysms associated with
dissection were smaller in diameter and had higher blood pressure than
patients with ruptured degenerative TAAAs (5.4 cm average vs 5.8 cm,
respectively) and had a higher mortality rate (90% vs 76%).38 Enlarge-
ment has also been found by others to relate exponentially to the size of
the aneurysm,25 correlating to a higher risk of rupture.39
In general, the growth rate of an intact TAAA is 19 mm per year (higher
if dissected) and the overall consensus is that the risk of rupture of
aneurysms of the descending aorta is significant when it reaches 5 cm to
6 cm. This lifetime risk is approximately 40% to 60% with a rupture-
related mortality well exceeding two thirds to three quarters of patients.
Those that will benefit from any repair must have a life expectancy of
greater than 25% over 2 years, regardless of the size of the aneurysm. This
is especially true for TAAAs, which have a lower risk of growth and
rupture when compared with a TAA.
COPD alone increases odds of rupture by 3.6 in TAAs and TAAAs,
even when smoking is accounted for in the risk assessment.34 Conversely,
COPD is repeatedly found to be 1 of the most important risk factors for
complications and death following open repair of TAAAs.40 When
evaluating the expansion rate of TAAAs, patients with COPD will
consistently have faster expansion rates.35 Ninety-four patients who were
not candidates for surgery were followed by Crawford and DeNatale.
They found that 80% of the subgroup that ruptured had COPD (Fig 7). Of
these, only 24% survived 2 years or more.41 Cambria and others followed
a series of 57 patients with TAAAs who were not considered operative
candidates. In addition to COPD, the authors found an association (P ⫽
0.06) between rupture and chronic renal failure.35 Conversely, preoper-
ative renal failure is also linked to having pulmonary complications after
TAAA repair.42 Smoking is common to both COPD and TAAAs, and
both share connective tissue weakness as their etiology. Perhaps the
combination of the 2 in a single patient may reflect the severity of their
connective tissue disease. Multivariate analysis has also identified COPD
as an independent predictor of impaired late functional status at 12
months after TAAA repair (P ⫽ 0.034, OR 5.0 [2.3-11.1]).43
Age alone is a risk factor for the rupture of aneurysms of the thoracic
aorta. The Mount Sinai group also demonstrated that the risk of
descending thoracic aortic disruption increased by a factor of 2.6 for
every decade of life,34 and the Swedish registry of healthcare demon-
strated that the incidence of ruptured thoracic aneurysms in Sweden was
100 per 100,000 in individuals aged 60 to 69, but this increased to 530 per
100,000 in patients over the age of 80.44 Although these findings may
only be a reflection of larger aneurysms being detected later in life, it is
possible that the debilitating effects on the aortic wall may be augmented
with age. Another possibility is that older patients may present later with
a symptomatic TAAA that is not diagnosed in a timely fashion. Although
the risk of rupture for untreated TAA and TAAA is higher with age, 1
review of the surgical outcomes in patients over the age of 79 (from a
high-volume referral center), age alone was not found to be a contrain-
FIG 7. Ruptured TAAA in a female patient with COPD. Three-dimensional CT angiogram and axial
images of a 6.5-cm ruptured, Crawford type III TAAA in a female patient with chronic obstructive
pulmonary disease. Letters A-D and their arrows correlate the axial CT images (left panels) with their
position on the 3D aortic reconstruction (right). AP, anteroposterior view; LAT, left lateral view. Dashed
line identifies the large retroperitoneal hematoma from the rupture seen in axial (B). (Color version of
figure is available online.)
dication for open repair since the mortality was 17%.45 This conclusion
has unfortunately not been reproduced by other high-volume surgeons,46
and multicenter sampling and population-based studies all conclude that
the risk of death after TAA and TAAA repair is indeed linked to age.4,44
Therefore, age is usually a criteria for “contraindication” for open repair
in endovascular trials involving the thoracic aorta. One other case series
concluded that older patients undergoing TAAA repair had the same
mortality as younger ones; however, the mortality for both groups was
higher (25% vs 28%, respectively).10 This again highlights differences in
outcomes of open repair from certain surgical groups and the complexity
involved in the appropriate management of TAAA, even though out-
comes have improved over time.12,44
Finally, the role of gender in the risk of TAAA rupture may be
understated. The Mayo Clinic’s evaluation of the outcomes of their
management of all 133 degenerative TAAs in Olmstead County revealed
that overall survival had improved over time. It also discovered that the
majority (79%) of all thoracic aortic aneurysm ruptures occurred in
women, and that they tended to be older than the male cohort.12 The
previously reviewed Swedish population-based study also found nearly
three quarters of TAA and TAAA ruptures occurred in older women.6
Another group to analyze female gender and TAAA was the University of
Texas group. They found in 355 open repairs of TAAA that the second
highest odds ratio for death was female gender (OR: 2.74).47 Research in
animal models has revealed different levels of aortic aneurysm matrix
metalloproteinases and collagen in a gender-related manner,48,49 demon-
strating early molecular evidence of differences between aneurysms in
men and women.
Threshold for Repair of TAAAs
Despite the aforementioned studies spanning more than 50 years, there
is still no uniform consensus as to an aortic diameter to repair asymp-
tomatic TAAAs, regardless of the operative technique. Due to the wide
ranges of the reported morbidity and mortality from various centers
performing the operation, the risk factors of the patient and the associated
presentation of the aneurysm must all be considered. Open repair of
TAAAs has been recommended for aneurysms with a range of diameters
that are based on conclusions of each authors’ experience (Table 3). In
1978, McNamara and Pressler reported their findings on 22 patients with
TAAs diagnosed with plain chest films that were not treated. They
suggested that because 8 of the 9 patients who did rupture had aneurysms
larger than 10 cm that this should be the threshold for repair.31
Crawford’s retrospective review of the outcomes of 86 ruptured TAAs
and TAAAs he treated challenged this conclusion, and based on his 8%
mortality rate concluded that a maximal diameter of the descending aorta
of 5 cm or greater should undergo surgery to maximize survival.9 This
conclusion was consistent with Mayo Clinic’s experience of the rupture
rate of 57 untreated TAAAs (18% risk of rupture for TAAAs greater than
5 cm).35 In Coady and colleagues’ first review of the Yale University
database, they recommend that TAAA diameters greater than 6.5 cm
should be reached before open repair.37 However, 5 years later, the same
group reviewed their surgical outcomes and the expansion rates of 720
TAAs. They concluded not only that there is a progressive risk of
expansion, dissection, rupture, and death with aneurysms greater than 6
cm, but that elective repair returned the survival rate back to baseline,
again lowering the threshold for surgical repair back to 6.0 cm.22 Our
practice at the University of Michigan is to offer a repair to patients with
TABLE 3. Studies evaluating the diameter threshold before operating for TAAA
Number of Diameter Recommended
patients recorded of diameter before
evaluated the TAA TAAA repair Study design
McNamara 22 89% of 10 cm (open repair) Retropective review of
et al31 ruptures untreated TAA
were (diagnosed by plain X
⬎10 cm ray) followed by the
authors over 10 y
Crawford 86 5-17 cm 5 cm (open repair) Retrospective review of
et al9 rTAA treated by the
authors
Mayo 57 3.4-7.8 cm 5 cm (open repair) Retrospective review of
Clinic35 nonoperated TAAA
Yale 230 3.5-10 cm 6.5 (open repair) Review of aortic imaging
University37 and outcomes from a
prospective database
Yale 570 6 cm cut 6 cm (open repair) Review of aortic
University22 off imaging and
outcomes from a
prospective
database
French 166 ⬍5 to ⬎6 17% were ⬍5 cm, Retrospective review of
Nationwide cm 21% were 5.1-5.9 all endovascular
Study50 cm (endovascular repairs of TAA in
repair) France
TAAA, thoracoabdominal aortic aneyurysm; TAA, thoracic aortic aneurysm; rTAA, ruptured
thoracic aortic aneurysm.
a reasonable life expectancy and surgical risk who have TAAAs that are
6 cm or greater in diameter, or patients with a symptomatic (pain,
hypotension, compression, etc) aneurysm.
Because all the above is based on the historic outcomes of open TAAA
repair, the “modern algorithm” for TAAA management may change when
we have long-term outcome data with greater experience in endovascular
repair. An example of this phenomenon is a report from an independent,
nationwide study from France that evaluated the outcomes of all thoracic
aneurysms treated with stent grafts. More than one third of the TAAs
were smaller than 6 cm (17% less than 5 cm, and 21% were 5.1 to 5.9
cm), which seems to indicate that stent grafts are more liberally used to
treat thoracic aneurysms by some groups. However, their reported
mortality in patients with TAA or TAAA less than 5 cm treated with
endografts was 4.7%, and 7.4% in patients with aneurysms that were 5.1
to 5.9 cm.50 With this in mind, the optimal time to repair a TAAA should
be when the predicted risk of rupture within 1 year is greater than the
anticipated mortality of the procedure itself, regardless of the technique
employed.34 How to accurately apply this principle to female patients
with TAAA is an area that deserves further study since the outcomes after
repair in women remain unclear.
Preoperative Evaluation of All TAAA Repairs

Patients with TAAAs frequently have significant coexisting medical
conditions, including hypertension, CAD, COPD, congestive heart fail-
ure, cerebrovascular occlusive disease, and peripheral vascular occlusive
disease. Cross-sectional imaging, mainly by computed tomography (com-
puted tomography angiography [CTA]), is the primary method to visu-
alize the thoracic and abdominal aorta for determining aneurysm diameter
and extent. Since most TAAAs are small when discovered, serial imaging
is often required to track growth patterns; however, level A and B
evidence regarding the timing of surveillance is lacking. Serial imaging is
typically performed at 6- to 12-month intervals, but varies depending on
the initial diameter and extent of the aneurysm.
Cardiac
Historically, the 2 most important predictors of mortality after surgery
of the thoracic aorta were emergent repair and history of cardiac
disease.19 In addition, poor myocardial function and atherosclerotic
disease of the coronary arteries are common in patients undergoing
TAAA repair,51 with one half of them having diastolic dysfunction before
surgery.52 A landmark publication by Hertzer and colleagues described
the findings of routine coronary catheterization in patients before under-
going elective abdominal aortic surgery. In this study, 42% of patients
with clinical evidence of cardiac disease had significant angiographic
CAD. However, 19% of symptom-free patients also had significant CAD.
Importantly, almost one half of the patients with AAAs that had coronary
disease were treated for it before open AAA repair.53 It is thus not
surprising that a cardiac etiology is the most common cause of death after
open TAAA repair, representing almost half of early deaths, as well as
one third of late deaths.54 Even if the patients have been revascularized,
they are not protected from increased mortality. Safi’s group evaluated the
incidence and effect of CAD, with or without coronary artery bypass
surgery (CABG), on patients undergoing TAA and TAAA repair. They
found that 34% of the patients undergoing surgery had CAD and that the
mortality in these was statistically significantly higher than those who did
not. More striking was that although the mortality of patients who had
undergone CABG was almost double (22%) that of patients who had not
(14%), patients with a cardiac ejection fraction less than 50% had the
highest 30-day mortality rate of both groups (26%) regardless of a
medical history of CAD and CABG (14%).55
Although cardiac complications are no longer the most important risk
factor for death after TAAA repair, all patients should undergo evaluation
of their coronary arteries and cardiac function before repair to best stratify
their cardiac risk. In the case of endovascular TAAA repair, this
recommendation may not be true because there are no data to direct the
approach of preoperative cardiac evaluation.
Standard evaluation of cardiac function includes a preoperative
electrocardiogram, transthoracic echocardiogram, and noninvasive
stress testing. These all help predict cardiac dysfunction and areas of
reversible ischemia. Coronary angiography in patients with suspected
atherosclerotic coronary disease may also be indicated based on the
results of the noninvasive testing or the patient’s symptoms. In the
elective setting, coronary revascularization, either by catheter-based
techniques or by surgical bypasses, should precede TAAA repair in
most cases. An important factor to consider when deciding to treat a
coronary artery includes the use of clopidogrel, which typically
requires a minimum of 6 weeks of antiplatelet therapy after stenting,
which would delay TAAA repair. Drug-eluting coronary stents have a
lifelong requirement of clopidogrel to avoid stent thrombosis and thus
should be avoided before TAAA repair. If the left internal mammary
artery was used for a coronary bypass graft, then patients with TAAA
stents that cover the subclavian artery first need a carotid-subclavian
or even a carotid-carotid-subclavian bypass to avoid subclavian-
coronary steal syndrome56 (Fig 8).
Transesophageal echocardiography (TEE) is helpful in demonstrating
left ventricular function and valvular abnormalities. TEE is also useful for
evaluating the ascending and descending thoracic aortic diameter. There
are many advantages to TEE over other modalities that evaluate the
thoracic aorta, including the ability to perform it quickly and continuously
in the operating room to detect sudden changes in cardiac function during
repair.57 Unlike x-ray-dependent imaging, it has no nephrotoxicity and
can be used to assess ascending and descending thoracic aortic size, as
well as identify the dynamics of aortic dissections. However, availability
of the esophageal ultrasound probes and a skilled operator may limit its
use in the emergency setting.56
Pulmonary
Single-lung ventilation is necessary to repair the descending thoracic
aorta. This is the most important reason preoperative spirometry is
FIG 8. Carotid-carotid-subclavian artery bypass to treat a type I TAAA involving the origin of the left
subclavian artery. Three-dimensional CTA reconstruction of a hybrid repair of a complicated
Crawford type I TAAA beginning at the left subclavian artery. This was treated with a right-to-left
retropharyngeal carotid-carotid artery bypass (CCB), as well as a right-to-left carotid subclavian artery
bypass (CSB) jump graft. The upper left and right panels demonstrate the preoperative appearance
of the TAAA and brachiocephalic arteries. The origins of the left carotid and the left subclavian were
occluded proximally via 2 endovascular plugs, as well as thoracic aortic endograft exclusion. (Color
version of figure is available online.)
necessary, to predict the patient’s ability to tolerate it. Patients with

COPD are at special risk of postoperative complications and death, and
patients with TAAA often carry this diagnosis. A patient with a forced
expiratory volume less than 1.4 L/s will likely be unable to be placed on
single-lung ventilation and have a poor outcome during their recovery.
Other useful predictors of postoperative respiratory failure include the
following: (1) a forced expiratory flow 25% less than 2 L/s; (2) PaO2 less
than 55 mm Hg at rest; and (3) PaCO2 greater than 45 mm Hg.58,59
Patients with these parameters should not be considered for open TAAA
repair and are even high risk for endovascular repair.
Renal
Second only to an emergent indication for TAAA repair, postoperative
renal failure is consistently the most important risk factor for 30-day
mortality by increasing the risk of death by a factor of 3 or more.4,60 The
risk of death after open TAAA repair that is associated with preoperative
renal failure is even greater than having a history of previous CABG,
whose odds ratio is less than 2.55 Developing new-onset renal failure, or
requiring renal replacement therapy after elective TAAA repair, is not
only a strong predictor of death, it is also an ominous marker for increased
length of stay, poor functional outcome after discharge, and elevated
hospital expense.2,61,62 There is a linear relation with the development of
postoperative renal failure after open TAAA repair to both preoperative
creatinine and age.63 Huynh and colleagues found that calculating the
patient’s preoperative glomerular filtration rate using the Cockcroft-Gault
equation was a more sensitive method to predict mortality when com-
pared with serum creatinine alone.61
A specific renal concern associated with endovascular repair is contrast-
induced nephropathy (CIN) from the use of iodinated contrast. Although
the incidence of CIN after TAAA has not been evaluated in published
reports of endovascular TAAA repair, CIN has been linked elsewhere to
increased length of stay, costs, number of cardiovascular events, and
mortalities ranging from more than 20% if temporary renal failure
develops to 80% if dialysis is required.64,65 Adequate measures to prevent
this complication should be attempted before an endovascular TAAA
repair, which often requires large amounts of iodinated contrast. Some of
these adjuncts include the following: avoidance of serial contrast loads
over short periods (from computerized tomography [CT] scans or
coronary angiography), ensuring the patient is well hydrated,66,67 avoid-
ing concomitant drugs that are nephrotoxic, or the use of nonnephrotoxic
contrast agents during aneurysm repair, such as carbon dioxide,68 when
imaging is obtained below the diaphragm. The need for intravenous
contrast dye and radiation for CTA requires that elective TAAA repairs
be delayed for a few days after iodinated contrast is administered. This
should minimize the cumulative injury to the kidney from the TAAA
surgery and recent exposure to contrast dye. Intravenous hydration with
0.9% saline solution and oral N-acetylcysteine (1200 to 2400 mg per day
for 2 days) are commonly used as innocuous strategies to limit CIN that
are sometimes combined with bicarbonate solutions in high-risk pa-
tients,66,69 although the etiology of CIN and therefore a good prevention
continue to be elusive.67,70 In summary, many risks associated with
preoperative renal failure are so great as to require surgeons to reconsider
the indications and treatment strategies before treating TAAAs in patients
who have preexisting renal dysfunction.
Imaging
The precise evaluation of the anatomy of TAAAs is mandatory to
determine the indications and approaches necessary for repair. Careful
evaluation of the location of the origin and end of the aneurysm, the
diameters, and the branches involved in the aneurysm must be determined
before any operation. Historically, conventional angiograms of the aorta
were a routine part of the preoperative evaluation of TAAA patients, but
currently this is reserved for special cases or obtained during endovas-
cular repair. Angiography has been used to identify the artery of
Adamkiewicz, or the great radicular artery, to ensure this branch was
included in the revascularization of the intercostal/lumbar branches.71
Mapping for the great radicular artery has mostly been abandoned
because preoperative evaluation of this artery has not had a significant
impact on postoperative neurologic complications of either open or
endovascular TAAA repair.
Spiral CTA with 3-dimensional (3D) reconstructions has now become
the principal imaging modality for rapidly evaluating the aorta in patients
with TAAAs and has a good correlation to the findings at the time of
operation.72 The additional benefits of CTA over angiography are that it
provides information on the diameter of the entire aorta and its relation-
ship to the surrounding organs, all of which may change the surgical
approach. It has also been noted that as many as 47% of CTAs discover
incidental findings that were previously unrecognized and unrelated to the
indication of the scan.73
Magnetic resonance angiography (MRA) can image the aorta using
gadolinium, which avoids iodinated intravenous contrast (used in CTA),
and therefore, theoretically has a lower risk of secondary renal dysfunc-
tion. However, this potential benefit over CTA is overshadowed by recent
concerns over the use of gadolinium in patients with preexisting renal
failure (common in patients with TAAA), which has rendered MRA74
overall a less attractive imaging modality than CTA. Another potential
benefit of magnetic resonance imaging is that it does not use radiation and
has also been used to evaluate the spinal cord circulation before TAAA
repair.75 These advantages of MRA over CTA are considered outweighed
by the facts that MRA takes longer to complete, is associated with
claustrophobia, and is more costly. Other advantages of CTA over
magnetic resonance imaging include that it is generally widely
available and does not have any contraindications in patients with
metallic implants.
Preoperative Considerations for Endovascular and

Hybrid Treatment of TAAAs
Anatomical evaluation and advanced planning are critical to the success
of purely endovascular and hybrid debranching procedures. Meticulous
preoperative planning must be done with high-resolution 3D CTA not
only to evaluate the proximal and distal aortic landing sites for the
endografts but also to consider the diameter, calcification, thrombus, and
angulations of the access vessels (both femoral and iliac arteries) to avoid
unnecessary complications.
Depending on the diameter of the endograft and the manufacturer, there
is a minimal vessel diameter ranging from 7 to 9 mm to introduce the
deployment device into the aorta. Complications associated with a
mismatch between the access vessels and the graft include inability to
advance the endograft, arterial rupture, dissection of the iliofemoral
arteries, prolonged occlusion of bypass grafts due to difficulties advanc-
ing the endograft, or embolization of mural thrombus while maneuvering
the endograft within the aorta. In cases where any of this is a concern,
creation of a conduit to deliver the graft without disrupting the flow to the
visceral bypasses will minimize these complications.
When the proximal aortic landing site is near the brachiocephalic
vessels, then care must be taken to evaluate if there is enough normal
thoracic aorta to land a graft (most manufacturers recommend more than
25 mm). If not, a preemptive bypass to the left subclavian, left carotid, or
even the right innominate artery may be needed first (Fig 8). There is
some controversy in the literature about the need and timing of when to
revascularize the left subclavian artery, or if it can just be covered without
consequence. Most would agree that bypasses are required in cases of a
dominant left vertebral artery, patent left internal mammary bypass graft,
carotid artery occlusions, extensive coverage of the aorta, patent dialysis
fistula in the left arm, or if there is thrombus near the left subclavian artery
that may embolize. In concert with the Society for Vascular Surgery
Practice Guidelines,76 we routinely revascularize the left subclavian
artery except in urgent cases since not doing so may increase the risk of
left arm claudication, vertebrobasilar ischemia, and possibly stroke and
spinal cord injury (SCI), albeit with a low risk of phrenic nerve injury.77
Regardless, failure to consider the anatomy and risk factors in these
patients may result in a preventable stroke or occlusion of critical vessel.
Complications Common to Open and Endovascular
TAAA Repair
There are multiple complications associated with a thoracoabdominal
incision that are related to an extensive, open surgical approach such as
those relating to the prolonged operative times, length of stay, and the
generally older patients that undergo these procedures. Although these
include wound-related complications and infectious complications,
among others, they are most overshadowed (and underreported) by other
complications that have been shown to predict their overall outcome. To
follow are the major complications that are common to both open and
endovascular repair of TAAA.
Renal Failure
It has been found that aortic cross-clamp times above the viscera as
brief as 40 minutes are associated with an increased incidence of
pulmonary (59%), renal (47%), hepatic (35%), and multi-organ dysfunc-
tion. In addition to the obvious increase in morbidity and mortality, these
complications significantly increase hospital and intensive care costs
above the expected cost of the surgery (an additional $US 31,000 to $US
88,000).78
The true incidence of renal failure after TAAA repair is hard to
determine since most authors define it differently. Due to so many
differing criteria, the reported risk of renal dysfunction ranges from 4% to
40%; however, all published series report a higher risk of mortality in
patients who develop renal dysfunction of any type.79 The risk factors and
effects of any postoperative renal dysfunction have been studied repeat-
edly during the evolution of TAAA surgery (Table 4). In the early stages
of open TAAA repair, when the surgical technique of TAAA repair only
included clamp-and-sew, the risk of needing dialysis was 14%. In 1
report, the development of renal impairment (defined by an elevation in
creatinine by 1 mg/dL per day for 2 days after surgery) after TAAA repair
increased the risk of death by an odds ratio of at least 6.7 (95% confidence
interval [CI] 3.2-14.2, P ⬍ 0.0001) and up to one half of patients who
require dialysis will die.80 Interestingly, 80% to 90% of the patients with
renal dysfunction after surgery who survive their hospitalization will
regain their preoperative creatinine within 1 month.80
For these reasons, much effort has been placed into understanding and
avoiding renal failure during TAAA repair, since the pathophysiology is
likely multifactorial and elusive. Although much emphasis has been
placed on the ischemic period during the aortic cross-clamp time, it is
TABLE 4. Notable studies of the effects of renal failure and outcomes following open TAAA repair
Number of Risk factor evaluated for
patients development of renal failure Finding
80
Safi et al 234 Postoperative creatinine Increased the risk of death—odds
elevation ⬎1 mg/dL ratio ⬎6.7
Huynh et 1106 Preoperative creatinine and Any preoperative renal dysfunction
al61 GFR led to increased risk of death—
odds ratio 3.2 but a low GFR
was more sensitive and
prognostic
Miller et 299 SSEP changes during cross- Odds ratio of 1.9 for renal failure
al82 clamp
Miller et 167 Use of nonocclusive femoral May benefit patients with
al83 cannula for bypass pump preoperative GFR ⬍60 mL/min/
1.73 m2 and elevated
postoperative myoglobin
predicts need for dialysis
Huynh et 540 Postoperative creatinine The most important predictor of
al2 ⬎2.9 LOS
SSEP, somato-sensory evoked potentials; GFR, glomerular filtration rate; LOS, length of stay.
often troublesome to find renal dysfunction appear despite short renal

ischemic times during repair of suprarenal AAAs and TAAAs. It is well
documented that acute ischemia-reperfusion via clamping the aorta above
the mesenteric and renal arteries results in an abrupt release of cytokines,
such as interleukin 1a, interleukin 6, interleukin 8, and tumor necrosis
factor ␣.59,81 However, these mediators are commonly elevated in a
myriad of disease processes that are not specific to TAAA repair or renal
failure so their significance after TAAA repair has yet to be determined.
Looking for a new etiology for renal failure after TAAA repair, Miller
and colleagues explored the role of lower extremity ischemia during open
in TAAA repair. They made the observation that the ischemic period to
the lower extremities is longer (since this clamp is the last to come off)
than for the kidneys themselves. From this, his group evaluated if renal
failure after TAAA was a result of underappreciated rhabdomyolysis,
which in turn explains postoperative renal failure in patients who had
brief ischemia to the kidney itself.82 This theory was tested using a
retrospective evaluation of 299 patients who had previous TAAAs. They
then looked at the previously recorded somatosensory evoked potential
(SSEP) that changed in the lower extremities during TAAA repair. These
recordings were used as surrogate markers for lower extremity ischemia,
and then they were compared with the development of renal dysfunction.
The authors found reversible changes in the SSEP in 36% of all the
patients included. Although poor preoperative renal function was the
greatest risk factor for postoperative renal failure, changes in SSEP during
TAAA repair was associated with a nearly 2-fold increased risk of renal
failure. The authors further explored this theory using a special femoral
artery cannula (for access to the perfusion pump) that had an orifice that
allowed some perfusion to the limb during its use, rather than nearly
occlude it. Subsequently, they compared 167 patients who received this
new perfusion cannula to 921 historic controls that were treated with the
standard cannula. They found no overall difference in mortality nor renal
failure, except in patients whose preoperative glomerular filtration rate
was less than 60 mL/min/1.73 m2. The authors also mentioned that the
risk of a higher creatinine level, or postoperative renal failure, in these
patients was reduced by 15% to 20%.83 This same group also prospec-
tively collected serum samples and tested them for myoglobin after
undergoing TAAA repair in another 109 patients. They found that the
only statistically significant predictor of postoperative need for dialysis
was found in patients with elevated serum myoglobin concentrations
(excluding the cases where myoglobin was the criteria for dialysis). There
was also a higher mortality in the patients who had an elevated myoglobin
(knowing that postoperative dialysis is a known risk factor for death after
TAAA repair). Patients with serum myoglobin levels greater than 1000
ng/mL 3 days after surgery had the highest risk of needing dialysis after
open repair. However, even as the authors attempted to identify muscle
ischemia as the culprit for renal failure after aortic cross-clamping, they
did not find a linear correlation between the absolute serum myoglobin
concentrations in 37% of the patients who recovered renal function before
discharge.84
At present, the etiology of renal failure after open TAAA repair remains
unclear, although the notion that simple renal ischemia alone is not the
cause is appealing and supported by not only the theory of rhabdomyol-
ysis mentioned above, but also by the findings of superiority with
crystalloid perfusion over blood. This multifactorial problem will con-
tinue to be the focus of surgeons who perform aortic surgery, due to the
high risks associated with renal failure.
Spinal Cord Injury
Surgeons are often daunted by the threat of having a patient undergo a
technically successful TAAA repair, only to have their patient emerge
from anesthesia paralyzed or present several months later with neurologic
impairment. The etiology of SCI after TAAA repair is believed to be due
to the combination of spinal hypoperfusion and an elevation of the
intrathecal pressure. Although this concept was first described 4 decades
ago, this complication still remains very difficult to overcome. This is
particularly true in extensive type II TAAAs where it is most commonly
reported. Poor spinal perfusion can occur at different intervals during
TAAA repair, including during perioperative hypotension, during aortic
cross-clamping, or secondary to permanent hypoperfusion after ligation
(open repair) or covering (endovascular stent grafting) of the origin
of intercostal and lumbar arteries critical for spinal perfusion.85 It has
also been directly linked to the length of time the aorta is clamped,
with neurologic injury appearing as early as 30 minutes after aortic
occlusion.86
Historically, it was suggested that paralysis after thoracic aortic surgery
was due to the occlusion of the largest intercostal-lumbar vessel described
by Adamkiewicz (also known as the great radicular artery). This “single”
vessel commonly arises from the aorta at the T8 to L2 levels and was
thought to be indispensable for spinal perfusion. Routine preoperative
angiograms of the intercostal/lumbar arteries71 or intraoperative hydro-
gen-saturated saline solution marker injections87 were used due to the
observational dogma that not revascularizing, or sparing this artery during
aneurysm repair, resulted in a greater than 50% incidence of spinal cord
complications.88 Since then, it has been shown that other factors are more
important in protecting from SCI89 and that neurologic injury occurs even
if the predicted artery is spared during repair.
Multiple authors report paraplegia rates of 2% to 8% following open
repair of TAAAs, but national averages are close to a sobering
12%.46,47,60,90 Purely endovascular repair of TAA has a lower incidence of
perioperative SCI, ranging from 6% to 12% of patients, most of which were
performed in patients considered “high risk” for surgery due to other medical
comorbidities.91-93 Although SCI is usually diagnosed within the first
postoperative day, up to 11% to 30% of affected patients can present in a
delayed fashion.94 In addition, multiple case reports also describe this phenom-
enon following endovascular TAAA repair.
Injury to the spinal cord after TAAA repair is directly linked to the
extent of the aorta that is involved in the TAAA according to the
Crawford classification of TAAAs. SCI is most common depending on
the number of patent spinal vessels available in the remaining aorta,
regardless of open or endovascular repair. SCI can also be much more
common after open TAAA repair when compared with the open repair of
isolated TAA (Table 5). The same is true when comparing the outcomes
of SCI in endovascular repair of a TAA versus TAAA (Table 6). Overall,
repair of Crawford type II TAAAs has the highest risk of SCI, regardless
of the technique used to repair it (open or totally endovascular).
TABLE 5. Odds ratio of developing spinal cord ischemia (SCI) syndrome after open repair of
thoracoabdominal aortic aneurysms (TAAAs) when compared with open repair of an isolated TAA
according to the Crawford classification, or history of previous aortic surgery of the distal aorta
Odds ratio of SCI after open repair of
a TAAAS when compared with open
Crawford type of TAAA repair of an isolated TAA
Type I 27
Type II 39
Type III 14
Type IV 1.8
Prior distal aortic surgery 1.8
Adapted with permission from Greenberg et al.95
TABLE 6. Odds ratio of developing spinal cord ischemia (SCI) syndrome after totally endovascular
repair of thoracoabdominal aortic aneurysms (TAAAs) when compared with endovascular repair of
an isolated TAA according to Crawford classification, or history of previous aortic surgery of the distal
aorta
Odds ratio of SCI after endovascular repair
of TAAAs when compared with endovascular
TAAAs repair of an isolated TAA
Type I 20
Type II 14
Type III 2.6
Type IV 2.6
Prior distal aortic surgery 3
Adapted with permission from Greenberg et al.95
Specifically, when compared with the risk of SCI after open repair of an
isolated thoracic aortic aneurysm, the odds ratio of SCI is 27 (95% CI
3-242) in open type I TAAA repair and 39 (95% CI 5-317) in open type
II TAAA repair. Even with a completely endovascular repair, type I and
type II have a drastically higher risk of SCI (type I TAAAs more than type
II TAAAs) when compared with the endovascular repair of an isolated
TAA (OR 20 with 95% CI 2-181 for type I TAAAs and OR 14 with 95%
CI 1.1-189 for a type II). The relative odds ratio of SCI after open repair
of a type III TAAA is almost one half of that of open repair of a type I
TAAA. The risk of SCI after totally endovascular repair of both type III
or IV TAAA are over one seventh the risk of the repair of a type I TAAA
when each is compared with the endovascular repair of a TAA. Mean-
while, the odds ratios of SCI in type IV TAAAs are less than 3 in both
open and endovascular repair when compared with the same type of repair of
TAAs.95 This exemplifies that TAAA repair has a many fold higher risk of
paralysis when compared with AAAS or isolated TAA repair.
However, spinal cord ischemia alone does not explain the superior
results that follow endovascular repair (where all involved lumbar
branches are unavoidably covered) with regards to neurologic injury.
A secondary etiology may be spinal cord reperfusion injury, where
ischemia alone is not the cause of neurologic injury, but rather
following reperfusion injury and the secondary spinal canal edema,
which may result in SCI and compression, respectively. The latter is
the basis for the use of spinal drainage as an adjunct to avoid SCI.
Several techniques have been advocated to attempt and protect the
spinal cord from edema, maximize spinal perfusion pressure, and thus
minimize spinal cord compartment syndrome.96 These adjuncts in-
clude elevation of systemic blood pressure,85 cerebrospinal fluid
(CSF) drainage, systemic hypothermia, spinal fluid cooling,97 and
administration of medications that decrease inflammation.98 It has
been suggested that spinal drainage may decrease spinal injury by
removal of the inflammatory mediators that aggravate it.
Of note, there are a few etiologies of SCI that are specific to endovascular
repair. The advancement of wires and catheters in a diseased aorta, in
addition to the expansion of the grafts within a thrombus-laden aneurysm,
may lead to embolization of debris into intercostal/lumbar vessels.99 This is
consistent with the findings of follow-up CT scans that reveal embolic
infarctions in the mesenteric, splenic, and/or renal infarctions after
deployment of thoracic and abdominal endografts in more than 9% of
cases—most of which are subclinical,100 but periprocedural embolization
to a critical vessel, such as the superior mesenteric artery (SMA), may
lead to the patient’s demise.101 Another characteristic seen after endograft
repair of the aorta is delayed neurologic events, sometimes months after
discharge.92 In these cases it may be that patent intercostal/lumbar
arteries that cause type II endoleaks spontaneously become throm-
bosed and there is abrupt cessation of blood flow into those vessels.102
Care must also be taken when covering the left subclavian artery
during proximal thoracic aortic endograft placement, since this may
decrease flow into the subclavian, vertebral, and internal mammary
arteries. This may lead to clinically important ischemia of the patient’s
left arm, brain (stroke or vertigo), or heart if a coronary bypass
originates from the internal mammary arteries. These patients likely
benefit from subclavian revascularization before endovascular TAAA
repair.77
Although the incidence of SCI is generally considered lower in
endovascular repair of TAAs compared with TAAAs, the extent of the
aneurysm (or the total amount of aorta covered) is still the most important
risk factor in developing SCI, regardless of the technique used to treat it.
Therefore, repair of Crawford type II TAAA has the highest rate of SCI
using either treatment modality.95
Pulmonary
COPD is common in patients with TAAA. In addition, pulmonary
complications are also commonly seen after open TAAA repair. This
complication is often not included in the reports of many case series or is
limited by referring to a respiratory complication, such as the incidence of
tracheostomy (implying prolonged ventilator dependence). Often not
included in the literature are other forms of respiratory complications,
such as patients who arrive on room air, but require oxygen upon
discharge, or those that develop new-onset shortness of breath on exertion
postoperatively.
One study that specifically evaluated risk factors for developing
postoperative pulmonary complications (prolonged ventilation and need
for tracheostomy) after TAAA repair found that the need for open TAAA
repair, preoperative renal failure, and TAAA rupture were all significant
risk factors.42 Sixty patients (27%) experienced respiratory complications
with prolonged postoperative ventilation (longer than 48 hours); 24
required tracheostomy (11%).
There is no known strategy that will obviate complications to the lungs
other than avoiding incisions that may lead to pain-induced respiratory
dysfunction, and eliminating general anesthesia. These 2 are the greatest
theoretical benefits to totally endovascular repair of TAAA since endo-
vascular repair can potentially be done with local/regional anesthesia and
only femoral and brachial artery incisions. Hybrid repair offers no need
for a thoracotomy, although a laparotomy is necessary so its benefit in
minimizing pulmonary complications is unclear. In reality, although the
use of endovascular tools for TAAA repair seems beneficial, there are
only small series available for review with limited data on pulmonary
complications. Whether or not pulmonary complications can be prevented
using endovascular techniques remains to be seen as these approaches are
used more.
Stroke
Although stroke may occur in open TAAA repair, it is an especially
ominous complication after endovascular procedures that involve the
thoracic aorta. Intravascular wires and large devices coming in contact
with mobile thrombus in the arch and brachiocephalic vessels and sudden
conformational changes in the arch that liberate loose mural thrombus are
suspected to be the most common etiology of stroke after endovascular
TAA and TAAA repair. Iatrogenic dissection of the carotid or
vertebral arteries, or even retrograde aortic dissections secondary to
iatrogenic trauma during stenting,103 are well-described, devastating
complications. Another potential etiology of stroke after endovascular
repair occurs when patients have their left subclavian artery covered
by a thoracic endograft. Stroke may occur because the brain depended
on cerebral perfusion originating from the left vertebral artery and is
reasoning for first performing a left carotid to left subclavian artery
bypass before deploying a thoracic endograft over the left subclavian
artery. The EUROSTAR database was used to evaluate the risk factors
for neurologic complications after deploying more than 600 thoracic
endovascular stent grafts in Europe. Investigators found that the 2
greatest risk factors associated with postoperative stroke were cases
lasting more than 2 hours and 40 minutes and female gender.
However, the most significant risk factor associated with having either
a stroke or a SCI was not performing a carotid subclavian bypass
before covering it with a thoracic endograft.104 A subsequent meta-
analysis of the literature confirmed that carotid subclavian bypass
before thoracic aortic stent grafting has not clearly demonstrated a
protective effect against developing stroke, although they may protect
patients from developing SCI.105
Adjuncts to TAAA Repair to Minimize

Complications
Prevention of Renal Dysfunction
Other than minimizing renal ischemia times by making the time the
aortic clamps placed above the renal arteries as short as possible, directly
perfusing the renal arteries with various solutions was studied over the
last 2 decades. In 1997, the Massachusetts General Hospital group
reported their outcomes in 143 open TAAA repairs using cold renal
perfusion alone as an adjunct to clamp-and-sew technique (without partial
left heart bypass or distal aortic perfusion) for renal protection. They
found they could prolong supraceliac clamp times before the appearance
of renal failure to 100 minutes, although 24% of the patients who did
develop acute renal failure (creatinine greater than 3 mg/dL or double the
baseline result) required dialysis. Interestingly, the odds ratio of renal
failure leading to mortality was greater than 9 (95% CI, 2.6-33; P ⬍
0.005).106
The theoretical potential that blood would be better to protect the kidney
during TAAA repair rather than crystalloid solutions remained. Coselli’s
group evaluated in a small randomized trial if warm blood perfusion was
superior to cold saline solution to prevent renal failure after Crawford
type II TAAAs with left heart bypass. In 30 patients, they evaluated
which group had an increase greater than 50% of the baseline serum
creatinine. Cold saline was superior to warm blood (21% in cold saline vs
63% in blood, P ⫽ 0.03) to prevent renal dysfunction, and cold saline was
actually protective (OR: 0.133).107 A follow-up randomized controlled
trial (86 patients in each arm) comparing cold renal perfusion versus cold
blood at 4°C by LeMaire and colleagues for the treatment of TAAAs with
left heart bypass revealed no difference in renal failure (31% in the blood
group vs 24% in the normal saline group had a rise ⬎50% of baseline),
nor mortality (8% in blood vs 6% in the saline groups) nor paralysis (6%
in the blood vs 0% in the saline groups).108 The authors concluded that
cold saline perfusion is sufficient to protect from renal failure during open
repair with TAAAs when compared with blood at any temperature. This
finding was echoed by Safi’s group, who retrospectively evaluated 359
patients undergoing TAAA repair that developed renal failure. All had
distal aortic perfusion and approximately one half of them had warm
blood (46%) versus 4°C cold (54%) blood perfusion via 9 to 12 F
cannulae placed into the renal (and visceral) arteries during cross-
clamping. They suggested that although there was no difference in the
incidence of renal failure, the patients who developed renal failure and
received cold blood renal perfusion had a significantly better survival
(21% mortality) versus the 46% mortality in those who received warm
blood.79
Finally, to determine if the effects on mortality and renal function were
due to the blood or the cold perfusate alone, Lemaire and colleagues
compared 172 patients with Crawford type II or III TAAAs and randomly
assigned patients to either 4°C blood versus lactated Ringer’s solution.
They found no difference in mortality (8% in the blood group vs 6% in
the lactated Ringer’s solution group) nor in significant renal failure (3%
each) and concluded that cold crystalloid perfusion is equivalent to cold
blood for the prevention of renal failure in TAAA repair.108
The definition of renal dysfunction is a moving target in the literature,
and the precise etiology of renal failure during open TAAA repair is still
unclear and likely multifactorial. For the moment, it seems to be that
continuous perfusion into the renal arteries during open TAAA repair
with cold crystalloid solutions seem to be sufficient to lower the risk of
renal dysfunction significantly.
Prevention of Spinal Cord Injury
Reattachment and Perfusion of Intercostal-Lumbar Arteries. SCI can
occur because of direct ischemia of the spinal cord during aortic
cross-clamping and ligation of the intercostal and lumbar arteries. The
spinal cord ischemia theory is the basis for implementing revasculariza-
tion of intercostal segments of the aorta and using cardiopulmonary
bypass oxygenation pumps to maintain perfusion distal to the immediate
area of the repair. During endovascular repair of the thoracic aorta,
covering more than 40 cm of thoracic aorta is an independent risk factor
for neurologic events, as is blood loss greater than 1000 mL.109
Furthermore, in support of the spinal ischemia hypothesis is that patients
who have had previous AAA repair followed by repair of a thoracic aortic
aneurysm have a relative risk greater than 11 (95% CI 3.8-32.3, P value
⬍ 0.0001), whereas it is almost 3 (95% CI 1.26-6.65, P value ⫽ 0.008)
if a TAAA is repaired after previous AAA repair.110 This is likely
secondary to an acutely greater total reduction in the aortic blood flow to
the spinal cord.
The first open TAAA repairs were performed by creating a side-to-side
aortoaortic bypass before placing the aortic cross-clamp in an effort to
minimize ischemia distal to the clamps.111 In the “clamp and sew”
technique popularized by Crawford, ischemia below the level of the
proximal aortic clamp is maintained until selective revascularization of
the intercostal and lumbar arteries (via posterior graft fenestrations) are
accomplished without any other adjunct; speed was critical to minimize
complications. Brief clamp times were also employed as the primary
technique for thoracic aortic surgery by other surgeons. Verdant and
colleagues reported the outcomes of 366 consecutive cases of open repair
of isolated, descending TAA using passive shunting alone with a 9-mm
Gott shunt. They reported no SCI and a 0.2% incidence of permanent
renal failure. These remarkable results in morbidity were unexpectedly
coupled with a more sobering 12% 30-day mortality, even though most of
the patients had less than one third of the descending aorta involved (10%
mortality when excluding emergent repairs of TAA). His success may
have been aided not only by the passive Gott shunt and the relatively
small amount of aorta covered, but also that his average cross-clamp time
was only 30 minutes.112
The dilemma is how to localize the necessary aortic and intercostal
segments without needless prolongation of aortic clamp time. Williams
and colleagues reported on the modern utility of preoperative angiogra-
phy to identify the great radicular artery. They had a low success rate
(43%) in finding the great radicular artery of Adamkiewicz. More
importantly, even when it was identified, it did not dramatically lower the
incidence of SCI (4.6%) when compared with other series.113
Monitoring SSEP during clamping of the aorta in TAAA repair has
been reported to assist in identifying the aortic segments that may be
important to maintain neural integrity. While predicting spinal injury,
revascularization alone of the suspected segments detected by SSEP did
not affect the incidence of postoperative neurologic injury.114,115 Safi and
colleagues found that in most cases, simply reimplanting the thoracic
intercostal arteries T11 and T12, as well as T9 and T10 if they are patent,
will lower the risk of late neurologic deficit.116
Decreasing Spinal Compartment Pressure. CSF drainage alone has
been suggested to minimize neurologic impairment after TAAA repair.
The data to support this are limited mostly by retrospective analysis from
single institutions. A Cochrane review in 2004117 demonstrated only 2
small trials that randomly compared spinal drainage alone to not draining
and the findings are conflicting. One report showed a paraplegia or
paraparesis rate of 12.2% (9 of 74 patients) without drainage versus 2.7%
(2 of 82 patients) with drainage.118 The other trial had a remarkably high
incidence of SCI in both groups (30% in CSF drainage vs 33% in
controls) albeit a small trial that only included 31 patients.
Crawford evaluated the effect of different spinal CSF pressures in a
prospective, randomized series of patients undergoing repair of Crawford
type I and II TAAA repairs. Twenty patients were maintained with a CSF
pressure under 10 mm H2O; 20 patients were kept at less than 15 mm
H2O, and 6 more were kept at greater than 15 mm H2O. Their outcomes
were compared with 52 control patients who did not have CSF drainage.
After evaluation of risk factors for paraplegia, neither reimplantation of
lumbar/intercostal arteries, use of atriofemoral bypass, nor CSF drainage
statistically influenced the outcome. The only statistically significant
factor contributing to neurologic injury was postoperative hypotension
(P ⫽ 0.006).119 This disparate finding may be due to the small numbers
of patients in each group compared with the large number of variables
that were evaluated simultaneously.
Adjuncts used to prevent SCI have also attempted to reverse delayed-
onset neurologic symptoms. Multiple case reports describe the use of
steroids, emergent CSF drainage,120,121 and elevation of systemic blood
pressure (to increase spinal perfusion pressure)91 have been reported to be
used alone or in combination to reverse acute paraplegia.89,92 Despite
these measures, open type II TAAA repair continues to be associated with
the highest risk of neurologic injury.122
Complications associated with drainage catheter placement, drainage of
CSF, as well as the removal of the intrathecal catheter, are not insignif-
icant. CSF drainage requires a 14-gauge needle be placed in the
intrathecal space. Reported serious complications of CSF drainage
include subdural or epidural hematoma at the puncture site and intracra-
nial subdural hematoma,123 which can be fatal.124 Intracranial bleeding is
thought to occur from excess negative pressure caused by CSF removal,
leading to tears of the delicate arachnoid plexus, either during active
drainage or unintentional leaks from the puncture site after removal of the
catheter. Bloody CSF may appear in approximately 5% of patients with
drains for TAAA repair, and one half of these may show blood on CT
scan of the brain without having a clinically detectable neurologic injury.
The incidence of neurologic deficits or subdural hematomas after CSF
drains for open TAAA management are 1% to 3.5% with a global
mortality of 0.6%, but the mortality associated with subdural bleeding
after CSF drain placement is 40% to 50%.125-127 To avoid this, care
should be taken when placing or proceeding with operation if bloody fluid
is obtained during drain placement before TAAA repair.128
Spinal Cord Cooling. Direct spinal cord cooling was evaluated by
Cambria and colleagues as another adjunct to the clamp-and-sew tech-
nique for lowering the incidence of spinal complications in open TAAA
repair. In a total of 70 patients, normal saline was cooled to 4°C and
infused into an epidural catheter placed at T11 to T12. In addition, they
simultaneously place an intrathecal catheter at L3 to L4 to monitor CSF
temperature and pressure, draining the spinal fluid as needed. All
operations (except 1 atriofemoral bypass) were performed with the classic
clamp-and-sew technique. The authors reported a very significant im-
provement in the incidence of neurologic defects (2.9% vs 23% in historic
controls, P ⫽ 0.0001).23 They subsequently reported a follow-up study in
2003 that included 337 patients. When compared with historic controls,
they documented that CSF cooling reduced the incidence of SCI to 10.6%
(19 of 180) versus 19.8% (18 of 91) in the historic controls.94 However,
this method is technically challenging since it can be difficult to
continuously infuse enough cooled fluid into the intrathecal space to reach
a goal temperature while still maintaining a low intrathecal pressure. This
often results in having to increase the systemic pressure to maintain a
stable spinal perfusion pressure. Results from the Mayo Clinic that
included 300 patients undergoing open TAA and TAAA repair revealed
no difference in spinal protection with CSF cooling in type I-II TAAAs
(11.6% without cooling vs 8.9%).129
Combination Therapies. Combining adjuncts to avoid SCI may be the
key to improving neurologic outcomes, although the data available are
mostly limited to single-institution series. Safi and colleagues compared
the outcomes of SCI before and after implementation of CSF drainage
with distal bypass while performing permissive hypothermia. They found
the incidence of neurologic deficit was 9 of 247 (3.6%) versus 33 of 493
patients (6.7%) in those who did and did not receive both modalities,
respectively.86 One of the lowest SCI rates using multiple adjuncts is
reported by Coselli and colleagues. This group retrospectively compared
their results after adding CSF drainage to their previous surgical protocol.
The latter was a combination of permissive hypothermia, left heart
bypass, and reattachment of patent “critical intercostal arteries.” In 145
risk-matched patients that were undergoing open repair of Crawford type
I and II TAAAs they obtained a 13.0% incidence of paraplegia or
paraparesis in the control group versus 2.6% (P ⫽ 0.03) in those who also
had CSF drainage. This resulted in a relative risk reduction of 80% with
CSF drainage.118 Thus, it would seem that although the cause of SCI is
multifactorial, the prevention (or reversal) can be obtained via a thought-
ful combination of avoiding intraoperative hypotension and keeping a low
metabolic consumption (corporal or spinal cooling) and elevated perfu-
sion pressures (low intrathecal pressure and mean arterial pressure greater
than 90 mm Hg).130
Currently, most high-volume aortic centers place a lumbar CSF drain in
elective, descending thoracic aneurysm repairs, particularly if they
involve an extensive length of the aorta,131 even in endovascular
repairs.132 Our protocol for open or hybrid endovascular repair includes
placement of the lumbar drain in lumbar spaces 3-4 or 4-5. The drain is
maintained less than 10 mm Hg during operation and ideally left in for
approximately 3 days with a range of 1 to 6. The pressure limit may be
lowered to 5 mm Hg by draining at a maximal rate of 15 mL/h if the
patient develops neurologic impairment. In these symptomatic patients,
concomitant measures are undertaken to maintain a mean arterial pressure
greater than 90 mm Hg and optimal oxygen delivery. The drain is then left
in for up to 7 days, but usually removed after 2 to 3 days of additional
treatment.91,126 The use of spinal cooling and evoked neural stimulators
is still institution-specific and we do not use these techniques. In cases of
open repair of TAAA, most centers (including ours) also advocate the use
of an extracorporeal pump if an extensive amount of aorta is being
replaced, visceral branches need reimplantation, dissections are repaired,
or there are other characteristics that make the case high risk for neural
ischemia.131
The Role of Hypothermic Circulatory Arrest
The use of hypothermic circulatory arrest (HCA) during open TAAA
repair has been advocated by some to lower the mortality and paraplegia
rates. In a series of 173 consecutive patients with aneurysms in the
thoracic aorta that included 110 TAAAs (64% of patients), HCA was used
during the aortic and visceral anastomosis. Both the operative mortality
and the stroke rates were 4%, and only 2.4% of the patients suffered
paraplegia.133 Renal failure that required renal replacement therapy
occurred in only 1%. The experience reported by the Mayo Clinic with 31
consecutive patients managed with HCA for TAAA repair resulted in no
paraplegia and a 3% rate of both stroke and long-term dialysis depen-
dence, albeit a higher mortality (6%) in this small series.134 Coselli and
colleagues retrospectively evaluated 111 patients undergoing HCA (only
9 of which were elective) and, while the minimal paraplegia rate (1%)
mirrored the findings of the above reports, they had a much higher overall
mortality (29%) and incidence of renal failure (15%).135 A series reported
by Cheng and colleagues included 63 consecutive patients with Crawford
type II TAAA that were repaired using both HCA and T6 to T12
intercostal arteries reconstruction. With a reported 100% follow-up, the
30-day mortality was 8%, temporary paraplegia was seen in 2 patients
(3%), and paraparesis was found in 1. One-, 2-, and 3-year survival rates
were 92%, 88%, and 86%, respectively, even with a 25% pulmonary
complication rate.136
HCA is therefore a reasonable technique for TAAA repair, espe-
cially when there is an inability to clamp the aorta. Although it offers
good spinal cord and renal protection, it is associated with increases in
other morbidities, such as respiratory failure and systemic coagulopa-
thy requiring reoperation. Another group of patients that may partic-
ularly benefit from HCA may be those undergoing reoperative TAA or
TAAA surgeries. In 1 series of 60 consecutive patients undergoing
repeat aortic intervention via thoracotomy, HCA offered a lower
complication rate than those treated with other surgical techniques
(clamp-and-sew, partial cardiopulmonary bypass, and partial left heart
bypass).137
In endovascular treatment of the thoracic aorta, little is written specif-
ically about the complication of SCI since it is very uncommon. However,
in both a large series of thoracic aortic endografts and a meta-analysis,
revascularizing the left subclavian artery before covering it lowers the
risk of SCI.104,105 Additional studies have suggested that women have a
higher (2 to 3 times) rate of SCI than men.
Open Repair of TAAAs
History. The 1950s were the beginning of the era for successful open
repair of aneurysms of the thoracic aorta. The first reported uses of an
aortic homograft to replace the thoracic aorta were by Swan and
colleagues in 1950138 and by Lam and Aram in 1951.139 Two years later,
DeBakey and Cooley used the first synthetic graft as a conduit to treat a
TAA.140 The first successful repair of a thoracic aortic aneurysm
involving a single visceral artery was reported 2 years later by Etheredge
and colleagues.141 DeBakey’s group again followed with the first tech-
nically successful repair of 4 TAAAs that involved the mesenteric, celiac,
and renal arteries using homografts.111 Their 23-page article meticulously
describes how they obtained a 50% mortality (from pulmonary edema and
upper gastrointestinal bleeding) with the routine use of aortoaortic shunts,
complete aneurysm excision, and permissive hypothermia (to 32°C). The
following 30 to 40 years have documented the progress in the classifica-
tion40 and development of most of the surgical techniques used today for
the open TAAA repair. In this regard, Svensson and colleagues54 were at
the forefront and continue to report the largest and most successful series
of open repair of TAAA.
Current Results of Open Repair of TAAAs. The best results published
after open TAAA repairs have been dominated by single-center, or even
single-surgeon experiences (Table 7). The first large series of open TAAA
repair published was from Baylor College of Medicine by Dr Stanley
Crawford. It included 1509 patients accrued over 31 years and obtained
a 30-day survival of 92% and the incidence SCI was 16%. A postoper-
ative creatinine level greater than 3 mg/dL or dialysis occurred in 18% of
the patients, and one half of them required dialysis.54 At the time, the
only adjuncts used were rapid repairs with short clamp times.
Crawford only used a clamp-and-sew technique with reattachment of
intercostal-lumbar branches. The visceral anastomoses were mostly
performed using patch grafts and the average, total aortic cross-clamp
time was only 43 minutes.
Currently the largest reported series is from Coselli and colleagues,
which evaluated the results of more than 2000 open TAAA repairs
performed by the senior author over 20 years. They had a nearly
irreproducible 95% 30-day survival, with more than 1400 of the cases
Crawford type I and II TAAA. The incidences of renal failure requiring
renal replacement therapy or spinal cord ischemia were 5.6% and 3.8%,
respectively.90 Coselli’s group aggressively advocates for the routine use
of left heart bypass with selective cold visceral perfusion, permissive
TABLE 7. Outcomes following open TAAA repair
Number of 30 d Renal failure
open TAAAs survival (need for SCI (%) Other Adjuncts reported
treated (%) dialysis)
Baylor College 1509 92 18% (9%) 16 GI complications Clamp-and-sew

of in 7% technique with brief
Medicine54 clamp times
(average 43 min)
and reattachment of
intercostal-lumbar
branches (perfusion
pump was used in
one third)
Coselli et al90 2286 95 5.6% needed 3.80 Pulmonary Left heart bypass with
dialysis complications selective cold
in 32%, visceral perfusion,
stroke in permissive
1.4% hypothermia,
reimplantation of
intercostal-lumbar
arteries, and spinal
fluid drains.
Selective HCA
University of 355 93 2.1% 2.3 (1.3% after Stroke 2.1% Left heart bypass with
Texas47 adjuncts selective cold
were added) visceral perfusion,
permissive
hypothermia,
reimplantation of
intercostal-lumbar
arteries, and spinal
fluid drains.
Selective HCA.
clamp time average
(36 min)
Cleveland 372 TAAs 92 NR 7.5% with Compares open Adjuncts varied
Clinic95 (64 open open to according to
repairs endovascular surgeon.
TAAAs) repair extracorporeal
pump, spinal
drains, hypothermic
arrest, and
reimplantation of
intercostals were all
included
NA, not reported; HCA, hypothermic circulatory arrest; GI, gastrointestinal.
hypothermia, reimplantation of intercostal-lumbar arteries, and spinal

fluid drains. His group has also reported the selective use of deep
hypothermic arrest for cases in which the proximal aorta does not have a
suitable place for clamping (especially in aortic dissections and some
ruptures). In this subset, a more sobering 21% 30-day mortality, paraple-
gia in 1%, postoperative renal failure in 15%, and a 9% incidence of
stroke were reported.135
Other large, single-center series are those from the University of Texas,
led by Dr Safi. His group reported the outcomes of 355 thoracic
aneurysms and also had a low mortality (93% 30-day survival), SCI rate
of 1.3%, and a renal failure rate of 2.1%. Meanwhile, the Cleveland Clinic
compared their outcomes after open TAA repair to those from endovas-
cular repair in 372 patients (64 were TAAAs) undergoing open repair
versus 352 undergoing endovascular repair. The open group had a 92%
1-month survival versus 94% in the endovascular group (P ⫽ 0.2). There
was also a 7.5% incidence of SCI in the open group versus 4.3% in the
endovascular (no statistical difference).95
Operative Technique for Open TAAA Repair. Our patients are rou-
tinely admitted the night before open TAAA repair and receive oral
polyethelyne glycol as a bowel prep and overnight intravenous hydration
to minimize prerenal azotemia during the surgery. Patients are also kept
from iodinated contrast agents for at least 48 hours before open TAAA
surgery.
Peri-anesthetic monitoring of the patient is critical to maximize the
ability of the anesthesiologist to support the patient’s changes in physi-
ology during the case. Patients should have an arterial blood pressure
monitor placed in the radial artery (right radial artery if the left subclavian
artery is planned to be clamped) and have large-bore central venous
access. A pulmonary artery catheter and/or a transesophageal echocar-
diogram probe are also placed to evaluate the patient’s cardiac function
throughout the case. At least 2 other large-bore (12 to 14 gauge)
peripheral intravenous catheters are placed to ensure good vascular access
is available for rapid fluid administration. Central core temperature
monitors should be placed in at least 2 locations (bladder, esophageal, and
rectal are options). The patient is intubated with a double-lumen endo-
tracheal tube. This enables single-lung ventilation for easier access to the
left thoracic cavity. Preoperative adjuncts to avoid spinal injury are
applied (we prefer spinal drainage alone to less than 10 mm H2O) before
positioning or even before entering the operating room.
A graft is selected based on the preoperative imaging (CT angiography
or magnetic resonance imaging). When all 4 visceral branches need
revascularization, we prefer to use a prefabricated Vascutek Coselli
thoracoabdominal tetrafurcate branched Dacron graft (Terumo Cardio-
vascular Systems Corporation, Ann Arbor, MI), or in its place a tube graft
is selected for the aorta and 4 branches are sewn on while the anesthe-
siologist is preparing the patient. In a sterile field, the branches are
manually sewn into the tube graft near the center of the graft to allow
appropriate length for the proximal and distal aortic anastomosis.
Positioning the patient can be the most important aspect to the
procedure because if it is not done appropriately, the patient can suffer
extremity nerve injuries142 or rhabdomyolysis.143 The patient is placed on
a bean bag, positioned so that it will support the patient during lateral
decubitus positioning. The room is cooled to obtain permissive hypothermia
during the aortic exposure with a target core temperature at the time of aortic
clamping of 32 to 33°C. The patient position is with the shoulders at 60° and
the hips rotated back to 30°. All contact points are padded and additional tape
is used on the shoulders and legs to secure the patient to the table. The patient
is then prepped and draped exposing the left chest from the spine to the
right anterior axillary line and from the left shoulder to both mid thighs
with access to both groins.
If the repair includes the proximal thoracic aorta (Crawford type I and
II TAAAs), then a thoracotomy at the level of the fourth to sixth
intercostal space is made (or above/below this if the sixth rib is to be
partially removed to allow a wider thoracotomy). However, if the TAAA
is lower (Crawford type III or a high type IV), then the incision is made
between ribs 7 and 9. Finally, if the aneurysm is localized to the abdomen
(Crawford type IV), then an approach can be made via an incision at the
9th or 10th intercostal space.
Once the left lung is deflated and entrance into the chest is made, a
self-retaining retractor is positioned for stable access to the aorta. The
diaphragm is divided from the costal rim, leaving a generous (more than
2 cm) margin for closure with care to preserve the phrenic nerve. Entrance
into the abdominal cavity is made with medial rotation of the left colon
to enter the retroperitoneum. Ideally, the left kidney is mobilized
anteriorly with care to avoid injuring the ureter when reflecting it to the
right. Although we prefer a retroperitoneal approach, especially to avoid
the need for enterolysis in patients with previous abdominal operations, a
transperitoneal approach can be used. The latter allows direct inspection of the
revascularized organs. The aorta is dissected free circumferentially and the
visceral arteries are identified. Lumbar veins are divided to maximize access to
the aorta during the repair. The thoracic aorta is also freed from the visceral pleura
and care is taken to identify the origin of the left subclavian artery, the phrenic
nerve, and the recurrent laryngeal nerve to avoid inadvertent injury. Once
identified, the vagus nerve can be cut distal to the origin of the recurrent nerve
and thus allow it greater mobility should it need to be moved out of the way.
Another structure that should be identified to avoid or ligate, if necessary, is
the thoracic duct, located near the aortic hiatus.
To obtain distal perfusion during aortic cross-clamping, we have used
an atrial-femoral artery bypass system with Carmeda-coated tubing that
includes an oxygenator. The tubing allows us to decrease the amount of
systemic heparin needed before starting distal aortic perfusion. Distal
aortic perfusion is usually maintained by an arterial cannula placed
directly into the left common femoral artery or via a conduit sewn into the
common femoral or iliac artery if the distal vessels are too small. A
venous cannula is placed in the inferior or superior pulmonary vein, the
left common femoral vein, or the right internal jugular vein, depending on
the extent of the operation. The patient is heparinized to an activated
clotting time greater than 250. We administer mannitol 12.5 g and
furosemide 20 mg intravenously before interrupting flow to the visceral
and renal branches. Taking a moment to clarify the time to cross-clamp
the aorta with the anesthesiologist helps prevent sudden changes in blood
pressure during unexpected clamping and unclamping. If possible, we
place our first cross-clamps just far enough to do the proximal aortic
anastomosis while still allowing distal perfusion into the visceral vessels
through the bypass circuit, thus minimizing ischemia to the intestines,
kidneys, lower extremities, and spinal cord. The proximal anastomosis of
the graft is sewn on to the aorta with a monofilament suture in an
end-to-end fashion with felt reinforcement.
It is worthwhile to attempt to identify intercostal or lumbar arteries in
order to ligate or clip them before entering the aneurysm. This is
especially useful in aneurysms associated with dissections since many of
these vessels tend to be patent and can bleed very briskly. After this, the
aorta is clamped distally above the visceral vessels and the aneurysm is
opened with electrocautery. Briskly bleeding intercostal lumbar arteries
are identified and oversewn in the high thoracic aorta. The proximal aortic
anastomosis is always performed in an end-to-end fashion with fine
monofilament suture and felt reinforcement. We usually reimplant
branches in the T10 to L2 range. The graft is then placed over the island
of intercostal lumbar arteries that will require reimplantation and a
fenestration is made with a thermal cautery at the intended implantation
site and anastomosed. Once this is accomplished, the proximal anasto-
mosis is surrounded with thrombin and gel foam and the proximal clamp
is brought down to allow direct inflow to the intercostal lumbar arteries.
To avoid late anastomotic aneurysmal formation, we avoid the use of
Carrel patches for the anastomosis, unless the case is deemed unstable or
emergent. We minimize the amount of aortic wall used in the repair and
prefer a “pickoff” technique for visceral branch revascularization. This
entails performing serial clamping of individual branches followed by
anastomosis of the proximal aortic graft to the left renal artery, SMA, and
finally the celiac artery (while the bypass pump continues to perfuse via
the femoral artery). This maintains continuous perfusion except when the
individual vessel is being revascularized. The aortic clamp is then moved
further down toward the terminal aorta when it is time to perform the right
renal artery anastomosis and minimizes lower extremity and lumbar
artery perfusion. The remaining aorta is opened; the ostia of the right
renal artery is identified, and the anastomosis is performed end-to-end.
Before creating each renal anastomosis, we infuse a cold solution
composed of 1 L of normal saline with 2000 U heparin and 50 mg
mannitol. At this point, the patient is allowed to be rewarmed by raising
the room temperature and using forced-air blankets and fluid warmers.
Finally, the anastomosis of the graft to the distal aorta is completed. The
bypass cannulae are removed (with repair of the femoral vessels is
completed as needed) and the heparin is reversed with protamine to an
activated clotting time less than 150 seconds.56
Endovascular Repair of TAAAs
History of Endovascular Intervention on the Thoracic Aorta. Al-
though endovascular treatment of thoracic aortic dissections and aneu-
rysms has been experimentally feasible since the 1980s,144,145 clinical use
in humans in the United States and Western Europe took almost 2 more
decades to become a reality. Volodos and colleagues from the Ukraine
published the first successful stenting of a thoracic aortic aneurysm via
the femoral artery in 1988 and subsequently published a series that
included 22 cases of transfemoral stenting of the iliac arteries, as well as
the thoracic and abdominal aorta.146,147
Advances in stenting the thoracic aorta was delayed in part due to
concerns about placing endografts over the intercostal arteries that may
lead to paralysis without any way to “reperfuse” the spine. There was also
a limitation in the available advances in engineering to design a way to
deliver a covered graft large enough and long enough to be deployed in
the thoracic aorta via the femoral artery.148 The fear of iatrogenic spinal
cord ischemia led to elaborate graft technologies that included retrievable
thoracic endografts. These grafts would be deployed in the aorta to
produce “test ischemia” for 20 minutes while evoked spinal potentials
were measured. If the evoked spinal potentials were stable, then the
removable graft would be exchanged for a permanent one (none of the
16 patients had changes noted).149 Another early technique used by
some to avoid spinal cord ischemia was to inflate 2 occlusion balloons
within the thoracic aorta above and below the intended landing site
and evaluate the response to spinal evoked potentials. To our knowl-
edge, neither of these techniques are being employed and are of
historical interest only.
As TAAAs tend to encroach or involve critical brachiocephalic or
visceral branches, it is clear that simple tube-shaped endografts would not
be sufficient to exclude the aneurysm. A Japanese group led by Inoe and
colleagues implanted the first handmade branched endograft that ex-
tended into the left subclavian artery for a proximal descending aortic
dissection150 in 1996, and later made a graft that extended into the celiac
artery to treat an 8-cm pseudoaneurysm151 in 1997. This paved the way
for the first description of a multi-branched endograft designed by Chuter
and colleagues that treated a type III TAAA with endovascular branches
into the celiac, superior mesenteric, bilateral renal, and bilateral common
iliac arteries.152 Of note, on the second postoperative day, the latter
patient presented with irreversible paraplegia, thus confirming that
patients who undergo endovascular TAAA repair indeed suffer from SCI,
albeit without the trauma of an aortic cross-clamp.
Current Results of Totally Endovascular Repair of TAAAs. Unlike
patients with infrarenal AAAs and isolated TAA, there are no branched or
fenestrated endografts approved by the US Food and Drug Administration
for the treatment of TAAAs. Surgeons have been gradually attempting to
create an endovascular treatment for aortic aneurysms involving the
mesenteric vessels since the mid 1990s.153,154 Most of the data that have
been generated internationally are from a collection of small case
series with few long-term data. Europe and Australia have led the way
in obtaining commercially available, custom-made endografts with
side branches or fenestrations to treat complex TAAAs. These
endografts are created to allow canalization of the mesenteric and
renal artery branches and extend covered stents into the branches
arising from the aneurysms. Although more than 1000 fenestrated
devices have reportedly been implanted, most have been used to treat
complex AAAs rather than TAAAs.131
William A. Cook (Cook Zenith, Pty Ltd, Brisbane, Australia) is the only
manufacturer to make commercially available custom-made branched
endografts. These grafts are not available in the United States; however,
ongoing clinical trials are being performed to approve their use. In 2001,
a clinical trial led by Muhs and colleagues from the Netherlands began to
treat aneurysms involving the visceral vessels that had increased risk
factors for open repair with custom-made endografts made by Cook with
fenestrations and branches.101 By 2005, 38 patients had been enrolled,
with a reported a 30-day mortality of 2.6% (aneurysm-related was 0%), a
92% visceral graft patency rate at 46 months, and with no change in the
serum creatinine. A group from Australia also reported their experience
with the completely commercially made, custom-designed Cook en-
dografts specifically for TAAA repair in 2005. However, Anderson and
colleagues reported the outcomes from repairing 3 Crawford type III and
1 Crawford type IV TAAA that involved 13 branch vessels. They were
able to perfuse 12 of the 13. However, 1 patient died of hemorrhagic
shock due to bleeding from an extraanatomic graft anastomosis. Regard-
less, the remaining 3 patients fared well and had patent grafts at 12
months without incidence of spinal cord ischemia.155
These results led to enthusiasm for endovascular techniques in the
management of TAAAs. The first report of an American trial of Cook’s
branched endografts included 73 branched grafts. Crawford types I-IV
TAAAs were included (more than half managed using regional anesthesia
alone) and the results included a 93% technical success rate, a 2.7%
incidence of paraplegia, 1.4% new-onset dialysis, and a 6% mortality.156
A subsequent series of 245 branched endografts from the Netherlands
included 34 patients with TAAAs.157 Of these, follow-up data were
available in only 30 (8 Crawford type I, 5 type II, 12 type III, and 5 type
IV). Thirty-day mortality was 7% (1 died of a ruptured arch and the other
died after discharge from bleeding from gastrointestinal ulcers). One patient
required dialysis due to rupture of the renal artery during stent ballooning in
a patient with a single kidney (4%). Paraparesis or paraplegia was seen in
16.7% patients (2 of the 5 patients had previous aortic surgery). Survival at
6 months and 1 year were 89% and 76%, respectively.
To date, branched and fenestrated grafts are handmade for each
individual case and require over a month before they can be delivered and
implanted. Many patients with TAAAs present with acute symptoms and
waiting this long is not advisable. However, in order to have “off the
shelf” availability, grafts must have prefabricated fenestrations or
branches placed in technically accessible areas. An underappreciated
contribution to the endovascular therapy of TAAAs that originated from
the Cook trials was the retrospective analysis of the most common
anatomical distribution of the branch vessels of the aorta. Sweet and
colleagues compiled data from 66 patients treated with fenestrated stent
grafts. They determined that to make an “off the shelf” graft feasible for
mainstream use, several conditions were necessary to access and stent
into vessels from brachial and femoral artery approaches: (1) no more
than 4 aortic branches should be attempted; (2) the celiac artery and SMA
should be 6 to 10 mm in diameter; (3) renal arteries should be 4 to 8 mm
in diameter; (4) the distance between the main graft and the branch vessel
should be less than 5 cm; and (5) that the angle of deviation to the branch
from the aorta be less than 45 degrees. They concluded that 88% of the
patients fulfilled these criteria and thus would be feasible candidates for
an “off the shelf” TAAA stent graft.158
Current Results of Surgeon-Initiated Fenestrated Endografts and
Adjunctive Branch Stenting of TAAAs. Until industry-made branched
endografts are made widely available, several groups manually create
openings (fenestratations) into endovascular grafts to treat suprarenal
AAAs and TAAAs primarily in patients who are unfit for standard, open
repair. Oderich and colleagues published a series of “surgeon-modified”
endografts, obtaining a technical success rate of 98% (85 total fenestra-
tions) with a 3.3% mortality in their first 30 patients with high surgical
risk.159 They compared these results with a cohort of 16 hybrid open and
endovascular debranching procedures that had a significantly higher 19%
mortality, but similar patency of the target vessels at 1 year (97% and
98%, respectively). This report was accompanied by editorials written by
the lead investigators of commercially available branched endograft trials
in the USA dissuading the creation of ad-hoc fenestrations. The authors
highlight the need for off-the-shelf fenestrated endografts in the United
States for patients with TAAAs that involve the visceral vessels.
A step-by-step technique to create these fenestrated endografts has been
described in the literature.160 This off-label technique requires very
careful preoperative planning and 3D CT imaging to determine the size
and location of the aortic branches. Once the desired location of the
braches is established, the endograft is removed from its factory-placed
sheath in a sterile fashion and either elliptical scallops at the top of the
endografts or orifices are created in the graft itself with a thermal cautery.
To see the new foramen once the graft is placed inside the patient’s aorta,
the fenestrations are outlined with radio-opaque materials. We prefer to
modify a commercially manufactured Cook Zenith thoracic cuff since
they are relatively easy to remove and reinsert into the sheath. An
endovascular gold snare is cut off the parent device and subsequently
secured to the perimeter of the fenestrations with interrupted 6-0 Prolene
sutures. This allows the target orifices to be identified to then access them
with wires once in the aorta. Most groups attempt to precannulate the
visceral arteries before deployment of the graft to have clear access and
localization of the aortic orifice. However, sometimes it is necessary to
partially deploy the stent graft first and get access to the orifice later. The
commercially available fenestrated/branched endografts are sometimes
precannulated with wires or have large, easily accessed side branches so
the visceral branches can be localized before complete deployment of the
endograft. Thus, treatment of TAAAs using noncommercially available
grafts requires very careful planning, advanced endovascular catheter
skills, and optimal imaging capacity to see the target vessels. Once the
graft is deployed and the visceral vessels are accessed, covered stent
FIG 9. Snorkel graft technique for aortic aneurysm repair. “Snorkel graft” technique used to treat a
suprarenal abdominal aortic aneurysm that followed a previous open repair. (A) Wire access and
stenting is done in the right renal artery (Rt RA), left renal artery (Lt Ra), and SMA before the aortic graft
is deployed. The 2 renal artery wires were positioned from the arms, while the SMA wire was placed
via the femoral artery. (B) Axial and coronal CT cuts demonstrating “snorkel” covered stent grafts
placed into both renal arteries and the superior mesenteric artery. They run parallel to the aortic
endograft to exclude the aneurysm without excluding perfusion to the organs. The small panels depict
axial cuts of the 3 patent snorkel grafts and their trajectory from the aorta into the branches. The large,
center image is a coronal cut demonstrating the snorkel stent grafts and their relation to the aortic
endograft. (C) Final, 3-dimensional reconstruction of the repair showing all grafts patent. (Color
version of figure is available online.)
grafts are deployed into the vessels to extend out of the main body of the
aortic graft and into branch arteries. These are oversized to effectively
seal the endograft and avoid endoleaks.
Another alternative to manual creation of fenestrations is to primarily
place long, covered stents that run parallel to the unmodified aortic graft.
The covered stent grafts can be used to protect the brachiocephalic,161
visceral, or renal arteries involved in the aortic aneurysm, while the main
aortic stent is purposely deployed over their origin.162 This technique has
been referred to as “snorkel” grafts, “paragrafts,” and “chimney grafts”
for their long extensions alongside the aortic graft that eventually reach
the aorta itself.163 Although the branch grafts can be configured to obtain
flow in an antegrade or retrograde manner, most reports are for suprarenal
AAAs (Fig 9) or Crawford type I TAAA, such that there is normal aorta
near (within a few centimeters) to the intended snorkel site. However, an
extreme use of chimney stents was reported by Lachat and colleagues to
treat a patient with a ruptured Crawford type IV TAAA who was unfit for
open repair. They accessed all 4 visceral branches via 2 sheaths placed in
the left subclavian artery and 2 more in the left femoral artery, followed
by stenting of the ruptured TAAAs via the right femoral artery. The final
configuration of the 4 chimney grafts was with 2 grafts perfusing the
bowel via antegrade flow and the 2 renal arteries being perfused in a
retrograde fashion.164
Hybrid Repair of TAAAs
History. Over the last decade, surgeons that were unable to have access
to branched endografts for TAAA, or who wanted to treat visceral vessels
with open surgical techniques, but still wanted to avoid performing a
thoracotomy and single-lung ventilation developed a combination of open
and endovascular techniques to repair TAAAs. This is the so-called
“hybrid,” or “debranching” technique and each stage (open debranching
and endovascular stent placement) is usually spread out over time, except
in cases of ruptured TAAA.
In this approach, the viscera and kidneys involved in the aneurysm are
sequentially revascularized via an open approach. The aortic branches are
individually treated to avoid cross-clamping the aorta and theoretically
not only spare the heart from acute afterload increase, but also keep the
spinal cord, viscera, kidneys, and extremities from prolonged ischemia
times. This technique also avoids a thoracotomy and single-lung ventila-
tion. With the aorta “debranched,” an aortic endograft is deployed to
exclude the TAAA. Hybrid repair of TAAAs has been particularly of
interest in patients who are poor candidates for open repair, especially if
there is significant pulmonary disease. However, despite the purported
advantages over open TAAA repair, the results for this technique are
varied, and the morbidity is not insignificant.
Inflow for the visceral bypasses is usually obtained from the common
iliac arteries using bifurcated prosthetic grafts with additional side
branches sewn on manually, or using 1 or 2 bifurcated grafts originating
from the common iliac arteries (Fig 10). Once the visceral and renal
arteries have been selectively revascularized and detached from the aorta,
an endograft is deployed to exclude the aneurysm.
The first 2 reported successful cases of hybrid TAAA repair were in
2002 by Watanabe and colleagues who first “debranched” the visceral
vessels off of the aorta using a bifurcated graft sewn into the aorta. In
addition, a retrievable thoracic stent graft was temporarily deployed in the
thoracoabdominal aorta to test for spinal cord ischemia using spinal
evoked potentials. When this was tolerated, a permanent endograft was
deployed.165
Current Results of Hybrid Repair of TAAAs. We recently published
our results of aortic visceral debranching to treat 36 consecutive patients
with aneurysms involving the renal and visceral vessels.166 There was 1
Crawford type I TAAA, 10 Crawford type II, 12 Crawford type III, 10
FIG 10. Hybrid (debranching) technique for aortic aneurysm repair. Three-dimensional reconstruction
of a CTA performed in a patient with end-stage renal disease, and a Crawford type II TAAA treated
with a hybrid technique. Open revascularization of the celiac and superior mesenteric arteries was
done via a single bifurcated Dacron graft originating from the left external iliac artery (arrow),
followed by endovascular exclusion of the TAAA. Left panel: Left lateral view. Center: Anterior view.
Right panel: Magnified, left lateral oblique view of the origin of the bypass graft and perfusion to both
the SMA and the celiac artery. (Color version of figure is available online.)
Crawford type IV, and 3 pararenal AAAs. One hundred twenty-three

bypasses were completed with an average of 3 per patient. These included
62 renal artery bypasses, 32 SMA bypasses, and 29 celiac artery
anastomoses. Although the in-hospital mortality was 8.3% (3 deaths), at
an average of 6 months after the procedure, survival was 80%. Primary
graft patency rate was 93% at 8 months. Five patients required dialysis
(14%) and 3 patients suffered ischemic colitis. Importantly, although
temporary paraparesis occurred in 1 patient, no patient suffered paraple-
gia. These results were compared with the outcomes of 73 open TAAAs
(19 Crawford type I, 50 type II, and 33 type III) repairs performed in the
same period (100% follow-up). We found that both techniques had equal
long-term survival by Kaplan-Meier curve, but the early morbidity and
mortality was directly related to HCA, open repair, and urgent presenta-
tion. In summary, hybrid TAAA repair was found to have a lower
complication rate with equal long-term survival.167
Another hybrid approach to the treatment of TAAAs was introduced by
Lachat in 2008.168 He described that after obtaining a suitable conduit for
inflow, rather than clamping the visceral or renal vessels, the end vessels
could be accessed under direct vision with a wire during laparotomy.
After this, a covered stent was deployed through the inflow graft, into the
target vessel. He suggested that this minimizes ischemia to these organs
and minimizes the need for extensive exposure of the vessels. The
technique used Gore Viabahn (WL Gore and associates, Inc, Flagstaff,
AZ) grafts for the visceral anastomosis, and they coined the term
“Viabahn Open Revascularization Technique (VORTEC).” Once the
abdominal portion was completed, the aorta was excluded with an
appropriate endograft at a later date. In a follow-up report in 2009, his
group reported the results of VORTEC in the repair of 30 TAAAs and 28
pararenal AAAs in which they revascularized 113 vessels (98 renal
arteries).169 They included 3 Crawford type I, 5 Crawford type II, 9
Crawford type III, and 13 Crawford type IV TAAAs. The primary
patency rate was 98% in the TAAAs and 96% in the pararenal AAA
repairs. Thirty-day mortality was 9% and this increased to 26% during a
wide range of follow-up (1 to 51 months). No patient required hemodi-
alysis; however, 3 patients developed reversible, delayed-onset SCI, and
another 2 patients (3.4%) suffered permanent paralysis of 1 or both legs.
Kuratani and colleagues were the first to report the long-term results of
hybrid TAAA repair. In 86 cases, they had no patient with paraplegia, 2%
operative mortality, 2% renal failure, and 1% graft occlusion. Long-term
survival rates were 95%, 86%, 80%, and 67% at 2, 5, 8, and 10 years,
respectively, with only 2 aneurysm-related deaths. The freedom from
aortic events was 91%, 81%, 71%, and 71% at 2, 5, 8, and 10 years,
respectively.170
A recent report of hybrid debranching TAAA techniques, which had
poor short-term survival, was reported by a group in Italy. Their outcomes
in 31 TAAA hybrid repairs (three quarters done in a single stage)
included a perioperative mortality of 19% (all from single-stage opera-
tions), 3% permanent SCI, and no cases of permanent renal failure.171
An evaluation of hybrid debranching procedures performed urgently in
42 patients with primarily (76%) arch involvement who were not
candidates for open TAAA repair revealed similar global outcomes (5%
mortality at 1 month and 5% incidence of permanent SCI). However,
hybrid repair requiring arch and abdominal (in some cases) debranching
was more prone to other serious complications, such as respiratory failure
(31%), and stroke or transient ischemic attack (19%). Remarkably, the
authors were still able to discharge home 58% of these patients who
otherwise would not have a surgical option.172 This report seems to
highlight the benefits of avoiding thoracotomies and sternotomies, espe-
cially in these poor operative candidates.
Albeit with mostly short-term follow-up, and small patient samples,
hybrid aortic debranching of visceral and renal vessels for the treatment
of TAAAs is feasible. It has favorable outcomes when compared with
open TAAA repair in terms of 30-day mortality (overall it is reported to
be 7% to 9%, except for one publication that reported a 26% mortal-
ity that included 3 deaths associated with ruptured TAAAs171,173),
permanent renal failure (0% to 14% dialysis need), and a particularly low
risk of permanent SCI (most reporting an incidence less than
3%).166,168,173,174 Also encouraging is that primary graft patency is nearly
90% or more in all series. Recognizing that hybrid TAAA repair
techniques are usually reported in patients who are poor operative
candidates for open TAAA repair, the results of these 2 techniques are not
entirely comparable. The data suggest that the higher mortality rates seen
more often in single-stage debranching and stenting may be mitigated by
separating the laparotomy from the endovascular portion of the repair.
In conclusion, although published data on debranching TAAAs are still
limited to small case series,175,176 until a commercially available endo-
vascular graft is available for TAAA patients, most centers find this
technique associated with good graft patency, relatively low complication
rates, and similar long-term outcomes as open TAAA repair.
Surgical Techniques for Hybrid Repair of TAAA. In this section, we
describe the surgical considerations and techniques involved in vessel
debranching that will allow deployment of a tubular stent graft to treat a
TAAA. The specific details of endograft deployment itself will be omitted
since they vary depending on the individual companies and are fairly
uniform.
When a case requires a carotid-subclavian bypass, we generally create
it the day before placement of the endograft using a 7-mm to 8-mm
polytetrafluoroethylene (PTFE) graft and generally do not ligate the
proximal subclavian artery unless there is clear visualization of the
prevertebral subclavian artery. Leaving it patent allows later placement of
a wire into the left brachial artery during the TAAA endograft to
continuously and dynamically mark the location of the left subclavian
artery. We then occlude the proximal subclavian artery using an Am-
platzer vascular plug (AGA Medical Corporation, Plymouth, MN). When
the planned date for placement of the endograft is remote, we cannot
reach the prevertebral subclavian artery to ligate it and do not wish to risk
thrombosis of the bypass due to competitive flow, we will access the
subclavian artery at the intended site for the bypass with a short 6-Fr
sheath and deliver the Amplatzer plug in a retrograde fashion. After
creating the subclavian artery bypass, we monitor the patient overnight
for any neurologic events that may modify our plan for TAAA stenting
and allow us to distinguish between endograft-related neurologic events
and those associated with the endograft. In cases of emergent endovas-
cular therapy, we have also created the subclavian artery bypass after first
obtaining endovascular coverage of the ruptured aortic aneurysm.
Regarding the following surgical techniques involved with visceral
debranching, we will omit the description of the aortic exposure via
laparotomy. We generally perform hybrid TAAA repairs in 2 stages
separated by a few days or weeks to allow our patients to recover from the
laparotomy before placing the endografts. The exception is in the cases of
stable ruptured TAAAs or symptomatic TAAAs, in which we will
perform the visceral debranching portion and immediately follow with the
endovascular portion in the same day.
We expose the common iliac arteries intended for bypass just enough to
place a side-biting clamp or, in lieu of this, 2 angled or straight clamps.
We generally avoid circumferential exposure of the common iliac arteries
to avoid injuring the iliac veins, sympathetic plexus, and ureters. Once an
inflow for the bypasses has been found, we begin to expose the visceral
vessels by retracting the bowel to the right and enclosing it in a plastic
bowel bag to contain and minimize evaporative losses to it. The aorta is
exposed near the suspected origin of the target vessels using electrocau-
tery, sharp dissection, and manual mobilization of the aneurysm. The
renal arteries are identified and encircled with vessel loops. At least 2 cm
of all arteries are exposed to have sufficient room to clamp and occlude
the proximal end, as well as a cuff to sew the bypass on. The SMA is
manually found on the inferior wall of the root of the mesentery and
dissected free. Care is taken to obtain as proximal a site as possible to the
aorta to not have inadvertent type II endoleaks from an unrecognized
branch. Finally, the celiac artery origin is identified and controlled with a
vessel loop. The patient is heparinized to an ACT greater than 250
seconds and then the common iliac is clamped. After an arteriotomy is
made, we use a 5-mm hole punch to ensure a wide-open orifice is created
for the anastomosis. Ideally, we create a large anastomosis to each common
iliac artery using a bifurcated, ringed PTFE graft (usually a 14 ⫻ 7 mm to 18 ⫻
9 mm). The graft is flushed and clamped off with a soft-jaw clamp. We
then individually anastomose the visceral and renal branches such that the
left renal and the celiac arteries originate from the graft from the left iliac
artery, while the right renal artery and SMA bypasses originate from the
right iliac artery. We generally tunnel our celiac artery anastomosis
retro-pancreatic in a “lazy S” configuration. The size of our grafts is
determined by both the size of the inflow arteries (iliacs or aorta) as well
as the visceral or renal branches. If the size mismatch between branches
is significant, then we will use the largest ringed PTFE and sew a smaller
one in an end-to-side fashion to maximize flow to the viscera. Several
other configurations can exist, such as bypassing to the hepatic artery,
originating both grafts from one iliac or establishing inflow in an
antegrade fashion from the thoracic aorta for aneurysms that involve the
iliac arteries. At times, there is only 1 iliac artery available as an inflow
vessel due to aneurysms or severe occlusive disease. In these cases, some
authors use serial jump grafts from 1 iliac artery that are created by
sewing on more branches end-to-side. We usually prefer to perfuse the
SMA and celiac arteries via the bifurcated graft from the iliac artery,
and revascularizing the renal arteries via left splenorenal and/or right
hepaticorenal artery bypasses. This may minimize the risk of renal
artery ischemia from the thrombosis of a visceral bypass graft.
If we determine during the preoperative evaluation that the external iliac
arteries will be too small to allow entry of the stent deployment device,
then we create a conduit from the best common iliac artery. It is then
tunneled into the groin and an anastomosis is created into the common
femoral artery. This will allow us to later reexpose the graft and directly
access the common iliac artery (ideally with minimal interruption of
the inflow to the debranched inflow grafts) with the endograft. Some
surgeons tie off the conduit graft after anastomosing it to the iliac
artery and then tunnel it in the subcutaneous tissue of the flank. When
the endograft is to be placed, they cut down on the graft (avoiding the
groin altogether), declot the graft, and control the conduit and sheaths
with tourniquet vessel loops.
Numerous other modifications of conduit or arterial inflow sources can
be created using a variety of bifurcated grafts to allow visceral perfusion
and stent deployment to treat TAAAs using the abdominal aorta,
VORTEC, or even the ascending thoracic aorta for inflow.177,178
Late Complications Following Open and Endovascular TAAA Repair.
Although most articles discuss events up to 30 days after open procedures
(perioperative outcomes), long-term outcomes after TAAA repair are
important to consider. A statewide review of the long-term outcomes after
TAAA repair in California revealed that, although 30-day mortality after
elective TAAA repair was 19%, 1-year survival was significantly lower
(31%). The mortality was affected by the age of the patient; it doubled
from 18% in patients 50 to 59 years of age to 40% in those 80 to 89 years
old. In ruptured TAAA cases, the mortality also changed from 48% at 30
days to 62% at 1 year (also worse in older patients).179 However, when
Zierer and colleagues examined the late functional status and quality of
life (QOL) of asymptomatic patients undergoing open, elective repair of
the thoracic aorta, they found slightly different findings.43 One hundred
ten asymptomatic patients underwent elective thoracic aortic replacement
of either the ascending,29 isolated TAA,23 or TAAA.48 Functional status
and physical and psychological QOL were measured using the Medical
Outcome Study 36-Item Short Form Health Survey, and survival using a
Kaplan-Meier curve were evaluated. They found that only 31% of
patients undergoing open TAAA repair returned to normal activities at 3
months. At 1 year, this increased to 85%. The return to normal activity
was independent of age and type of procedure. At a mean of 35 months,
psychological QOL was no different among the surgical treatment groups,
but physical QOL was lowest after TAAA surgery (P ⬍ 0.02). Overall,
age did not affect the physical QOL, and older patients even had an
improved psychological QOL, whereas 20% of TAA patients reported
their current health status as poor (3 to 20 times more than the other
surgical repairs). Overall survival was 70% at 4 years, but was lowest and
statistically different in the patients who underwent open TAAA repair
(53%) compared with either ascending (77%) or isolated TAA (91%).
Thus, although age alone did not affect the QOL after TAAA repair, those
that survive open TAAA repair fare worse than other types of aortic
surgery, which is a stimulus to improve the procedure.
Addressing QOL issues between open aortic repair and endovascular
repair of the thoracic aorta, Dick and colleagues performed a post-hoc
analysis of a prospectively collected consecutive series of 136 patients
who underwent surgical management of the descending thoracic aorta
over 4 years. They evaluated perioperative and late mortality rates and the
long-term QOL using the Short Form Health Survey and the Hospital
Anxiety and Depression Score questionnaires. There was no difference in
mortality rates (9% for open vs 8% for endovascular repair). Cumulative
long-term mortality rates were not statistically significantly different.
Overall QOL was also not significantly different among TAAA repair
types. Finally, anxiety and depression scores were not higher after open
TAAA repair. Thus, both endovascular and open aortic repair provide
comparable long-term results in terms of QOL in the treatment of thoracic
aortic disease.180
Outcomes Related to Operative Volume
Several complex surgical procedures, including pancreatoduodenec-
tomy, esophagectomy, coronary bypass, and abdominal aortic aneurysm
repair, have been shown to have better outcomes when performed at
high-volume centers.181 At first, it would seem obvious that outcomes for
open TAAA repair would also be predicted by the surgical volume of the
center. Certain authors have shown very low complication rates in both
elective and emergent open TAAA repairs. The cases range from
hundreds to thousands and have mortality and paraplegia rates of 5% to
9% and 2% to 8%, respectively.46,47,60,90 However, when evaluating a
nationwide database, or smaller published series, the mortality rate for
open TAAA repair is drastically higher (20% to 35%).1,4,182
In general, patients with ruptured TAAAs still have a dismal outcome.
Overall 30-day mortality rates in the USA after open surgical manage-
ment of ruptured TAAAs (rTAAA) are greater than 50%, with one half of
those dying within 24 hours and more than one quarter suffering acute
renal failure. In a report using the nationwide inpatient sample database,
these outcomes were not affected by hospital volume of TAAA or AAA
repairs, and globally echoed the results from most case series that report
a greater than 40% mortality.183-185 This notwithstanding, an outlying
27% mortality has been reported in at least 1 small, modern series of 40
rTAAA,10 which is only comparable to Crawford’s report in 1991 (24%
30-day mortality in open repair of rAAA).9 Therefore, improved out-
comes in rTAAA surgery may not completely be explained by readily
available surrogate measures related to volume or the organization of the
institution where the repair is done (as used by the Leap Frog initiative). In
TAAA outcomes, it may be more important to consider the specific surgical
teams performing the procedure and whether the repair is done in a training
program or not, since both of these consistently demonstrate better out-
comes.186,187 Presently, there are no data published on the outcomes of
centers using endovascular or hybrid techniques for TAAA repair related to
surgical volume. This is due to the small number of cases to date, and the
overall lack of widespread application of this technology. This technique is
also too young to have accrued significant long-term outcomes data.
Future Perspective
Currently, TAAA repair is still associated with high morbidity and
mortality, with a very wide range of outcomes reported by surgical
groups. Although the simplest answer may be to refer all patients to
high-volume TAAA surgeons, there are only a handful of people in the
world who can claim a lifetime experience of even 100 open or
completely endovascular TAAA repairs. Because of this wide inequality
in operative experience, the outcomes in open TAAA repair are widely
disparate. A completely endovascular repair is mostly unavailable in the
United States since there are no US Food and Drug Administration-
approved endovascular options available to treat TAAAs that involve the
visceral and renal branches. Reports from Europe, Australia, and a few
specialized centers in the USA are demonstrating the feasibility of
endovascular approaches to TAAA repair with better outcomes than open
repair (when compared with the national average). However, many
regulatory obstacles remain. These custom-made grafts take a long time
to fabricate, prolonged exposure to radiation to place them, and their
longevity is still unknown, so true comparisons to open repair are not yet
available. Over time, it is likely that the extensive endovascular gymnas-
tics currently required to treat a TAAA via a completely endovascular
technique will be overcome, as they have been for endovascular AAA
repair.188 Until this happens, we must realistically curb our enthusiasm
for purely endovascular TAAA treatment until both long-term data and
off-the-shelf grafts are available.
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Management of Thoracoabdominal

Curr Probl Surg 2011;48:70-133.

70 Curr Probl Surg, February 2011

Crawford type I TAAA involves most of the descending thoracic aorta

chronic obstructive pulmonary disease (COPD), and atherosclerotic

each).21 The Yale University Thoracic Aneurysm Database also revealed

Risk Factors for TAAA Rupture and Death

Initial reports from the 1970s by Pressler and McNamara documented

Preoperative Evaluation of All TAAA Repairs

necessary, to predict the patient’s ability to tolerate it. Patients with

Preoperative Considerations for Endovascular and

often troublesome to find renal dysfunction appear despite short renal

Adjuncts to TAAA Repair to Minimize

Baylor College 1509 92 18% (9%) 16 GI complications Clamp-and-sew

NA, not reported; HCA, hypothermic circulatory arrest; GI, gastrointestinal.

hypothermia, reimplantation of intercostal-lumbar arteries, and spinal

Crawford type IV, and 3 pararenal AAAs. One hundred twenty-three

Curr Probl Surg, February 2011 133

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