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21 Endovascular Repair oftheThoracic Aorta
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helpful in navigating wire positioning and ensuring appropriate stent placement in the aorta [66].
Intraoperative Anticoagulation
A concern in blunt thoracic aortic injury or cases of rupture
is the timing, if any, for anticoagulation. In routine TEVAR,
systemic anticoagulation with heparin is standard once the
CFA is successfully accessed either percutaneously or via
surgical exposure. Anticoagulation is important to prevent
lower extremity thrombosis given the large caliber delivery
systems required. Additionally, full anticoagulation minimizes the incidence of thromboembolic events with wire and
catheter manipulation across the aortic arch.
It is not uncommon for patients presenting with BAI to
have multiple injuries including closed-head injuries. Full
systemic anticoagulation in these cases can lead to devastating hemorrhagic complications. In these settings, discussion
with other consulting services, particularly neurosurgery, is
critical for best patient outcome. Generally, when anticoagulation may still be used, a lower dose may be considered.
Some centers have reported successful outcomes of TEVAR
for BAI without the use of systemic heparinization [67].
Deployment
Once access is obtained, aortography is performed in the left
anterior oblique projection. This allows for identication of
the aortic branch vessels and landmarks for appropriate
endograft deployment. Additionally, it can serve as a check
to conrm the estimated length of endograft needed.
Each endograft has specic directions for accurate
deployment. These should be reviewed carefully prior to any
procedure. There are, however, a few general “pearls” for
successful endograft deployment. In patients where more
than one endograft will need to be used, deployment of the
smaller diameter graft should precede the larger graft. This
will decrease the risk of subsequent type III endoleak.
Temporary reduction of the mean arterial pressure during
deployment can reduce the windsock effect. This is particularly important for endografts such as the Medtronic Valiant,
where the graft opens one stent at a time from proximal to
distal. Maintaining forward pressure on the graft and avoiding excessively slow deployment can also assist with target
landing.
Completion angiogram is performed to assess placement
of the endograft and evaluate for endoleaks. Type I or type III
endoleaks should be addressed during the initial procedure
with additional ballooning or extension with an additional
endograft. Type II endoleaks usually result from ow from
the intercostal arteries and can often be managed conservatively with monitoring on follow-up imaging. Type IV
endoleaks usually resolve once the procedural anticoagulation has been reversed.
Postprocedure
Immediately postprocedure, patients are sent to the ICU for
close monitoring of their hemodynamics and neurologic status. Most patients can be transferred to the oor within
2–3 days of the procedure and discharged home within a
week.
Immediate postprocedure imaging is generally not needed
unless there is a technical concern during the procedure.
Scheduled follow-up imaging is recommended at 1month,
6 months, and annually with CTA.Ideally, the CT should
have a noncontrast, arterial, and delayed phase to appropriately assess for endoleak.
Clinical Outcome
Randomized comparison of TEVAR versus open surgical
repair of the thoracic aorta has never been done. While a
large body of literature exists on both procedures, the patients
treated with TEVAR are often higher risk than those undergoing surgery, making direct comparison difcult [36, 68].
TEVAR has excellent technical success rate, quoted up to
98% [36]. Early experience with TEVAR in high-surgicalrisk individuals reported 30-day mortality of 9–12% [69,
70]. More recent data report 30-day mortality signicantly
lower at 2% [24]. Mid-term outcomes demonstrate an advantage for TEVAR in aneurysm-related survival with a reported
95% at 1year versus 89% for open repair [24].
Conclusion
TEVAR has become the preferred approach to thoracic aortic
pathology in patients with appropriate anatomy. Careful preprocedural planning including appropriate diagnostic imaging, proper device sizing, appropriate access planning, and
evaluation for appropriate landing zones is key to a technically successful procedure. Patient management with preprocedural consideration of potential complications
including spinal cord ischemia and stroke and early recognition of these complications are key to the best patient outcomes. Endografts continue to improve, expanding the
patient population eligible for this treatment modality.
338
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A. H. Fairchild and R. A. Hieb
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Aortocaval Fistula
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KristineClodfelterOrion andJamesH.Black III
22
Introduction
Aortocaval stulas are a life-threatening and difcult problem to address surgically. Description of the rst major
abdominal AVF was reported by Syme in 1831. Although
aortocaval stulas are rarely encountered during the career
of a vascular surgeon, there are several viable management
strategies. While the most common etiology may be attributed to penetrating trauma or iatrogenic injury, this chapter
will focus on the aortocaval stulas in the setting of aortic
aneurysmal disease.
Epidemiology
Aortocaval stulas occur in <1% of all abdominal or iliac
aneurysms. However, among ruptured abdominal aortic
aneurysms, aortocaval stulas are appreciated at a higher
incidence of 2–7%. To gender, they are more common in
men with an average age of 65years.
Historically, the mortality of this disease ranged from
16% to 66% [1, 2]. The higher estimates may have been
driven by operative intervention and postsurgical cares
because until the turn of the last century, most aortocaval
stulas were repaired with open surgery and limited appreciation of the cardiac effects. Improved outcomes of both
open and endovascular techniques will be reviewed.
Anatomy
An aortocaval stula is an unnatural connection between the
aorta and, most often, the infrarenal vena cava. Fistulization
can also occur between the aorta and the iliac veins, the iliac
veins and iliac arteries, and most uncommonly the aorta and
renal veins (Fig.22.1). This phenomenon is a result of spontaneous erosion of an expanding arterial aneurysm into the
neighboring venous structures. The slow necrosis of the aortic wall involves adventitial inammation and resultant
adherence to adjacent veins. Calcication of the arterial wall
may not be protective from stula development.
Physiology
Multiple studies have evaluated arteriovenous stula physiology [3, 4] demonstrating a relationship between ow and
size of the stula.
If the cross-sectional area of the stula is less than 1.5
times the diameter of the artery, ow in the proximal artery
increases vefold, and the direction of arterial ow distal to
the stula is maintained. As the area of the connection
approaches three times that of the artery diameter, the proximal arterial ow can increase by a factor of 8, whereas the
distal arterial ow can be diminished or reversed. In the setting of an aortocaval stula, compensatory increases in cardiac output are required to maintain blood pressure.
K. C. Orion
Department of Surgery, Yale University, New Haven, CT, USA
Division of Vascular Diseases and Surgery, The Ohio State
University, Columbus, OH, USA
J. H. Black III (
Vascular Surgery and Endovascular Therapy, Johns Hopkins
Hospital, Baltimore, MD, USA
© Springer Nature Switzerland AG 2019
R. S. Dieter et al. (eds.), Diseases of the Aorta, https://doi.org/10.1007/978-3-030-11322-3_22
*)
Pathophysiology
Physiological changes to the body are many, and understanding them is essential to prompt diagnosis and selection of
therapy. The initial effect of a central AVF is the decrease in
peripheral vascular resistance and a marked increase in cardiac output. Increased cardiac output is both a result of
increased venous return and an attempt to maintain peripheral perfusion via uid retention by the kidneys; signicant
341
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a
b
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K. C. Orion and J. H. Black III
Aortocaval
fistula
Aorto-iliac
fistula
c
Aorto-renal
fistula
Fig. 22.1 (a) Aortocaval stula, (b) aortoiliac stula, (c) aortorenal stula
22 Aortocaval Fistula
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weight gain and peripheral edema may be mistaken for diastolic heart failure. The net effect of increased cardiac output
is accompanied by signicant increases in total blood volume as the venous system pressurizes and venous dilation
produce a large increase in capacitance. As the right heart
develops high-output failure, pulmonary hypertension may
also develop. In end-stage right heart failure from an AVF,
rapid decrease in the stula ow from occlusion may not be
tolerated without hemodynamic collapse.
Diminished renal function has been described and thought
to be related to both impaired plasma ow and renal venous
hypertension [5, 6]. Finally, there is increased risk of pulmonary embolism, both from the deep venous system and
atheromatous mural thrombus routinely residing within the
aortic aneurysm.
Patient Presentation
Unfortunately, because of the elusiveness of the disease,
there is frequently a signicant delay in diagnosis. However,
because of the mass introduction of computed tomography
imaging for abdominal pain, surgeons can now make a preoperative diagnosis more commonly.
Patients may present in acute fashion or with a chronically
evolving picture over time. An acute rupture of an abdominal
aortic aneurysm typically causes unrelenting abdominal or
back pain. Hemorrhagic shock may or may not be present. If
the patient ruptures into the vena cava causing an aortocaval
stula, the classic symptoms and physical exam have been
described: pulsatile abdominal mass, abdominal machine-like
bruit, femoral thrill, lower body or leg edema, and heart failure. Only a minority of patients will present with a full spectrum of symptoms; however, most will demonstrate at least
one. Variable presentation can occur in the chronic patient
with high-output cardiac failure accompanied by increased
jugular pressure, dyspnea, pulmonary edema, and a widened
pulse pressure. Long-standing venous hypertension can cause
varicose veins, hematuria, and even rectal bleeding.
Workup
Timely diagnosis and surgery before the onset of shock markedly increases survival. Traditionally, abdominal ultrasound
is useful to diagnosis of both abdominal aortic aneurysm and
can readily demonstrate an aortocaval stula. Computed
tomographic angiography (CTA) is now the primary imaging
modality because of the availability and ease, and threedimensional imaging may allow the practitioner to diagnose
the location and diameter size of the AVF (Fig.22.2). Timing
of contrast can limit the diagnosis of smaller stulas on CTA
as reux of contrast proximally and distally into the vein lim-
343
Fig. 22.2 Aortocaval stula on CTA. (From Orion etal. [7]. Reprinted
with permission from Elsevier)
its exact visualization. Magnetic resonance imaging (MRI)
provides detailed views and may give a sense of the amount
of local inammation, which can be helpful when planning an
open repair, especially if infection is thought to be present.
Invasive angiography, albeit a historical gold standard, is
rarely needed to demonstrate the presence an aortocaval stula given CT and MRI omnipresence.
Preoperative Care
Because of the risk of high-output cardiac failure, aortocaval
stulas should be repaired. Fastidious preoperative evaluation of cardiac function by echocardiography is vital. Unless
there is prohibitive coronary artery disease, patients should
be evaluated by a surgeon for operative repair. In many
instances, correction of the AVF may normalize the preload
and afterload imbalance of high-output failure; thus, there is
little role for coronary intervention. Angiotensin-converting
enzyme inhibitors and diuretics should be used to manage
volume overload and improve cardiac contractility.
Surgical andEndovascular Care
The largest contemporary review of aortocaval stulas evaluated both open and endovascular repairs, their outcomes, and
complications [7].
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K. C. Orion and J. H. Black III
Open Repair
In 1955, Dr. Cooley performed the rst reported successful
open repair of an aortocaval stula. Forty years later, Dr.
Wholey described the technique of aortic exclusion when he
unexpectedly diagnosed an aortocaval stula intraoperatively.
Patients are under general anesthesia and require invasive
arterial blood pressure monitoring as well as adequate central
venous access. Most recommend an intraoperative transesophageal echocardiogram and a pulmonary catheter intraoperatively (Fig.22.3). These greatly assist the anesthesia team to
monitor cardiac output as well as physiologic changes that
occur upon closure of the stula. The availability of an autotransfusion device, or cell-saver, is also critical for these cases.
The transperitoneal approach works best as this allows
access to the vena cava; however, a thoracoabdominal incision is the safest approach if a supraceliac aortocaval stula
is suspected or extensive juxtarenal/pararenal AAA. More
commonly, a generous midline incision is made in the traditional fashion for infrarenal abdominal aortic aneurysm
repair. The aorta is exposed by placing the transverse colon
cephalad and all small intestines to the patient’s right upper
quadrant. The ligament of Treitz is divided and left renal vein
mobilized as needed. Proximal and distal control of the aorta
and iliacs is compulsory; however, circumferential control
and clamping of the cava should not be attempted as there is
signicant risk for injury of the very hypertrophied lumbar
and renal veins. There is a palpable thrill in the cava which
facilitates external assessment of the stula location and can
Fig. 22.3 Intraoperative transesophageal echo showing markedly
dilated right atrium. (From Orion etal. [7]. Reprinted with permission
from Elsevier)
be manually compressed at the time of opening the aneurysm
for control. After systemic heparinization, the aorta is
clamped and the aneurysm opened. Evacuation of mural
thrombus should be undertaken carefully as embolism,
including both debris and air, can occur. If the aortocaval
stula was not preoperatively diagnosed, massive dark
venous blood will be issued forth, and the location of the
aortocaval stula is promptly apparent. Manual compression
with sponge sticks or nger is performed to stop the venous
bleeding. The stula is then repaired primarily from within
the aneurysm sac with pledgeted mattresses of polypropylene suture (Fig.22.4). Given the degeneration of the aortic
wall and the IVC wall, no attempt should be made to surgically separate the two structures from the stula site as the
tissues will be too fragile to work with independently. It is
infrequent that the vena cava needs a patch angioplasty even
in large stulas. In such cases, balloon control proximally or
distally into the stula can isolate the area needed for patch
angioplasty. The abdominal aortic aneurysm is then replaced
with a tube or bifurcated Dacron graft.
Aortoiliac, iliac-iliac, or iliocaval stulas are challenging
because of close adherence among the vessels at the aortic
bifurcation. Again, circumferential control may come at a
fatal bleeding risk. These may do well with endovascular
venous control (see section “Hybrid Approach”). In difcult
cases, ligation of the aorta with extra-anatomical bypass is an
option of last resort.
Open Repair: Outcomes
Although long-term patency rates for patients surviving surgery are excellent, postoperative complications are many.
Renal failure, respiratory failure, bowel obstruction, acalculous cholecystitis, pseudomembranous colitis, wound infection, paralysis, and lower extremity ischemia are typical and
are seen in frail patients whose preoperative heart failure is
signicant.
Historically, high rates of mortality were reported for
open repair. There were many reasons for this, including
massive and unexpected exsanguination upon opening the
aortic aneurysm if preoperative diagnosis was not achieved.
If there is a delay in diagnosis, the 30-day mortality markedly increases. Second, the concern for how to handle the
overloaded right ventricle and pulmonary hypertension was
far less manageable postoperatively. Today, critical care has
vastly improved, and the issues of heart failure and resuscitation are commonly confronted issues in a surgical intensive
care unit.
Thankfully, the pathophysiologic changes are quickly
reversed upon closure of the arteriovenous stula. In most
patients, central venous pressure, pulmonary artery pressure,
stroke volume, and cardiac output all decrease immediately.
Given the low SVR of the periphery to facilitate perfusion
distal to the AVF, many patients may require pressors in the
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Aortocaval
fistula
Fig. 22.4 Repair of aortocaval stula from within the aneurysm sac
early postoperative period. Within 1–4days, systemic vascular resistance increases and often may result in excessive
hypertension. Therefore, it is paramount that there is continuous and clear communication between the surgical and
anesthesia teams intraoperatively, as well as critical care specialists in the ICU.
Endovascular Repair
Since the advent of the endovascular era, many surgeons
now look to this option rst when faced with an aortocaval
stula. Endovascular repair negates the need for laparotomy,
less blood loss, and perhaps less postoperative complications. Essentially, an appropriately sized aortic endograft is
deployed within the aorta in the usual fashion for an abdominal aortic aneurysm. There may be an increased difculty in
opacication of the renal arteries if in close proximity to the
aortocaval stula. Stent graft and wire manipulation should
be minimized if possible to avoid potential dislodgement of
mural thrombus and pulmonary embolism. It is anticipated
that after endovascular repair, cessation of the highly pressurized aortic inow to the stula will allow the concomitant
aneurysm to seal.
Endovascular Repair: Outcomes
Discounting delay in diagnosis, 30-day mortality for the
endovascular repair of aortocaval stulas is <5%. The
main challenge with this approach, however, remains
endoleak. While early studies showed only a small or
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Fig. 22.5 Endograft stents
within the aorta and
Amplatzer™ plug within
aortocaval stula
K. C. Orion and J. H. Black III
moderate risk of endoleak [8, 9], a more contemporary
analysis [7] showed a rate of 50%. Unlike the more benign
type II endoleak, these continued endoleaks frequently
lead to sac enlargement or the need for secondary intervention such as deployment of an Amplatzer™ occluder
from the transfemoral venous approach (Fig. 22.5). To
address the high incidence of endoleak, some surgeons
have modied their endovascular approach in these
patients. Placement of an intravenous stent graft in addition to the aortic stent graft has been described, but the
risk of venous thromboembolism from the IVC stent graft
is a signicant worry. With sparse data that guide us on
anticoagulation for such rare conditions, the question of
anticoagulation is unsolved both in the acute postoperative period and in the long term.
Despite increased endoleaks, there seems to be certain
clinical situations where endovascular repair is benecial to
open repair. Certainly, many surgeons believe that patients
with a ruptured abdominal aortic aneurysm may do better
with an endovascular approach despite the IMPROVE trial
which did not show a signicant reduction in 30-day mortality [10]. Furthermore, ruptured inammatory aneurysms have
a higher occurrence of aortocaval stulas. Surgical dissection
of an inammatory aneurysm or retroperitoneal brosis is
technically demanding with increased bleeding risk or injury
to ureters. These particular patients may be best served with
an endovascular repair with close attention to endoleaks.
Hybrid Approach
Today’s surgeons have become more and more creative, now
employing both their endovascular skills to assist them with
denitive open repair. An occlusion balloon can be inserted
from the femoral veins and inated across the stula at the time
of opening the aneurysm sac to decrease blood loss. Alternatively,
a covered stent graft can be deployed within the inferior vena
cava prior to open repair. This approach was described in 2009
by Siepe etal. in a patient who presented with malperfusion and
rapid deterioration. The aneurysm’s juxtarenal anatomy
excluded it from an additional aortic stent graft [11].
Conclusion
Aortocaval stula is an uncommon aortic pathology. The
ubiquitous nature of CT scans for diagnosis or evaluation
have secured the diagnosis prior to surgery in most cases. It is
incumbent for surgeons to communicate closely with anesthesia and critical care physicians to manage the conse-
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quences of preoperative high-output cardiac failure and to
monitor hemodynamics in the postoperative period.
Endovascular and open surgery remain viable treatment strategies, but the effect of endoleak after endovascular repair may
require secondary procedures to address aneurysm growth.
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