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Endoleak
BrianC.Gardner andSaherS.Sabri
19
Pathophysiology
Abdominal aortic aneurysm is the abnormal enlargement of
the aorta, most often due to weakening of the vessel wall.
Pathologically, wall degeneration is a complex combination
of inammation, smooth muscle cell death, and extracellular matrix changes. These typically occur in the elderly and
more often in males. The leading risk factor for development is a smoking history [1]. They tend to run in families.
Abdominal aortic aneurysms are only detected on physical
exam in 30–40% of patients as a pulsatile abdominal mass
[1]. Clinically, patients sometimes present with abdominal
pain, although they can also be completely asymptomatic.
Due to unreliable physical exam ndings, the United States
Preventive Task Force recommends screening ultrasound be
performed in male smokers age 65–75 [1]. Abdominal aortic aneurysms should be treated if equal to or greater than
5.5cm or if the aneurysm has enlarged more than 1cm in a
year due to the increased risk of rupture [1]. There is a
greater than 50% mortality rate for patients with abdominal
aortic aneurysm rupture prior to even presenting to a hospital, and of the patients that do make it to a hospital, there is
about a 50% mortality rate during attempted repair [1].
Historically, abdominal aortic aneurysms were repaired by
open surgery; however, up to 70% of repairs are now performed
using covered stents deployed within the aortic lumen known
as endografts [2].
Endografts serve as a conduit within a vessel to exclude a
diseased segment from systemic arterial pressurization. Juan
B. C. Gardner · S. S. Sabri (*)
University of Virginia Health System, Department of Radiology
and Medical Imaging, Charlottesville, VA, USA
e-mail: bg5h@virginia.edu; saher.s.sabri@medstar.net
Key Point
The USPTF recommends screening US in male smokers
65–75years of age to evaluate for AAA.
Parodi developed the rst endograft in 1990 [3]. Endografts
can also be used in the setting of arterial dissection to maintain patency of the vessel true lumen. Endograft placement is
much less invasive than the traditional open surgical repair.
In the appropriate patient, endografts can be deployed using
only percutaneous access with introducer sheaths in the
bilateral femoral arteries.
Endoleak is a term used to describe a condition following
endovascular repair of the aorta in which blood ow is maintained outside the lumen of the endograft and within the
excluded portion of aneurysm sac [4]. Endoleaks usually
need to be treated or at least monitored, because they allow
for pressurization of the excluded vessel and, in the setting of
aneurysm, can lead to continued aneurysmal expansion and
eventually rupture [5]. According to a recent review, endoleaks are detected in about 25% of patients following endovascular repair of an aneurysm of the abdominal aorta [6].
Endoleaks are classied based on the mechanism of the
leak (Fig. 19.1). Type I endoleaks are dened by leakage
around either the proximal (type Ia) or the distal (type Ib)
aspect of the endograft. Type II endoleaks occur when the
excluded sac is pressurized by afferent and efferent arteries
excluded by the graft. Afferent arteries bring blood into the
excluded aneurysm sac, and efferent arteries drain blood
away from the aneurysm sac. This constant afferent and
efferent arterial ow prevents thrombosis of the excluded
aneurysm sac. Type III endoleaks involve a defect in the
graft, either between components of the endograft or secondary to a puncture of the graft itself [7]. Type IV endoleaks are
© Springer International Publishing AG, part of Springer Nature 2018
N. A. Keefe et al. (eds.), IR Playbook, https://doi.org/10.1007/978-3-319-71300-7_19
219
220
B. C. Gardner and S. S. Sabri
Fig. 19.1 Types of endoleaks
dened by leakage through the covered endograft material
due to porosity, but are uncommon with modern endograft
materials [8]. Type V endoleaks are secondary to a phenomenon known as endotension [9]. The exact mechanism of
endotension is somewhat controversial, but when present,
there is continued expansion of the excluded aneurysm sac
without an identiable source of endoleak on imaging [10].
The most common type of endoleak is type II, making up to
around 44% of all endoleaks [7, 11]. Type II endoleaks most
commonly involve the lumbar and inferior mesenteric arteries [11]. Endoleaks are also characterized according to the
timing of onset, with “early” endoleaks occurring within
30 days of endograft placement and “late” endoleaks presenting thereafter [11].
Arterial anatomy of the proximal and distal attachment
sites or “landing zones” can determine the endograft
treatment strategy; some types of landing zones can increase
the risk of endoleak occurrence [7]. Abdominal aortic
aneurysms can be categorized based on the location of the
aneurysm in relation to the renal arteries. Infrarenal
abdominal aortic aneurysms are aneurysms located below
the level of the renal arteries with a segment of normal aorta
between the renal arteries and the aneurysm. This segment is
also known as the “neck,” which is used as the proximal
attachment site for the endograft [12]. Characteristics of the
proximal neck that increase the risk of type Ia endoleak
include a relatively short neck (typically dened as <1cm),
an angulated neck (>60 degree angulation), and intraluminal
calcication or thrombus [13]. Additional types of abdominal
aortic aneurysms include juxtarenal aneurysms which
terminate just below the level of the renal arteries, pararenal
aneurysms which extend up to and involve the renal arteries,
and suprarenal aneurysms which extend above the renal
arteries. In some of these cases, special endografts such as
fenestrated endografts with suprarenal xators can be used to
repair these types of aneurysms, with an uncovered portion
of the endograft at the level of the renal arteries to maintain
blood ow to the kidneys (refer to Chap. 17 for more information on aneurysms) [13].
Key Point
Increased risk of type Ia endoleak:
• Short proximal neck
• Angulated proximal neck
• Intraluminal calcication or thrombus of the landing
zone
Increased risk of type Ib endoleak:
• Aneurysmal or tortuous iliac arteries
19 Endoleak
221
Consideration must also be made for the distal landing
zone. Today’s endografts are bifurcated grafts made up of
modular components with two limbs that extend into the
common iliac arteries [11]. Deployment of an endograft can
be difcult in the setting of aneurysmal or tortuous iliac arteries, which make poor landing zones and can lead to a poor
seal with the arterial wall [8]. In the setting of a poor distal
landing zone, one of the endograft limbs can be extended
inferiorly beyond the common iliac artery into the external
iliac artery. Prior to endograft deployment into the external
iliac artery, the ipsilateral internal iliac artery, also known as
the hypogastric artery, should be embolized to prevent a
future type II endoleak [1]. Extension of an endograft into the
bilateral external iliac arteries is not routinely performed due to
concerns for buttock claudication and erectile dysfunction,
although this can be performed in some high-risk patients [1].
Clinical Indication
Patients with endoleaks can present with abdominal pain due
to an expanding aneurysm, but most endoleaks are asymptomatic and identied on routine imaging, either during the
placement of the endograft with digital subtraction angiography (DSA) or on follow-up evaluation using CT, MRI, or
ultrasound.
Type I–IV endoleaks can be diagnosed by digital subtraction angiography at the time of endograft deployment. Type
V endoleaks, on the other hand, are diagnosed in the setting
of a continually expanding aneurysm sac without another
endoleak type identied on imaging during follow-up CT
angiography, MRI, or ultrasound. In type Ia and Ib endoleaks, contrast will be seen quickly ling either the superior or
inferior aspect of the aneurysm sac around the endograft during the injection of contrast. In type II endoleaks, a vessel
excluded by the endograft (usually a lumbar artery or the
inferior mesenteric artery) is identied either lling or draining the aneurysm sac. In type III endoleaks, contrast lls the
aneurysm sac through a defect in the endograft, either at a
junction of the components or at a defect in the graft. Type
IV endoleaks could be historically identied on DSA immediately post endograft placement, but are uncommon with
modern graft materials [8].
Key Point
CTA is the gold standard for evaluation of endoleak.
Following placement of endografts, patients must be followed with surveillance imaging to detect an endoleak that
was not identied during deployment, any further growth of
Table 19.1 Imaging surveillance modalities for endoleaks
Imaging surveillance modalities for endoleaks
Advantages Disadvantages
CTA Gold standard
Rapid
examination
MRI No ionization
radiation
Ultrasound No ionization
radiation
Exposure to ionization radiation
Use of potentially nephrotoxic IV
contrast
Susceptible to beam hardening artifact
Use of potentially nephrotoxic IV
contrast
Risk of nephrogenic sclerosing
brosis (NSF)
Susceptible to artifacts
Higher cost and longer exam time
Accuracy dependent on skill of
technologist
Limited in large patients and extensive
bowel gas
the aneurysm sac, or evidence of device complication such
as graft migration [6]. Surveillance imaging modalities
include CTA, MRI, and ultrasound (Table19.1). Currently,
CT angiography is the most commonly used imaging modality for follow-up and is considered the gold standard [6, 11].
Multiphase CT angiography examinations are employed
with unenhanced, arterial phase, and delayed phase imaging
[8]. The recommended follow-up interval using CT angiography is at 1month, 6months, and 1year following endograft deployment, with annual examinations thereafter for
lifelong surveillance [8].
The potential adverse effects of CT angiography include
exposure to ionizing radiation and the use of intravenous
contrast agents that can cause renal damage, particularly in
the setting of acute kidney injury or baseline chronic kidney
disease [6, 14]. Another issue with CT angiography is the
endograft material, and embolization materials can cause
beam hardening artifact that can obscure potential sources of
endoleak [14]. Ultrasound is another imaging modality that
can be used to detect endoleaks with the benet of no ionizing radiation exposure. Duplex ultrasound and contrastenhanced ultrasound are methods of performing ultrasound
evaluation. Duplex ultrasound utilizes the Doppler effect of
sound waves to detect ow, such as around the endograft in
cases of endoleak. Contrast-enhanced ultrasound uses microbubbles that are injected intravenously as a contrast agent to
detect ow [6]. MRI is another imaging modality, which
unlike CTA does not involve exposure to ionizing radiation.
Some studies have shown MRI superiority compared to CT
at detecting endoleaks, particularly type II [8, 14]. MRI can
be limited by susceptibility artifacts caused by the endograft
material that disrupt MRI signal characteristics particularly
near the endograft, potentially blocking visualization of an
endoleak [15]. Other drawbacks to MRI include the higher
cost compared to other modalities and the longer examination times [6, 16].
222
B. C. Gardner and S. S. Sabri
Conventional Therapy
Compared to the traditional repair of abdominal aortic aneurysms using open surgery, endografts have superior perioperative and early morbidity and mortality rates [17, 18, 19].
However, multiple randomized control trials have not shown
a signicant difference in overall long-term mortality
between endovascular and surgical repairs [20]. Additionally,
randomized control trials have shown a signicant increase
in secondary interventions following endograft repair when
compared to open repair of abdominal aortic aneurysms
[21]. The most common complications in endograft repair
that necessitate secondary intervention are endoleaks and
graft migration [21]. For this reason, endograft patients must
be followed with lifelong imaging surveillance [19].
With regard to endoleak treatment following endovascular
stent placement, type I and type III endoleaks must be treated
immediately as these types of endoleaks are characterized by
high pressure within the aneurysm sac. The other types of
endoleaks do not necessarily need to be treated immediately
and can be followed as long as the aneurysm sac size is stable.
In fact, persistent type II endoleaks have not been shown to
have an increase in aneurysm-related mortality [22]. Also,
stable type II endoleaks demonstrate a comparable rate of rupture compared to stable aneurysms without an endoleak [23].
If the decision is made to perform a repair for an endoleak,
endovascular techniques are usually attempted rst instead of
surgical repair (Table 19.2). Many patients initially selected
for endograft placement have signicant comorbidities that
make them poor surgical candidates [24]. However, elective
open surgical repair of type I or III endoleaks or endograft
migration following endograft placement in which further
endovascular treatment is not possible has been shown to have
similar mortality rates of about 3% as a primary open repair of
abdominal aortic aneurysm [18, 25].
Interventional Therapy
Endovascular treatment of endoleaks depends on the type of
endoleak encountered:
Type IEndoleaks
Type I endoleaks are typically high-pressure endoleaks and
therefore warrant treatment immediately upon detection
(Fig.19.2).
There are a variety of endovascular treatment options for
type Ia endoleaks. First, the proximal endograft can be
secured to the vessel wall using a relatively noncompliant
balloon [1]. A large vessel balloon expandable stent can be
used to reinforce the proximal aspect of the endograft.
Endovascularly placed staples can also be used to secure the
stent to the vessel wall. Additionally, the proximal aspect of
the endograft can be extended superiorly with an additional
Table 19.2 Management of type II endoleaks
Decrease in sac size No therapy
Increase in sac size Endovascular/surgical treatment
Stable sac size Consider treatment in the presence of
predictors of persistent endoleaks:
Numerous collaterals (>3 vessels)
Large central nidus (>15 mm)
High ows (velocities >100 cm/sec)
Chronic anticoagulation
Fig. 19.2 (a) Angiography demonstrates a type Ia endoleak along
the proximal aspect of the endograft below the left renal artery
(white arrowheads). (b) Following deployment of a Palmaz balloon
expandable stent within the proximal aspect of the endograft, the
endoleak is no longer present
19 Endoleak
cuff if the neck provides enough space for deployment [16, 19].
If the neck is not sufcient, fenestrated extension cuffs or
chimney grafts can be placed in order to extend the endograft
superior to the renal arteries [2, 19]. Alternatively, embolic
agents including coils, Onyx (Medtronic, St. Paul MN), or
cyanoacrylate can be placed to ll the space between the
endograft and the aortic neck [11, 16]. This space is accessed
by catheterization from the aorta or using translumbar aneurysm puncture (see below). Of note, coils and embolic agents
can create beam hardening artifact on follow-up CT angiography that can possibly limit future surveillance examinations [19].
Type Ib endoleaks can be treated with many of the same
techniques as type Ia endoleaks, but are usually treated by
extending the distal portion of the affected endograft limb
with additional stents [1, 16]. If the additional stents extend
over the internal iliac artery, this vessel should be embolized
prior to covering to prevent a type II endoleak [16].
Type II Endoleaks
Type II endoleaks are typically low-pressure endoleaks with
a lower rate of aneurysm sac expansion and rupture compared
to type I and III endoleaks [1]. Some type II endoleaks will
resolve without further intervention and therefore do not
require immediate treatment [1, 16]. However, treatment is
indicated if a type II endoleak results in continued sac expansion [1]. In persistent type II endoleaks, there can be more
than one inow and outow vessel, making eradication of
type II endoleaks difcult [16]. Treatment options include
transarterial embolization of the artery supplying the
endoleak, translumbar direct percutaneous puncture of the
aneurysm sac with embolization, and transcaval puncture of
the aneurysm sac with embolization [1]. Choice of technique
to use depends on operator preference. Some anatomic
factors may favor one technique over others.
The transarterial approach is the most common technique
used to treat type II endoleak (Fig.19.3) [26]. In this method,
the aneurysm sac and feeding vessel are accessed using endovascular technique. For example, through a femoral artery
approach, the inferior mesenteric artery can be accessed from
the middle colic artery branch of the superior mesenteric
artery via the arc of Riolan [16]. The lumbar arteries can be
accessed via the internal iliac artery through the iliolumbar
arteries [16]. Once the feeding vessel is accessed, it is embolized, with additional embolization, when possible, of the
aneurysm sac. Embolization materials include coils, cyanoacrylate, Onyx, and thrombin [19]. Another method of transarterial approach is accessing the aneurysm sac and feeding
vessel from a femoral arterial access by navigating a catheter
into the potential space between the distal aspect of the endograft and the common iliac artery wall [19].
223
Key Point
Key vascular connections for type II endoleak repair:
SMA ->arc of Riolan ->IMA.
Internal iliac ->iliolumbar arteries ->lumbar arteries.
The How To
Transarterial Embolization of Type II Endoleak
1. Prior to endoleak repair, patients usually undergo
cross-sectional imaging, most commonly multiphase CT angiography to characterize the endoleak
and identify a possible endoleak source and potential target for intervention.
2. The patient is placed supine on the angiography
table, and the bilateral groins are prepped and
draped. A Foley catheter may be placed as procedure times can be long.
3. Ultrasound-guided puncture technique is used to
access the femoral artery via the Seldinger technique (refer to Chap. 8 for more information).
4. After placement of a sheath and pigtail catheter,
an aortogram is performed. Additional selective
angiography may be needed to identify the artery
supplying the type II leak.
5. The supplying vessel of the endoleak will determine subsequent steps. If the endoleak source is
the inferior mesenteric artery, the superior mesenteric artery will be selected. If the source is a lumbar artery, the internal iliac artery will be selected
(alternatively the aneurysm sac is directly accessed
by navigating around one of the distal limbs of the
endograft directly into the aneurysm sac).
6. The superior mesenteric artery is selected, and
angiography of the SMA is performed.
7.
microcatheter and microwire.
8. The inferior mesenteric artery is selected and
angiography of the aneurysm sac is performed.
9. At this point, hopefully the afferent and efferent
most commonly a lumbar artery and the inferior
mesenteric artery. Results are superior if all can be
occluded.
10. The afferent limb, efferent limb, and aneurysm sac
are embolized using coils, Onyx, cyanoacrylate,
thrombin, or a combination thereof.
11. Follow-up angiography should demonstrate stasis
224
B. C. Gardner and S. S. Sabri
Fig. 19.3 (a) Angiography with a microcatheter advanced into the ilio-
lumbar collaterals using access from the internal iliac artery (black
arrowheads) demonstrates a type II endoleak with inow from a lumbar
artery (white arrow). (b) Through the microcatheter (black arrow-
heads), embolization is performed with Onyx (black arrow) and placement of a coil within the lumbar artery (white arrow). (c) On
post-embolization imaging, the Onyx appears as radiopaque material
within the aneurysm sac
19 Endoleak
225
The How To
Translumbar Embolization of Type II Endoleak
In the translumbar approach, the aorta is directly
punctured with the patient in the prone position using
either CT or fluoroscopic guidance (Fig. 19.4) [27].
The approach is usually from the patient’s left side
along the lateral aspect of the vertebral bodies to avoid
the inferior vena cava, although a right-sided approach
is also possible which traverses the IVC en route to the
aorta [16, 26]. Once access of the aneurysm sac is
established, angiography is performed. Embolization
materials include coils, cyanoacrylate, Onyx, and
thrombin [16]. One of the risks of this technique is
retroperitoneal hemorrhage [16].
1. Prior to endoleak repair, patients usually undergo
cross-sectional imaging, most commonly multiphase CT angiography to characterize the endoleak
and identify a possible endoleak source and potential target for intervention.
2. The patient is placed prone on the angiography
table. The patient’s back is prepped and draped.
3.
aneurysm sac, usually on the patient’s left side,
with the needle running closely alongside the verte-
-
ing that corresponds with the aneurysm sac.
4. Once the aneurysm sac is accessed, successful nee-
blood return. Then the needle is exchanged for a 4
or 5 French catheter.
5. Angiography is performed to identify the afferent
and efferent branches.
6. The afferent limb, efferent limb, and aneurysm sac
are embolized through a microcatheter as needed
using coils, Onyx, cyanoacrylate, thrombin, or a
combination thereof.
Type III Endoleaks
Type III endoleaks are diagnosed by injecting the graft to
identify contrast quickly exiting the graft into the aneurysm
(Fig. 19.5). Type III endoleaks are typically high-pressure
endoleaks and therefore are treated immediately upon
diagnosis, just like type I endoleaks [30]. Type III endoleaks
are usually treated by covering the defect in the graft or the
separation of the endograft components with an additional
endograft component [1]. Embolization is almost never
performed in the setting of type III endoleaks [16].
The How To
Transcaval Embolization of Type II Endoleak
In the transcaval approach, the inferior vena cava is
accessed via the femoral vein, and the abdominal aorta
aneurysm sac is punctured using a transhepatic
portosystemic shunt kit [28]. This method is useful in
patients without an identifiable transarterial approach
and when the aneurysm sac is located to the right of
midline, limiting use of the transarterial or translumbar
approaches [28]. These patients require the inferior
vena cava to directly oppose the aneurysm sac [28].
Risks of this technique include retroperitoneal
hemorrhage and graft puncture with the needle [28].
Another risk is deployment of embolization material
such as coils within the IVC, which could potentially
migrate to the pulmonary arteries [29].
1. Prior to endoleak repair, patients usually undergo
cross-sectional imaging, most commonly multiphase CT angiography to characterize the endoleak
and identify a possible endoleak source and potential target for intervention.
2. The patient is placed supine on the angiography
table. The patient’s groins are prepped and
draped.
3. The femoral vein is accessed using the Seldinger
technique, and a pigtail catheter is advanced into
the inferior vena cava. A venogram of the iliac vein
and inferior vena cava is performed.
4. Using a transhepatic portosystemic shunt kit, a needle is directed from the inferior vena cava transversely into the aneurysm sac at a level in which the
inferior vena cava and the abdominal aortic aneurysm sac are opposed based on preoperative
imaging.
5. The transhepatic portosystemic shunt kit is
exchanged for a catheter, and angiography of the
aneurysm sac is performed to identify the afferent
and efferent branches.
6. The afferent limb, efferent limb, and aneurysm
sac are embolized using coils, Onyx, cyanoacrylate, thrombin, or a combination thereof, with
care not to deploy embolization material within
the inferior vena cava. A successful embolization
appears to prevent retroperitoneal hemorrhage in
most cases.
Type IV Endoleaks
Type IV endoleaks due to endograft porosity are uncommon
with modern endograft materials. When these types of
endoleaks were encountered in the past, they typically
226
B. C. Gardner and S. S. Sabri
Fig. 19.4 (a) Preoperative CTA demonstrates a type II endoleak with
contrast enhancement of the aneurysm sac (white arrow). (b)
Intraoperative cone beam CT with the patient placed prone demonstrates direct sac puncture using a needle (white arrowhead). (c)
Fig. 19.5 Type III endoleak between the components of the endograft
on angiography, with contrast lling the excluded aneurysm sac (white
arrows)
resolved without intervention [1, 16]. Additionally, type IV
endoleaks are not associated with increased risk of aneurysm
rupture [11].
Type V Endoleaks
Type V endoleaks due to endotension are difcult to treat, as
the source of the continued sac expansion is not readily
Angiography through the access needle (black arrow) in a lateral view
demonstrates enhancement of the endoleak (black arrowheads) with
enhancement of a lumbar artery and the IMA. (d) Embolization material (Onyx) is seen within the aneurysm sac post-embolization
apparent. These endografts can be treated either by extending
the limbs of the endograft or relining the endograft with an
additional endograft [1, 11]. If this is not successful, explantation of the endograft and open surgical repair may be the
only option [1, 16].
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Traumatic Aortic Injury
MichaelJ.Hagar, AbhijitL.Salaskar, andShawnSarin
Pathophysiology
The rst known description of a traumatic aortic injury was
made in 1557 by Vesarius who described a patient that died
of aortic rupture after falling from a horse [1]. Traumatic aortic injuries can occur from blunt or penetrating trauma.
Today, the most common etiology of traumatic aortic injury
is blunt trauma. In 274 cases of aortic transections collected
from 50 trauma centers over a 2.5-year period, 81% of cases
were caused by motor vehicle collisions (MVC). The severity of injury varies with the extent of vessel wall involvement, which can range from a small intimal tear with subtle
hemorrhage to a complete aortic transection resulting in
rapid exsanguination [2].
Aortic transections are extremely rare. On average two to
three cases are seen per year in major trauma centers in the
United States [3]. However, in a study of 387 blunt trauma
deaths, traumatic aortic transections were found to be the
second most common cause of death behind head injuries
[4]. The risk of death following a traumatic aortic injury is
greatest immediately after the accident. It is estimated that
only 10–20% of patients with aortic injuries make it to the
emergency department alive, and of those, only 60–70% survive [5].
Blunt aortic injuries can result from rapid deceleration
injuries such as with a MVC and fall from signicant height
M. J. Hagar
George Washington University Hospital, Department of Diagnostic
Radiology, Washington, DC, USA
A. L. Salaskar
George Washington University Hospital, Department of
Interventional Radiology, Washington, DC, USA
S. Sarin (
George Washington University Hospital, Department of Vascular
and Interventional Radiology, Washington, DC, USA
e-mail: ssarin@gwu.edu
*)
20
or from compression in crushing injuries of the chest [6, 7].
There is no consensus on the exact mechanism of blunt aortic
injury; however, there is agreement that the pathophysiology
is complex and likely involves a combination of factors
including sheer, hydrostatic forces, rapid deceleration, and
direct compression [8]. Rapid deceleration results in aortic
injury at points of xation, most commonly at the isthmus [9,
10] which is at the junction of the ligamentum arteriosum
and the takeoff of the left subclavian artery. Compression can
result in aortic injury when the aorta is pinched between the
spine and the sternum, clavicle, or rst rib.
Key Point
Aortic injuries secondary to rapid deceleration most
commonly occur at the isthmus.
The common sites of aortic transection according to
autopsy studies are reported to be 45–56% at the isthmus,
19–23% ascending aorta, 9–13% descending aorta, 6–8%
transverse aortic arch, and 4–5% abdominal aorta [9, 10].
However, these distributions are drastically different when
the site of aortic injury is directly observed during surgical
repair where 93–97% of aortic injuries were observed at the
isthmus [2, 10]. This disparity suggests that patients with
aortic transections in sites other than the isthmus rarely survive long enough to reach the hospital [11].
There are various grading systems for traumatic aortic
injuries. The most widely accepted grading system proposed
by Azizzadeh etal. [12] has been endorsed by the Society for
Vascular Surgery. Grading system is as follows (Fig.20.1):
• Grade 1—intimal tear
• Grade 2—intramural hematoma or large intimal ap
• Grade 3—pseudoaneurysm
• Grade 4—free rupture
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N. A. Keefe et al. (eds.), IR Playbook, https://doi.org/10.1007/978-3-319-71300-7_20
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