Surg Clin N Am 84 (2004) 1337–1352
What is the significance of endoleaks
and endotension
Maarit A. Heikkinen, MD, Frank R. Arko, MD,
Christopher K. Zarins, MD*
Stanford University Medical Center, 300 Pasteur Drive,
H3600, Stanford, CA 94305-5642, USA
The primary purpose of endovascular aneurysm repair (EVR) is to
prevent death from aneurysm rupture. Endoleaks are defined as the
persistence of blood flow outside the lumen of the endoluminal graft but
within the aneurysm sac [1–3]. Thus, the aneurysm sac is not completely
excluded from the systemic circulation, and blood may fill the sac either
from around the graft (type I) or as back bleeding through small vessel
arising from aneurysm sac (type II). Often the pressure in the aneurysm sac
in patients with an endoleak is the same as systemic arterial pressure [4],
raising concerns of possibile aneurysm enlargement and rupture. Endoleaks
can be identified in 15% to 52% of patients after endovascular repair [5–13].
Endotension is defined as pressure within the aneurysm sac without
evidence of endoleak as the cause. The aneurysm may increase in size under
these circumstanses. Endotension with sac enlargement raises the the
possibility of an aneurysm rupture. The phenomenon of endotension is
unusual, and is seen in only 2% to 5% of patients after EVR [11,13–15]. At
present, the significance of endoleaks and their relationship to aneurysm
enlargement and rupture is unclear. Some authors conclude that reduction
in the size of the aneurysm is the only absolute indication of stent graft
treatment success [16]. However, aneurysm rupture can be seen in
aneurysms that decrease in size [14]. Here, we have reviewed the current
literature on endoleaks and endotension in relation to their their influence
on the primary outcome measures of EVR, which are aneurysm-related
death and aneurysm rupture.
* Corresponding author.
E-mail address: zarins@stanford.edu (C.K. Zarins).
0039-6109/04/$ - see front matter Ó 2004 Elsevier Inc. All rights reserved.
doi:10.1016/j.suc.2004.04.009
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Classification and incidence
A widely accepted classification of endoleaks divides endoleaks into four
categories according to the origination of flow into the aneurysmal sac
[2,3,17]. Type I endoleaks are those in which flow into the aneurysm sac
originates a stent graft attachment site to the infrarenal neck or iliac arteries
(Fig. 1). Separation of the space between the arterial wall and the stent graft
allows the direct flow of blood from the aorta into the aneurysm sac. Type I
endoleaks can be divided further divided into type IA endoleaks, which
occur at the aortic neck attachment site, and type IB endoleaks, which occur
at the distal iliac attachment sites. Type II endoleaks are those in which
blood flows into the aneurysm sac in a retrograde direction through normal
branches of the excluded segment of the aorta (Figs. 2 and 3). The most
common branches that give raise to type II endoleaks are the inferior
mesenteric artery and lumbar arteries. Accessory renal arteries can also give
rise to type II endoleaks. In subgroup type IIA endoleaks only, one branch
vessel can be detected. In more complex type IIB endoleaks, flow can be seen
through two or more branch vessels. Type III endoleaks occur when there is
a structural failure of the endovascular device. Type III endoleaks can be
subdivided into three groups: type IIIA endoleaks are due to disruptions or
holes in the fabric of the device, type IIIB endoleaks arise from separation of
modular devices and junctions, and type IIIC endoleaks are due to suture
holes in the fabric. Type IV endoleaks are caused by graft porosity, and is
usually identified on completion of angiography at the time of implantation
while the patient is fully anticoagulated.
Endotension indicates the there is tension exerted on the aneurysm wall
with or without an endoleak. The exact cause of endotension, when no
Fig. 1. Computer tomography images (coronal view left; 3D image in middle) show insufficient
proximal fixation and poor patient selection (angulated neck) resulting to type I endoleak (axial
views of computer tomography right).
M.A. Heikkinen et al / Surg Clin N Am 84 (2004) 1337–1352
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Fig. 2. Type II endoleak is visualized with Doppler ultrasound (top) and computer tomography
(bottom).
endoleak can be found, is unknown, but some authors think it is a missed or
sealed endoleak [7,18,19]. However, there are reports of endotension
patients who have undergone surgical conversion for aneurysm enlargement
without any evidence of blood inside the aneurysm sac [20]. Pressure may
remain high in the excluded aneurysm sac due to transmission of the pressure
through thrombus at or around the ends of attachment zones of the
prothesis [21,22]. This has been particularly associated with angulation of
the proximal aspect of the graft [20]. It has also been suggested that an
infectious process may be the cause of endotension, although the mechanism
is not clear [23,24]. Endotension has also been noted as a late phenomenon
several years after EVR [20].
The incidence of type I and II endoleaks at the time of discharge
following endovascular aneurysm repair ranges between 4% to 7% and
27% to 37%, respectively [25,26]. The incidence of type I endoleaks varies
between 4% to 6% at 1 month, between 1% and 4% at 12 months, and
between 1% to 3% at 24 months follow-up. The incidence of type II
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Fig. 3. Anterior (top left) and posterior (top right) 3D computer tomography view on type II
endoleak. 2D sagittal view showing the right (bottom left) and left (bottom right) iliac arteries.
endoleaks are 8% to 12% at 1 month, 5% to 32% at 12 months, and 13% to
26% at 24 months [23,26–28].
Natural history of aneurysms with endoleak
The natural history of aneurysms with endoleak after EVR remains
poorly defined. Aneurysm sac enlargement is more often seen in patients
with endoleak compared with those without an endoleak [4,14,29]. Sac
enlargement has been found in 20% of patients with type I/III endoleak
compared with 10% of patients with type II endoleak and 5% of patients
with no endoleak [4]. However, aneurysm enlargement following endovascular repair may not always be associated with an increased risk of
aneurysm rupture [14]. Also, there have been reports on patients with
shrinking aneurysms with no endoleaks with aneurysm rupture [30–33],
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1341
although type I/III endoleak has been found to be associated with aneurysm
rupture [8]. These ruptures have more often been seen in tube grafts or first
generation grafts, which were more prone to total graft displacement, graft
fractures, and severe kinking [4,9,34]. In the EUROSTAR study of 2862
patients, the risk ratio for late aneurysm rupture for proximal type I
endoleak was 7.59 (P = 0.001) and for type III endoleak 8.95 (P = 0.001)
[35]. However, distal type I endoleak was not significantly associated with
rupture (P = 0.8). In a study of 398 patients who had undergone EVR with
the AneuRx stent graft, that the presence or absence of an endoleak did not
predict patient survival or aneurysm rupture rate after EVR [16]. Thus, it
was felt that the endoleak in and of itself was not a predictor of the primary
outcome measure after EVR.
Type II endoleaks are the result of continued blood flow within the
aneurysm sac from the inferior mesenteric artery (IMA) or lumbar arteries.
Type II endoleaks are often seen immediately after placement of an
endovascular device, and are more likely to be seen and persist in patients
with large IMA or multiple lumbar arteries [36]. The long-term significance
of type II endoleaks is unknown. The risk of aneurysm rupture in patients
with pure type II endoleak is not increased compared with patients with no
endoleak [4,14]. In a comparison of three groups of patients with type II
endoleaks—those with a persistent type II endoleak, those with a transient
(\1 month) type II endoleak, and those with no endoleak—Arko et al found
that aneurysms with a persistent type II endoleak increased in diameter and
volume compared with the two other groups, both of which decreased [36].
There were no aneurysm ruptures in patients with type II endoleak and no
correlation between type II endoleaks and stent graft migration, proximal
neck enlargement, or aneurysm. Although aneurysm rupture in patients
with type II endoleak has been described [37], the overall risk of rupture has
not been found to be increased in patients with a pure type II endoleak
compared with patients with no endoleak [4].
Intrasac Doppler flow velocities can be used to predict if type II
endoleaks will spontaneously seal [38]. Low-velocity endoleaks (\80 cm/s)
have been found to be more likely to seal spontaneously compared with high
velocity (>100 cm/s) endoleaks. High-velocity endoleak is often related to
large-branch vessel diameter or number, and are also often resistant to
treatment with transarterial embolization [38].
In the EUROSTAR registry, 91 patients have been reported to have
endotension, and no aneurysm ruptures were seen during the mean followup of 15.4 months [4].
Risk factors and prevention
Short or angulated infrarenal aortic necks are the most significant
preoperative risk factors for a type I endoleak [4,39,40]. A neck length less
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than 20 mm is significantly more likely to result in a proximal type I
endoleak compared with longer neck lengths [40]. Large-diameter aortic
necks (>28 mm) can lead to an endograft migration and endoleak [40].
Smaller amounts of mural thrombus in the aneurysm sac also have been
found to correlate with device-related endoleaks. Ouriel et al found in
a study of 700 patients that patients with a large (>5.5 cm) aneurysm more
often developed a late type I endoleak than patients with a small aneurysm
[41]. There was no difference in frequency of the type I endoleak seen on
intraoperative angiograpgy or postprocedure CT scans. Shames et al
compared the endoleak rate between transrenal and infrarenal endograft
fixation [42]. They found no difference in the endoleak rate between these
two, and concluded that patient selection is more important than the type of
proximal fixation in preventing endoleaks.
The most important issue in preventing a type I endoleak is careful
patient selection. Aortic neck dimensions and quality of proximal and distal
fixation sites are the most critical factors. Patients should have infrarenal
necks longer than 15 mm, a common iliac artery diameter smaller than 18
mm, with minimum continuous length of 15 mm. Other factors that must be
evaluated are neck angulation, tortuousity and transmural calcification, and
thrombus. Patients with an aortic neck less that 15 mm in length should be
treated with caution because of concern about security of proximal fixation
and a type I endoleak. Furthermore, the aortic neck contour and angulation
are of particular concern because angulation increases the risk of a type I
endoleak, particularly when neck length is short. Security of the proximal
endograft, graft fixation, is the most important factor in preventing acute
and late type I endoleaks (Fig. 4). Thus, it is recommended that the
Fig. 4. Example of poor proximal fixation. Optimal place for proximal stent graft is
immediately under renal arteries (white dashed line). Insufficient proximal fixation leads to
migration and a type I endoleak in many cases.
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endograft be placed as close to the renal arteries as possible and extended to
the hypogastric arteries. The use of suprarenal fixation may be beneficial in
patients with short and angulated necks to improve proximal fixation. Type
I/III endoleak can sometimes occur after mechanical trauma. Krajcar and
Dougherty (2003) reported four patients in whom mechanical trauma was
identified as a factor in the development of late complications after EVR
[43]. Two patients had sustained blunt abdominal trauma in a car
accident,one had suffered a traumatic fall, and one had been participating
in vigorous rowing activity. However, a clean relationship between traumatic
events and endograft complication has not been established.
A type II endoleak is more likely to occur and persist if there is patent
IMA or two or more patent lumbar arteries. To avoid type II endoleak,
IMA or large lumbar arteries can be embolized before stent grafting [15,16]
(Fig. 5). However, because the risk of an aneurysm rupture with a type II
endoleak is so small, preoperative embolization is rarely performed.
Fig. 5. Preoperative coil embolization of patent inferior mesenteric artery (IMA). Preoperative
angiogram shows patent IMA (white arrow, top left), which has been selectively cannulated (top
right) and coil-embolized (bottom). After embolization, endografting is performed as usual.
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Diagnosis
The diagnosis of an endoleak is based on the observation of contrast
medium or blood flow within the aneurysm sac on angiography, computer
tomography (CT), or duplex scanning. In the operating room after EVR,
completion angiography is performed. A high-flow power-injected run and
filming through the venous phase usually shows if there are any endoleaks
present. When an endoleak is seen, further analysis on the type of endoleak
is needed. With selected injections near attachment sites and with multiple
projections, the source of the endoleak usually can be found. Sometimes, if
there are patent lumbar arteries an attachment site leak can mimic a type II
endoleak. Thus, careful evaluation of the direction of flow in the branch
vessel will show the true source of the leak. Sometimes contrast material
does not disappear from the aneurysm sac until after the first postoperative
day. Thus, postprocedure CT scans can mimick an endoleak, due to residual
contrast material in the aneurysm sac from the previous day’s angiograph
procedure and endograft placement. A noncontrast CT scan will identify
such a circumstance (Fig. 6).
Duplex ultrasound (US) and spiral CT are the most important tools for
recognizing endoleaks during postoperative surveillance [44,45]. Highquality duplex US scanning has been found to be comparable to CT
angiography for the assessment of aneurysm size and endoleaks after EVR
[45]. As an adjunct to CT in evaluating endoleaks, duplex US provides
hemodynamic information that enables further characterization of the type
of endoleak [44,45]. CT and US are more sensitive than angiography for the
detection of endoleaks [46]. Angiography can be employed selectively to
define the source of the endoleak when it is uncertain and when further
procedures are considered.
With CTA, the direction of the flow cannot always be identified. Thus,
the type of endoleak that is present might be misdiagnosed. Time-resolved
magnetic resonance angiography (TR-MRA) has been found to be as
sensitive as CTA for detection of endoleaks [47,48]. Furthermore, TR-MRA
Fig. 6. Contrast material can be sometimes seen in the aneurysm sac at first postoperative day
mimicking endoleak (left), but image without contrast shows that there is no endoleak (right).
M.A. Heikkinen et al / Surg Clin N Am 84 (2004) 1337–1352
1345
can visualize the direction of flow in the aneurysm sac, making the endoleak
characterization more accurate with TR-MRA than CT [49]. However,
MRI imaging is limited to patients with nitinol-based supported or
unsupported devices, and cannot be used in patients with a pacemaker.
Patients with stainless steel devices are unable to be followed with MRA
because of the significant metallic artifact caused by the stainless steel
components. Similarly, patients who have undergone embolization procedures with stainless steel coils may be difficult to follow with MRA because
of the artifact from the coils [50]. Platinum embolization coils are nearly
invisible for MRA, and create no artifact [49].
Endotension can cause sac enlargement, and the diagnosis is made by
measuring the intrasac pressure. Intraaneurysm sac pressure assessment is
performed using direct translumbar access through the aneurysm sac or
selective cannulation of the inferior mesenteric or lumbar arteries via
either the superior mesenteric artery or hypogastric arteries, respectively
[20,51].
Treatment
The primary objective in treating patients with aortic aneurysms is to
prevent aneurysm rupture and death from aneurysm rupture. Thus,
treatment of the endoleaks should be based on that same basic principle:
if the endoleak increases the risk of rupture, it should be repaired as soon as
possible, but the risk of death or severe complications of the chosen
treatment should never exceed the risk related to the endoleak itself.
Unfortunately, decision making is seldom straightforward due to several
factors. The difficulty lies in the fact that the true natural history of
aneurysms with an endoleak is poorly understood, and there is not a clear
consensus on treatment guidelines. Also, predicting the risk associated with
secondary intervention for each individual patient is difficult. The risk of
aneurysm rupture depends primarily on the size of the aneurysm [14], the
pressure within it, and the force applied to the aneurysm wall [52]. The
clinical consequence of rupture, however, depends on the potential for lifethreatening hemorrhage. The amount of hemorrhage in the case of an
aneurysm rupture should depend on the flow rate to aneurysm sac, that is,
the endoleak volume. Thus, clinical significance of the endoleak or
endotension is based on the risk of rupture and on the possibility of lifethreatening hemorrhage if rupture occurs.
Most endoleaks will seal spontaneously without any treatment. Two of
three endoleaks that are seen at the time of the discharge seal during the first
month after the procedure [8,16]. Arko et al found that low velocity type II
endoleaks (\80 cm/s in Doppler ultrasound) were likely to have thrombosis
without treatment [38]. However, 20% of leaks that spontaneously seal
reopen at 12 to 18 months [53]. New type II endoleaks can occur at any time
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after the procedure. The timing of endoleak occurrence does not significantly influence the rate of spontaneous endoleak resolution [54].
Type I/III endoleaks have been found to be associated with aneurysm
rupture in several studies [4]. Thus, treatment of these endoleaks is
indicated.
If a type I endoleak is recognized at completion of angiography, it should
be treated during the initial operation with endovascular techniques, if
possible. If the endoleak is from the proximal attachment site, balloon
angioplasty, Palmaz stent, or stent graft extension to the proximal site will
often eradicate the leak. Sometimes, however, a proximal leak is resistant to
immediate procedures, and in these cases it can be followed some time after
operation, because most of these endoleaks seal spontaneously [8].
With the development of a late type I endoleak, there often can be
treatment with additional stent graft modules to improve the proximal
fixation. There should be sufficient native aorta available proximal to allow
placement on an extender module. Type I endoleaks have been treated with
coil or glue embolization with fairly good results [47,55–58]. At the same
time of the embolization of the perigraft space, patent outflow vessel,
including lumbar arteries and IMA, can be embolized [59]. However,
recanalization of the endoleak site or transmission of systemic pressure
through thrombus has been seen [57]. Acute complications, such as colon
ischemia, has been reported in the treatment of a type I endoleak with glue
[57,60].
When there seems to be a proximal endoleak despite proximal restenting,
periaortic ligature can seal the leak [61,62]. Although aortic clamping can be
avoided in this procedure, it is more invasive than the above described
endovascular techniques, and 30-day mortality has been even 30% [61].
Persistent type I endoleaks resistant to endovascular repair may require
open surgical conversion. However, surgical conversion is associated with
a high (20%) mortality rate [35,63,64]. Patients who are at especially high
risk for open surgery may, on occasion, be observed with careful, ongoing
monitoring. However, the ongoing potential for aneurysm rupture must be
recognized.
Although the long-term significance of a type II endoleak is unknown,
thus far they have been associated with low risk of an aneurysm rupture
[4,38]. However, patients with type II endoleaks associated with an
aneurysm enlargement are of concern, and should be treated and carefully
observed.
Endovascular treatment of a type II endoleak includes selective catheterization of feeding vessels and embolization with glue or coil [65]. (Fig. 7).
Another method is to use a translumbar approach via either a left-sided or
right-sided (transcaval) approach [66]. Type II endoleaks are often resistant
to embolization, and new type II endoleaks can occur after treatment
[67,68]. Baum et al compared transarterial and direct translumbar embolization in the treatment of a type II endoleak [69]. In their series, 80%
M.A. Heikkinen et al / Surg Clin N Am 84 (2004) 1337–1352
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Fig. 7. Patent inferior mesenteric artery has been selectively cannulated (left) and successfully
coil-embolized (right).
(16 of 20) of endoleaks treated with transarterial embolization were
unsuccessful with recanalization of the original endoleak cavity over time
compared with 8% (1 of 13) in the translumbar group during the median
follow-up of 8 months (P = 0.0001). [69] High velocity (>100 cm/s in
Doppler US) type II endoleaks are more persistant and also resistant to coil
embolization [38]. A lower recurrence rate can be achieved if the entire
aneurysm sac is glue- or coil-embolized [69]. Also, thrombin injection into
the leak by a percutaneous approach directly into the aneurysm sac using
Doppler US has been described [70]. A more effective, but also more invasive, treatment method is feeding vessel ligation or clipping, which can be
performed using laparoscopy or laparotomy [71–74].
Treatment of type II endoleaks is not complication-free, and severe
consequences, although rare, have been associated with migration or distal
embolization of the agent being used. Paraplegia, colonic necrosis, and
ischemic colitis subsequent to embolotherapy for type II leaks have been
reported [75–77].
A type III endoleak increases the risk of aneurysm rupture significantly
[8]. With the first-generation endografts, severe migration has been
a relatively common problem, causing kinking and graft separation
followed by a type III endoleak. In many cases, these can be treated with
an extender cuff or an entirely new endograft inside the old one [78]. If
endovascular means are unsuccessful or are not appropriate, then open
conversion is indicated.
Type IV endoleaks, which are seen at the time of completion of
angiography when the patient is fully anticoagulated, are self-limited, and
no treatment is needed [79].
In the case of endotension, the clinical consequences of rupture are
unclear. Some authors favor open surgical conversion in the case of
endotension and aneurysm enlargement [20]. Endotension is clinically
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significant if associated with the potential for hemorrhage in the event of
aneurysm rupture, or if it causes progressive enlargement of the aneurysm
and aneurysm neck so that the security of endograft fixation is compromised
[53]. Because of the absence of an endoleak, the only treatment method in
the case of endotension is open surgical conversion. However, the risk of
death and severe complications of open repair may be greater than the risk
of observation of the endotension. Our conclusion from currently available
data is that open conversion in endotension is rarely justified. In the case
that the aneurysm enlargement leads to compromised proximal fixation and
a type I endoleak, treatment is indicated.
Summary
Endoleaks remain a challenging issue following endovascular aneurysm
repair. Careful patient selection is the most important factor in preventing
endoleaks. The natural history of aneurysms with different types of
endoleaks is unclear, and endoleaks may not be reliable indicators of the
success of endovascular repair. The primary objective of aneurysm repair is
prevention of aneurysm rupture, and endoleaks are only indirect measures
of success. An endoleak, however, is a good secondary outcome measure
after EVR. Treatment of type I and III endoleaks is indicated, and should be
done with minimally invasive technique, if possible. If open conversion is
required, risks and benefits must be carefully evaluated. Type II endoleaks
are associated with aneurysm enlargement, but may not be indicators of an
increased risk of rupture.
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