Endoleak Following
AAA Repair
Problems detected during follow-up
affect treatment durability and success.
BY ELLEN D. DILLAVOU,
MD; NAVYASH GUPTA, MD; AND MICHEL S. MAKAROUN, MD
To view the table and figures
that correspond to this article, please refer to the print
version of our November/December 2002 issue, page 44.
As the prevalence of endovascular aneurysm repair (EVAR)
increases, so does our understanding of the benefits and
limitations of this technology. Initial clinical trials
have reported high success rates for endovascular exclusion
of AAAs,1-4 but problems detected during follow-up care
leave the long-term durability and success of this treatment
yet to be determined.5-7 A recent review of ruptures after
endograft placement for AAA exclusion noted that 44 out
of 47 known ruptures showed previous evidence of an endoleak
(the persistence of blood flow around the endograft within
the aneurysm sac).8 White et al originally classified
endoleaks,9 and this classification system has recently
been updated (Table 1).10
TO TREAT OR
NOT TO TREAT?
The presence of an endoleak can expose an aneurysm sac
to systemic arterial pressure after EVAR.11,12 This persistence
of pressure (or reintroduction of pressure after the sac
has collapsed, in the case of late endoleaks) may be the
cause of endoleak-related rupture. However, most endoleaks
found in early follow-up do not lead to rupture, and the
presence of an endoleak is not a predictor of mortality.3
A great deal of controversy persists regarding the most
appropriate diagnostic and treatment modalities for an
endoleak from various endografts. Between 20% and 40%
of patients undergoing EVAR experience an endoleak at
some point after endograft deployment.4,11,13 Consequently,
the detection and treatment of endoleaks has become a
major consideration in endovascular surgery.
Most surgeons agree that patients should be evaluated
with a high-quality CT scan using intravenous contrast
within 1 month after EVAR, and then again at 6 months
if there are any problems detected at the first postprocedure
scan. If no problems are detected, future scans can be
performed on a yearly basis. The following summary provides
information on the various types of endoleaks, with evaluation
and treatment recommendations for each type.
TYPE I: SEAL
FAILURE
A type I endoleak comprises a failure to seal the attachment
sites of the endograft to the native vessels. These are
widely recognized as the endoleaks most closely linked
to rupture and are the most aggressively treated.8,13
Type I endoleaks can occur at proximal or distal attachment
sites, and have been correlated to short aneurysm neck,
large vessel diameter, aneurysm neck angulation, and tortuosity
of the iliac arteries.14,15
Type I Endoleak in Unsupported Grafts
The characteristics of a type I endoleak vary by the type
of endograft involved; subsequent treatment should be
individualized with the particular device in mind. For
example, proximal (type IA) endoleaks detected intraprocedurally
with the Ancure endograft seem to have a more benign clinical
course than others.16 A review of cases at the University
of Pittsburgh showed that 7% of patients who underwent
EVAR with Ancure grafts had an intraprocedural proximal
endoleak after graft deployment and ballooning of the
attachment site. At 1-month follow-up, a CT scan showed
resolution of 82% of these leaks. The subsequent clinical
outcome of these patients is essentially the same as those
who never had a proximal endoleak. Figures 1 and 2 demonstrate
an intraprocedural type IA endoleak and its spontaneous
resolution on the 1-month follow-up CT scan.
The Ancure graft has a proximal low radial force and a
sharp change in compliance between the attachment system
and the unsupported graft. This combination of features
may make the graft vulnerable to early endoleaks that
resolve subsequently during remodeling of the proximal
attachment site. Therefore, we feel comfortable observing
small type IA leaks around Ancure grafts for at least
1 month after placement; if there is no sac enlargement,
we continue the observation for 6 months. If a leak is
still present at 6 months, the physician should investigate
the problem angiographically and provide treatment.
Unsupported grafts do not demonstrate the same pattern
of spontaneous resolution of distal (type IB) endoleaks.
Many early Ancure ruptures were linked to type IB endoleaks
seen with first-generation tube grafts.8 Due in part to
this problem, bifurcated or monoiliac grafts are now the
standard of care. It is imperative to create an adequate
distal seal between the graft and iliac artery; type IB
endoleaks can be a persistent problem with unsupported
grafts, and the majority require reintervention.11 Late
endoleaks can occur at the distal attachment site when
the length of the seal is short. We have recently encountered
two patients at 4 and 5 years post-EVAR with late type
IB endoleaks in aorto-monoiliac devices; these leaks resulted
in rupture. Many distal endoleaks can be avoided by selecting
patients with suitable iliac anatomy or by placing limb
extenders at the time of EVAR deployment. If the interventionalist
finds a type IB endoleak at the time of deployment of
an unsupported graft, it should be treated at that point.
Coils have been successfully used to obliterate the space
between a vessel wall and graft, but this strategy is
primarily used for type II endoleaks.
Type I Endoleak in Supported
Grafts
Fully supported grafts such as the AneuRx (Medtronic,
Minneapolis, MN) and the Excluder (W.L. Gore and Associates,
Flagstaff, AZ) perform differently than nonsupported grafts
when associated with type I endoleaks. Type IA endoleaks
seen in this setting rarely exhibit spontaneous resolution
and may lead to rupture.8 Therefore, these should be treated
at the time of implantation. Treatment of type IA endoleaks
most often involves ballooning the site; if a leak persists,
additional stents or extension cuffs can be deployed over
the attachment areas. Type IB endoleaks in fully supported
grafts are generally easily treated with modular extensions.
Any type I endoleak that arises during follow-up of a
previously excluded AAA is probably due to aneurysm remodeling
and possible graft kinking with a loss of seal between
the graft and vessel. These endoleaks should be promptly
treated.
TYPE II: RETROGRADE
FLOW
Type II endoleaks are a result of retrograde flow from
small arteries such as the lumbars or the inferior mesenteric
artery (IMA). Detection of a type II endoleak is accomplished
by routine duplex ultrasound, but is more commonly performed
by CT scanning. Both methods have some disadvantages;
however, the most serious problem is related to CT scanning.
The timing of contrast injection during the CT scan will
determine whether a type II endoleak is visible. Due to
the nature of retrograde flow, these can be very low-flow
systems. Delayed films may be necessary to assess late
perfusion within the sac and should be performed with
any suspicion of type II endoleak.
Interventionalists debate the significance of type II
endoleaks, as many of these leaks will spontaneously resolve,
regardless of graft type. Additionally, some patients
will demonstrate stability or even shrinkage of the aneurysm
sac in the presence of a patent type II endoleak.17 Current
treatment of type II endoleaks is based on the behavior
of the aneurysm sac, most of which can be safely observed
for 6 months. However, if the sac expands during this
time or at a later date, there is little doubt that the
patient should undergo angiography and treatment usually
in the form of embolization of feeding and draining vessels.
Figure 3 illustrates successful coil embolization of a
type II leak. Occasionally, a presumed type II endoleak
is actually noted at angiography as a type I requiring
prompt treatment.11
More controversy surrounds the best course of action when
a type II endoleak is detected without an increase in
sac size during follow-up. I favor an aggressive approach
to treating all persistent endoleaks at 6 months and would
consider further conservative treatment only when a type
II endoleak is difficult to treat and the aneurysm sac
is shrinking in size. The lessons learned through patients
lost to follow-up and returning with rupture are difficult
to ignore.
It is important to remember, however, that most type II
endoleaks have a benign course and aggressive treatment
should not involve excessive patient morbidity. In this
setting, successful embolization performed via transarterial
or translumbar techniques can be technically demanding,
and should not be attempted by a beginning interventionalist.
A recent comparison of the two techniques found that a
significantly higher percentage of the translumbar embolizations
resulted in durable exclusion of perigraft flow.18
There has been an interest in pre-EVAR embolization of
patent lumbar arteries and IMA in an effort to prevent
type II endoleaks,19 and also in laparoscopic ligation
of patent lumbars and/or IMA.20 Currently, this is not
the standard of care and preprocedural ligation of potential
feeding vessels has not resulted in a significant decrease
in type II endoleaks.
As with type I endoleaks, the surgeon should promptly
evaluate and treat any new type II leak arising in a previously
excluded aneurysm sac, as these may be more serious endoleaks
appearing as type II. This is particularly important in
modular grafts that may develop late type III endoleaks.
TYPE III:
GRAFT DEFECT
Type III endoleaks arise from a defect within the graft.
This flaw can be a disjunction between modular components
(type IIIA), or a hole in the fabric of the graft (type
IIIB). Type III endoleaks are very graft-specific and
can be serious because they are invariably associated
with a sudden elevation of intrasac pressure.
All type III defects should be repaired as soon as they
are detected. The interventionalist can successfully correct
most of these defects with a modular extension or covered
stent.
TYPE IV: FABRIC
POROSITY
Type IV endoleaks are caused by fabric porosity and subside
within 30 days. No specific treatment is necessary.
No Demonstrable Endoleak
Occasionally, the patient's aneurysm sac will increase
in size without a demonstrable endoleak. If the aneurysm
is large and the increase in sac size is significant (>5
mm), the physician should perform an angiographic evaluation.
An endoleak detected on angiography should be treated.
Difficulty arises when no endoleak can be found on either
CT scan or angiogram, and the aneurysm sac continues to
expand. At this point, the physician can assume that the
aneurysm is pressurized either from an unapparent endoleak
or from endotension.
The term endotension was initially coined to refer to
continued pressure within an aneurysm sac, with or without
demonstrable flow. This term, however, has now evolved
to mainly represent the concept of a pressurized aneurysm
sac without apparent endoleak. Possible sources of this
pressure include transmission through clots from side
branches, attachment sites, or porosity of ultrafine graft
fabric.21 Although most leading endovascular surgeons
agree that an embolized or spontaneously thrombosed endoleak
is no longer problematic,10 the true nature and clinical
consequence of endotension is unknown. In this situation,
the interventionalist should consider performing a second
endograft within the first, or converting to open surgical
repair.
ENDOLEAKS ARE
HERE TO STAY
Endoleaks are intrinsic to EVAR and require clear methods
of evaluation and treatment. CT scans should be performed
shortly after EVAR, and then yearly if there are no abnormalities
detected. Any abnormalities (including sac expansion)
demand intensive investigation. From the first mention
of EVAR as a treatment option, physicians should clearly
explain to patients the need for frequent evaluation and
the possibility of further intervention.
RECOMMENDED
TREATMENTS
Type IA endoleaks should be repaired
in the operating room if fully supported grafts are used.
Unsupported (Ancure) grafts have a high rate of spontaneous
closure of type IA endoleaks and can be observed for up
to 6 months if no sac expansion is noted. Type IB leaks
should be repaired at the time of detection.
Type II endoleaks noted on the first
postoperative CT scan can be safely observed for 6 months
if there is no sac expansion. Further observation is appropriate
only in the presence of sac shrinkage.
Type III endoleaks are seen with modular
grafts and should be treated at the time of detection.
Ellen D. Dillavou, MD, is a Vascular Fellow at the
University of Pittsburgh in Pittsburgh, Pennsylvania.
Dr. Dillavou may be reached at (412) 648-8420; dillavoued@msx.upmc.edu.
Navyash Gupta, MD, is Assistant Professor at the University
of Pittsburgh in Pittsburgh, Pennsylvania. Dr. Gupta may
be reached at (412) 648-9012; guptany@msx.upmc.edu.
Michel S. Makaroun, MD, is Professor and Chief in the
Division of Vascular Surgery and Director of Endovascular
Surgery at the University of Pittsburgh in Pittsburgh,
Pennsylvania. Dr. Makaroun may be reached at (412) 648-9015;
makarounms@msx.upmc.edu.
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