Management of endoleaks following endovascular aneurysm repair
John Rose1 and Robin Williams2
1Lead Clinician in Interventional Radiology and Head of
the Department of Clinical Radiology, Freeman Hospital,
Newcastle upon Tyne, UK
2Interventional Radiology Fellow, Freeman Hospital,
Newcastle upon Tyne, UK
Address for correspondence:
Dr Robin Williams
Freeman Hospital, High Heaton
Newcastle upon Tyne, NE7 7DN, UK
Tel: +44-(0)191-233-6161 Fax: +44-(0)191-213-1968
Email: Rob.Williams@nuth.nhs.uk
Abstract
The term endoleak was defined in 1996 as the persistent perfusion of the
aneurysm sac after endovascular aneurysm repair (EVAR) due to the incomplete
sealing or exclusion of the aneurysm sac or vessel segment. An endoleak
implies failure to exclude the aneurysm and the patient may be at continued
risk of aneurysm rupture. Treatment depends on the type, site and size
of the endoleak. Treatment of type I and type III endoleaks is mandatory,
while treatment of type II endoleaks is only necessary in the presence
of increasing aneurysm sac size. This article discusses the various options
for treatment that are available.
Introduction
The aim of aortic aneurysm repair is to exclude the aneurysm from the
systemic circulation. Endovascular aneurysm repair (EVAR) first came into
clinical use in the early 1990s [1]. In this procedure, the aneurysmal segment
of the aorta is relined with a covered stent graft, held in
place by radial force, friction and (in some devices) barbs. Figure 1
illustrates an example of a successful EVAR before (a) and after (b) the
procedure has taken place.
The term endoleak was defined in 1996 as the persistent
perfusion of the aneurysm sac after EVAR due to the incomplete sealing
or exclusion of the aneurysm sac or vessel segment [2]. An endoleak
implies failure to exclude the aneurysm and the patient may be at continued
risk of aneurysm rupture.
Classification and treatment
The classification of endoleaks is based upon the source of the inflow
into the aneurysm sac and may be proximal or distal. The initial definition
differentiated between four types of endoleak [3,4] but was expanded
in 1999 to include endotension (type V) [5].
There is evidence that endoleak and late rupture are linked. A review
of EUROSTAR data suggested that the presence of an endoleak can predict
rupture, since 69% of patients whose aneurysm ruptured following EVAR
had a pre-existing endoleak [6].
Type I endoleaks
These are caused by failure of the seal at the fixation points of either
the proximal graft (type IA) or the
distal graft (type IB). This may be a primary failure at initial deployment
or late failure due to graft migration.Treatment is mandatory because
the aneurysm sac is at systemic pressure. Untreated type I or III endoleaks
are at high risk of rupture and a rupture rate of 3.37% has been quoted [7].
The treatment requires satisfactory circumferential apposition
between the endoluminal surface of the vessel and the external aspect
of the stent-graft. Gentle expansion of the device with a compliant moulding
balloon will seal the majority of primary leaks. Occasionally, despite
prolonged moulding, the leak will persist. A giant Palmaz® stent may then be used to prevent recoil and encourage stent apposition
to the proximal neck. If this procedure fails, and the leak is significant,
a limited laparotomy will enable an external band to be placed around
the proximal neck, without opening the aneurysm sac.
Open conversion was
occasionally required in the past for very large endoleaks due to the
migration of home-made devices. If the endoleak is due to
graft malposition or moderate distal migration, the stent graft is extended
to increase the length of neck contact or the distal seal in the case
of a leaking limb. Hence,a proximal aortic cuff or a graft extension limb
may be required and these are generally oversized by 10-20% to prevent
further endoleaks.
Type II endoleaks
In this type of endoleak, one or more cavities are formed within the organised
thrombus inside the aneurysm sac, via retrograde flow through small aortic
side-branch vessels. The leak always communicates with another outflow
vessel and most commonly involves the inferior mesenteric artery (IMA),
lumbar or internal iliac arteries. These are the commonest endoleaks,
affecting up to 43% of cases [8]. They are associated with a low
(0.52%) risk of rupture [7] and a significant rate of spontaneous closure.
The current consensus is that treatment is required only for endoleaks
that persist for more than a year in an aneurysm of increasing size [9].
Intervention is usually by percutaneous embolisation, either
by a trans-arterial or a trans-lumbar route. The trans-arterial approach
requires catheterisation either of the IMA or a lower lumbar artery. These
are super-selected with a micro-catheter passed into the superior mesenteric
artery (SMA) or an ascending iliolumbar branch of the internal iliac artery,
respectively. Catheterisation of the aneurysm sac may occasionally be
possible by passing a catheter directly alongside the
stent graft limb from a trans-femoral approach. The trans-lumbar route
involves direct needle puncture of the cavity in the aneurysm sac under
CT or US guidance (Figure 2). After passage of a guidewire and catheter
under fluoroscopic control, the inflow and outflow vessels can be occluded
and the problematic cavity directly embolised. Many different embolic
materials have been used, including platinum coils, usually with an additional agent
such as thrombin or Gelfoam® .
Type III endoleaks
This type of endoleak is caused by structural failure of the stent-graft due to separation of the modular components of the graft (type IIIA) or a tear in the graft material (type IIIB). As in the case of type I endoleaks, type III leaks represent direct perfusion of the aneurysm sac at systemic pressure and have a relatively high rupture rate [7].
Primary type III endoleaks are readily apparent during the initial procedure but can be difficult to differentiate from a type I leak. They are usually caused by inadequate overlapping of the junctional sections of a modular stent-graft, but rarely there may be defects in the graft material.
Primary type IIIA leaks almost always resolve after balloon moulding of the junction(s). If there is insufficient overlap of the components then an additional component may be required. If the leak is from the main body of the graft or at the flow-divider, a second stent graft needs to be deployed within the first. Use of an aorto-mono-iliac device and a surgical fem-fem crossover helps reduce the total amount of graft material. If no suitable graft is available, open surgical conversion must be considered.
Delayed type III endoleaks were seen commonly in the first generation of devices. They are generally due to sac remodelling causing the graft components to separate or mechanical stress causing stent and fabric failure. They should be treated as primary type III leaks, accepting that there is a significant open conversion rate (Figure 3).
Type IV endoleaks
Type IV endoleaks are caused by porosity of the graft fabric during the primary procedure. They were reported almost exclusively with first-generation devices and were seen most commonly while the patient was anticoagulated. Rupture has not been reported.
Type V endoleaks
This type of endoleak is caused by continued expansion of the aneurysm sac in the absence of a visualised endoleak on conventional imaging. The term endotension has also been applied to this phenomenon [10], which is thought to reflect the continued pressurisation of the aneurysm sac. It is important to exclude the presence of a subtle endoleak by further investigation such as contrast enhanced ultrasound [11]. If found, these need to be treated as described previously.
In some cases, the expansion may be due to ultra-filtration through a first-generation ePTFE graft, resulting in the formation of a hygroma [12] or tiny endoleaks through suture holes in the graft material [13]. Sac expansion due to ultrafiltration of serous material can be left untreated even if rupture occurs. However, the inside of the endograft can be re-lined with a second device and open surgical conversion remains an important option.
Conclusion
The treatment used is selected according to the type of endoleak (Table 1). As a general rule, all endoleaks where the aneurysm sac is in direct communication with the systemic arterial circulation and other leaks causing aneurysm sac expansion should be treated. Endoleaks with no sac expansion or a reduction in sac size can be left untreated.
| Endovascular | Open surgery | |
| Type I | Moulding balloon angioplasty Giant Palmaz stent Stent-graft cuff/ extension |
External banding of aneurysm neck Surgical conversion |
| Type II |
Trans-arterial embolisation Trans-lumbar injection | 30% decrease |
| Type III | Angioplasty/ stenting of junctions Secondary graft placement |
Open conversion |
| Type V | Co-axial graft (re-lining) |
Evacuation of hygroma Open conversion |
| Table 1. Treatment of endoleaks. | ||
- Endoleaks are defined as persistent filling of the aneurysm sac after EVAR.
- Type I endoleaks indicate direct communication with the circulation and cannot be ignored. They require timely treatment, most often by the endovascular route.
- Type II endoleaks need only be treated if the aneurysm is increasing in size.
- Type IIIA endoleaks are extremely unusual with accurately deployed modern endograft. Holes in the graft are very rare but must be considered when other sources of endoleak have been discounted.
References
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Current and future developments in the endovascular repair of aortic aneurysms
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