Endoleaks are characterised by persistent blood flow within the aneurysm sac following endovascular aneurysm repair (EVAR). Normally the aortic stent-graft used for EVAR excludes the aneurysm from the circulation by providing a conduit for blood to bypass the sac.
An endoleak is a common complication of EVAR and is found in 30-40% of patients intraoperatively (seen on the on-table angiogram after stent deployment), and in 20-40% during follow-up. It has been referred to as the “Achilles heel” of the endovascular approach to aneurysm treatment. Some endoleaks seem to be unavoidable due to the presence of pre-existing patent branch vessels arising from the aneurysm sac, whilst others occur as a result of poor patient/graft selection.
Endoleaks are often asymptomatic, however as flow within the aneurysm sac is at systemic or near- systemic pressure, if untreated, the aneurysm may expand and is at risk of rupture. As such aneurysm expansion following EVAR always warrants investigation for endoleak.
Endoleak may become evident intra-operatively, years down the track, or anywhere in between. Therefore lifelong imaging surveillance is necessary. This is usually performed with CT angiography.
There are several causes of endoleak and can be classified into five types as follows:
type I: leak at graft attachment attachment site
- Ia: proximal
- Ib: distal
- Ic: iliac occluder
type II: aneurysm sac filling via branch vessel (most common)
- IIa: single vessel
- IIb: two vessels or more
type III: leak through defect in graft
- IIIa: junctional separation of the modular components
- IIIb: fractures or holes involving the endograft
- type IV: leak through graft fabric as a result of graft porosity.
- type V: continued expansion of aneurysm sac without demonstrable leak on imaging (endotension)
Type I endoleaks occur as a result of an inadequate seal at the site of the graft attachment. It may occur at the proximal end, distal end or where the components overlap. Blood flow leaks alongside the graft into the aneurysm sac. It occurs in as many as 10% of cases. They are often the result of unsuitable patient (aneurysm) selection or device selection, but can also occur if the graft migrates. Type I leaks are always considered significant as they do not tend to resolve spontaneously.
Type II endoleaks are the most common after an abodminal aortic repair 5, accounting for 80% of cases. Retrograde flow though branch vessels continue to fill the aneurysm sac. The most common culprit vessels are lumbar arteries, inferior mesenteric artery or internal iliac artery. This type of leak has been reported in up to 25% of cases. It usually resolves spontaneously over time and requires no treatment. Embolisation of the branch vessel is indicated if the aneurysm sac continues to expand in size.
Type III endoleaks are caused by mechanical failure of the stent-graft. There may be a fracture of the stent-graft, hole or defect on the graft fabric, or junctional separation of the modular components. Causes may relate to defective device material, extreme angulation of a segment predisposing to fracture, or improper overlap of the modular components during insertion.
Type IV endoleaks occur when blood leaks across the graft due to its porosity. It does not require any treatment and typically resolves within a few days of graft placement.
Type V “leak” (also referred to as endotension) is not a true leak but is defined as continued expansion of the aneurysm sac without evidence of a leak site. It is also referred to as endotension. It is a poorly understood phenomenon but is believed to be due to pulsation of the graft wall with transmission of the pulse wave through the perigraft space (aneurysm sac) to the native aneurysm wall.
Endoleak is seen on CT angiography (most common modality for follow up and investigation of potential endoleaks), MR angriography and DSA as contrast opacification of the aneurysm sac outside the graft. Flow in the sac may also be detected on ultrasound.
The key to accurate diagnosis and evaluation of a suspected endoleak is multiphase imaging (typically three-phase: non-contrast, arterial phase and delayed phase). Non-contrast is necessary to establish a base line of density within the (hopefully) thrombosed sack, presence of calcification can mimic contrast.
Contrast may be seen as a focal region of enlarging increased density or a more generalized increase in the density of the sac, in cases where most of the sac has not thrombosed. This may require placement of a ROI to measure density.
Treatment and prognosis
Treatment depends on the type of endoleak:
Type I leaks (above, below of between graft components) are generally treated as soon as detected. Extension cuffs or covered stents can be inserted at the leaking graft end to improve the seal, or embolisation of the leak site with glue or coils can be used. Rarely, if detected intra-operatively during EVAR, conversion to an open procedure may be required if endovascular methods of sealing the leak are unsuccessful.
Type II leaks (retrograde flow through branch) usually spontaneously thrombose. As such at many institutions these leaks are not treated immediately; watchful waiting is employed and if the leak persists it is treated by embolising the branch vessel with glue or coils. Pre-emptive embolisation of potential sources of collateral flow is sometimes performed prior to stent-graft insertion, particularly the internal iliac artery in select cases. Pre-emptive embolisation of other branch vessels is controversial.
Type III leaks (graft mechanical failure) do not spontaneously resolve and are therefore treated immediately, usually with additional stent-graft components.
Type IV leaks (graft porosity) require no treatment.
Type V leaks (endotension) are controversial but when continued growth of the aneurysm sack is demonstrated further treatment with additional endoluminal components (cuffs or extensions) may be successful 3. Alternatively, conversion to an open repair may be necessary 4.
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