Cath Lab Digest

author:
Frank J. Criado
Editor-in-Chief
Vascular Surgery and Endovascular Intervention; Union Memorial Hospital/MedStar Health,
Baltimore, Maryland
frank.criado@medstar.net

Endoleaks have been at the center of developments with endovascular aneurysm repair (EVAR) from the outset — even before the term had been coined.1 The definition is rather simple: persistent (or recurrent) blood-flow perfusion of the aneurysm sac after endograft implantation. Type I (stent-graft seal failure at a proximal or distal fixation site) and type III (from graft holes or modular component separation) are universally characterized as high-pressure, graft-related, and dangerous. Treatment (if possible) must be undertaken without delay. Type II endoleaks, on the other hand, have not been met with such clear understanding and consensus of opinion. They are quite common (10–25% of EVAR cases) and result from persistent patency of one or more endograft-excluded aortic branches (lumbar arteries, inferior mesenteric artery, and others) that continue to perfuse the aneurysm sac via retrograde blood flow. The nature and significance of such endoleaks remain the focus of considerable disagreement (if not controversy), with the main question relating to the real potential for aneurysm rupture (and death) when a type II endoleak fails to resolve.2

In the early days of EVAR (1990’s), the detection of an endoleak — any endoleak — was thought of as ‘treatment failure’. Such concepts changed with growing experience, and systematic review and analysis of patients over time.3 In this decade, the prevailing view has shifted steadily in the direction of considering type II endoleaks as largely benign, with the requirement for observation and follow up only, in most cases, reserving invasive intervention (or surgical conversion) for a very few, where risks of serious consequences seem higher.4 Endoleaks originating from inferior mesenteric or hypogastric arterial backflow may be in a slightly different category, and perhaps justify a more aggressive attitude.5 When indicated, endoleak intervention can be performed via a transarterial catheterization approach or with direct translumbar puncture of the sac. The latter has been increasingly favored in recent years, as has the use of liquid embolic agents. The article by Barge et al,5 appearing in this issue of VDM, is especially interesting in this regard.

While recognizing that we are still far from reaching consensus, or even a complete understanding, currently available evidence and a preponderance of expert opinion make the following observations safe and reasonable:

- Type II endoleaks occur frequently after EVAR, in up to 25–30% of patients;

- Type II endoleaks tend to be benign in nature, carrying little, if any, potential for aneurysm enlargement and rupture. As such, most patients require follow up and observation only;

- Diagnosis of a type II implies that a type I or III has been ruled out (through CT and conventional angiography). This is perhaps the most important aspect of endoleak management. Likewise, there must be an awareness that combinations of type II with a type I (or III) do occur at times, explaining why certain type IIs may seem to behave more like high-pressure leaks;

- Significant aneurysm sac enlargement (in the face of a persistent type II endoleak) is generally viewed as an indication for treatment; this is reasonable. But it must be pointed out also that sac enlargement alone may correlate little (if at all) with the risk of aneurysm-related mortality.