Answer: Endoleak
The CT scan depicts an endoleak, which is persistent filling of contrast into the aneurysm sac after stent graft exclusion. They are classified into 5 types. Type I refers to a leak across the seal zone either proximally or distally. Type I leaks are usually seen at placement or years later after migration of the proximal attachment. If seen during initial placement, they should be treated prior to terminating the operation because they rarely spontaneously resolve.
Type II endoleaks are due to retrograde flow through branch vessels, which are either lumbar arteries or the inferior mesenteric artery (IMA). They occur in approximately 20% of patients after endovascular stent graft repair of abdominal aortic aneurysm.1 Type II endoleaks are typically followed with serial CT scans, and many are seen to close spontaneously. Some surgeons will treat if the endoleak persists for greater than 6 months, some will treat for growth in the aneurysm sac, and others require both. The treatment goal is to close the endoleak allowing complete exclusion of the aneurysm sac. Options for nonsurgical treatment include embolization using coils or fibrin glue by a transarterial or translumbar approach. Surgical options range from a laparoscopically placed clip to conversion to an open vascular repair.
Type III endoleaks are secondary to leakage between the modular components or between the main body and the docking limb of a stent graft. Like type I endoleaks, these either occur early or late. If detected at the time of the procedure, typically further angioplasty is needed to form a seal. If detected late, it is usually due to material fatigue and then fracture of the stent or suture breakdown. Late type III endoleaks require additional cuff or limb placement, sometimes requiring placement of an aortouniliac device within the original stent graft with a femoral-femoral crossover graft.
Type IV endoleaks are caused by graft porosity. Very frequently this is seen on completion arteriogram at the time of placement due to transgraft migration of contrast. Type IV endoleaks do not require therapy because they resolve when the heparinization from the operation is allowed to reverse.
Type V endoleak was originally used to describe an aneurysm sac that was growing in size secondary to endotension—or persistent systemic pressurization of the sac—but a discrete cause could not be found.
Our patient was found to have a type II endoleak from his IMA on his first postoperative CT scan. This was followed with serial CT scans. Two years after endograft placement, a repeat CT scan was performed, which showed a persistent type II endoleak with a slight increase in sac size (Figure, A).
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Figure. Computed tomography of the abdomen and pelvis (A) and superior mesenteric artery arteriogram (B).
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The patient was then taken to the Interventional Radiology Suite where an abdominal aortogram was performed followed by selective catheterization of the superior mesenteric artery. The superior mesenteric artery arteriogram demonstrates a blush—contrast pooling in the midline aneurysm sac from retrograde filling of the IMA—which is by definition a type II endoleak (Figure, B). A microcatheter was then advanced through this collateral pathway to embolize the origin of the IMA using Tornado microcoils (Cook, Bloomington, Indiana), with follow-up arteriogram showing immediate technical success.
The initial technical success of transarterial embolization is 79% in patients where all sources can be accessed via collaterals.2 The question of whether pressure will still be transmitted across coils to increase endotension is currently not answered as long-term follow-up has not yet been reported.
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