Type II Endoleaks After EVAR

Do stable type II endoleaks require treatment after EVAR?

By Richard A. Baum, MD

CEndovascular repair has significantly altered the way patients with aneurysms are identified, classified, and treated. As with other interventions, postoperative surveillance is an important way to maximize long-term outcome. After endovascular aneurysm repair (EVAR), patients undergo routine postoperative CT scanning at regular intervals to check the status of the aneurysm sac and to ensure the continuing integrity of the endograft. An aneurysm sac that is shrinking without flow between the stent graft and the aneurysm wall is a hallmark of a successful repair.

Flow identified within the aneurysm sac (endoleaks) can represent a failure of the attachment sites (type I) or device (type III). There is general agreement that these failure modes necessitate urgent repair because blood flow and systemic pressure will continue to be transmitted into the aneurysm sac, putting the patient at continued risk for aneurysm enlargement and rupture.1,2 An additional way that flow can enter the aneurysm sac after endograft placement is through aortic branch vessels (type II endoleaks). The diagnosis, treatment, and significance of type II endoleaks continues to generate lively discussion a decade after the introduction of EVAR.

There are three essential independent questions that must be answered in every patient that has been treated with a stent graft.

What Is the Status of the Size/Volume of the Aneurysm?
The purpose of EVAR is to prevent aneurysm rupture. This is why it is critical to monitor the status of the aneurysm sac after repair. This is most often done with axial CT scanning. Recently, volumetric analysis comparing preoperative and postoperative CT imaging has proven to be useful in following these patients. Because postendograft aneurysms change configuration in longitudinal as well as axial dimensions, volumetric analysis may provide a more sensitive method for determining whether an aneurysm is enlarging, shrinking, or remaining stable.

Has the Stent Graft Migrated?
It is important to determine whether the stent graft is in the same position that you left it in the operating room. Migration and device failure can occur without the presence of an endoleak or any other signs or symptoms. A fracture of a hook or barb at a proximal attachment site, for example, could eventually lead to proximal migration. Identifying these problems early may prevent catastrophic failures.

Is There an Endoleak?
Failures at attachment sites and the graft itself can manifest themselves as endoleaks. These failures require immediate attention and repair. Collateral endoleaks can have a benign self-limiting course or can lead to aneurysm enlargement and rupture.

The diagnostic accuracy of CTA for the presence or absence of endoleaks is high. Unfortunately, the same cannot be said regarding endoleak classification. CT angiography is extremely sensitive for the presence or absence of endoleaks but lacks the specificity to determine the origin of an endoleak, which is critical for proper classification.3 This is because CTA produces static images, making it impossible to determine which vessels serve as endoleak ingress and egress. Just because an endoleak cavity is in continuity with a lumbar or inferior mesenteric artery does not indicate a collateral endoleak. It is important to remember that all endoleaks, regardless of type, can have lumbar and/or inferior mesenteric artery egress. For this reason, ultrasound may prove a better tool to classify endoleaks once they are diagnosed on CTA.4-6

Because the significance and treatment options depend on endoleak type, it is critical to separate types I and III endoleaks from type II endoleaks. Because CTA cannot accurately distinguish between these types, it is recommended that all patients demonstrating an endoleak at 30 days should undergo contrast angiography or ultrasound examination to determine the etiology of the leak to classify it.

Once there is confirmation that an endoleak is from collateral vessels (type II), the next step is to determine when to intervene. It is clear that if left alone, some type II endoleaks will thrombose spontaneously. Some endoleaks will persist, leading to aneurysm enlargement and rupture. A very useful time-point to help make this decision is the 6-month CT scan. If the endoleak continues to be present on the 6-month scan, there is very little likelihood that it will spontaneously thrombose.7 Because of this, many interventionalists choose to intervene if a type II endoleak is present on the 6-month scan regardless of the status of an aneurysm sac. Others will avoid treating type II endoleaks as long as there is no evidence of sac enlargement. There is little debate regarding treatment of type II endoleaks in the setting of an enlarging aneurysm sac.

Once a decision has been made to treat a patient with a type II endoleak, there are several treatment options available.8 One approach is to embolize the artery feeding the endoleak cavity by a transarterial route (eg, the femoral artery). This technique has proved ineffective, providing only short-term response. Endoleaks treated in this fashion will recur by recruiting additional aortic branch vessels. In this way, endoleaks are very similar to vascular malformations and represent dynamic structures that change feeding and draining blood supply frequently.

Several years ago, a technique was introduced in which the endoleak cavity itself was entered directly through a translumbar needle stick.9,10 Embolization coils and glue (Trufill, Cordis Corporation, a Johnson & Johnson company, Miami, FL) are used to completely thrombose the endoleak cavity. This technique differs significantly from the transarterial embolization; instead of treating feeding vessels, the endoleaks themselves are being embolized. With the translumbar technique, the connection between ingress and egress vessels, as well as the endoleak cavity, is destroyed. Again, this is very similar to how vascular malformations are treated. The endoleak cavity acts as a ?nidus,? and thrombosing this nidus is what provides a successful and durable response.

Translumbar Endoleak Embolization Technique
The patient is placed in the prone position on a fluoroscopy table. After review of the CT images, a left-sided or right-sided approach is made.9 Angles, depth of penetration, and distance from the midline are all determined from the CT scan. A small skin incision is made, and the aneurysm sac is punctured using a translumbar needle/sheath system. The needle is advanced from the skin to a vertebral body. It is then slowly advanced anteriorly along the bone, eventually entering the aneurysm sac. The entry of the needle into the aneurysm sac is transmitted through the needle because the aneurysm wall is usually calcified. Care must be taken to avoid the transverse processes of the spine because this can deflect the needle, making access to the aneurysm sac impossible. A right-sided translumbar approach is also possible through the inferior vena cava (Figure 1).

Once in the sac, the needle is advanced slowly, using both anteroposterior and lateral fluoroscopic views to position the needle in the endoleak cavity. It is very important that the tip of the needle-sheath system reside in the endoleak cavity. This is generally signaled by rapid pulsatile blood flow through the end of the catheter. At this point, a confirmatory angiogram is obtained in the endoleak cavity by injecting 10 mL of contrast material. This will show the entire endoleak cavity, as well as the ingress and egress vessels. Pressure measurements should be obtained at this point to serve as a baseline for the embolization procedure.

The endoleak cavity is then embolized using a mixture of embolization coils and glue. The combination of glue and coils is desirable because it would take dozens of coils to completely thrombose an endoleak cavity, and glue alone could migrate down the lumbar vessels causing neurologic injury. With a coil/glue combination, coils are first used to slow the flow in the endoleak cavity. The glue is then used to completely thrombose the cavity and the proximal ingress and egress vessels.

There are two morphologic types of endoleaks identified using direct endoleak angiography. The first has a small cavity and has ingress and egress from a single vessel. An example of this would be an inferior mesenteric artery simple type II endoleak. Blood travels during systole into the endoleak cavity, swirling around, and leaving the endoleak cavity during diastole. The physiology of this endoleak cavity is very similar to that of a pseudo-aneurysm. Many of these ?simple? collateral endoleaks will spontaneously thrombose prior to the 6-month CT scan. The more common type of type II endoleaks is characterized as ?complex.? These endoleak cavities have multiple ingress and egress vessels, and behave like arteriovenous malformations and can easily recruit and redirect blood flow through additional aortic branch vessels. It is this type of collateral endoleaks that persists longer than 6 months.

The significance and treatment of type II endoleaks has been debated for nearly a decade. As our knowledge of type II endoleaks has increased, the areas of disagreement among experts are now minimal. The presence of a type II endoleak in the setting of an enlarging aneurysm sac seen on a 6-month CT scan is an indication for treatment. An endoleak that is present in the setting of a shrinking aneurysm sac does not need to be treated. The only disagreement that currently exists is whether to treat a type II endoleak in the setting of an aneurysm sac that is neither enlarging nor shrinking. Learning more about these “stable” aneurysm sacs and the role that endoleaks play in aneurysm sac physiology are crucial to determining the significance of these types of leaks and which patients should undergo treatment. 

Richard A. Baum, MD, is the Herbert L. Abrams Director of Interventional Radiology at the Brigham & Women’s Hospital, Boston, Massachusetts. He holds no financial interest in any product or manufacturer mentioned herein. Dr. Baum may be reached at (617) 732-7263; rbaum@partners.org.

1. Veith FJ, Baum RA, Ohki T, et al. Nature and significance of endoleaks and endotension: summary of opinions expressed at an international conference. J Vasc Surg. 2002;35:1029-1035.
2. Veith FJ, Baum RA. Endoleak and Endotension: Current Consensus on Their Nature and Signifacance. New York: Marcel Dekker; 2002.
3. Stavropoulos SW, Carpenter JP, Fairman RM, et al. Can CTA be utilized to classify endoleaks? J Vasc Surg. (in press).
4. Garret HE, Jr., Abdullah AH, Hodgkiss TD, et al. Intravascular ultrasound aids in the performance of endovascular repair of abdominal aortic aneurysm. J Vasc Surg. 2003;37:615-618.
5. von Segesser LK, Marty B, Ruchat P, et al. Routine use of intravascular ultrasound for endovascular aneurysm repair: angiography is not necessary. Eur J Vasc Endovasc Surg. 2002;23:537-542.
6. Sato DT, Goff CD, Gregory RT, et al. Endoleak after aortic stent graft repair: diagnosis by color duplex ultrasound scan versus computed tomography scan. J Vasc Surg. 1998;28:657-663.
7. Makaroun M, Zajko A, Sugimoto H, et al. Fate of endoleaks after endoluminal repair of abdominal aortic aneurysms with the EVT device. Eur J Vasc Endovasc Surg. 1999;18:185-190.
8. Baum RA, Carpenter JP, Golden MA, et al. Treatment of type 2 endoleaks after endovascular repair of abdominal aortic aneurysms: comparison of transarterial and translumbar techniques. J Vasc Surg. 2002;35:23-29.
9. Baum RA, Cope C, Fairman RM, et al. Translumbar embolization of type 2 endoleaks after endovascular repair of abdominal aortic aneurysms. J Vasc Intervent Radiol. 2001;12:111-116.
10. Baum RA, Carpenter JP, Stavropoulous SW, et al. Diagnosis and management of type 2 endoleaks after endovascular aneurysm repair. Tech Vasc Intervent Radiol. 2001;4:222-226.


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