Point-Counterpoint: Type II Endoleaks - To treat or not to treat

The management of Type II endoleaks remains controversial. At the Charing Cross meeting this year Jean- Pierre Becquemin and Hence Vehagen debated whether Type II endoleaks should be treated. Dr. Verhagen suggested that results of endoleak treatment are so poor and the natural history of Type II endoleaks so benign that perhaps we shouldn’t even try to treat them. Dr. Becquemin felt that an attempt at treatment for some endoleaks was still necessary. This prompted our editors to suggest a U.S. version of the debate. As you will see both Dr. Geraghty and Dr. Kwolek feel that there is merit in pursuing treatment but with certain caveats. We appreciate their insight into this important subject.

– Dr. Russell Samson is the medical editor of Vascular Specialist.

A slow start can be salvaged

Our group recently published the midterm outcomes of our series of percutaneous glue and /or coil embolizations to treat type II endoleaks (T2EL) accompanied by continued aneurysm sac growth.¹ Painstaking retrospective data collection, augmented by blinded review of all follow-up CT scans, demonstrated that at 23 months post intervention, T2EL had persisted or recurred in 72% of patients. Furthermore, the rate of aneurysm sac growth was not altered by the percutaneous intervention.

Other institutions have also reported significant rates of T2EL persistence/recurrence following embolization, and in the Cleveland Clinic experience, continued sac growth in excess of 5 mm in diameter was documented in 56% of patients who had undergone an attempt at T2EL ablation.^2-4 In light of this data, one might logically question why I continue to support intervention in this setting.

The midterm reappraisals of T2EL interventions are certainly sobering. We can no longer accept apparent procedural success as a guarantee that these endoleaks will remain clinically and radiographically dormant. Yet these studies were not without their bright spots. In our series, diagnostic angiography (via transfemoral and translumbar approaches) detected occult type I or type III endoleaks in 21% of patients, prompting definitive repair by additional endograft placement. Similar angiographic elucidation of type I and III endoleaks was confirmed by the University of Chicago experience, with a 16% detection rate.² The diagnosis and treatment of these highly pressurized leaks likely contributed to the low incidence of aneurysm rupture and aneurysm-related mortality seen in most of these series.

Bright spots aside, current midterm results for T2EL intervention leave much to be desired. I would contend, however, that these interventions should be refined, not abandoned. We now appreciate that T2EL mimic the behavior of complex arteriovenous malformations in several ways: the presence of multiple feeding and draining branches, the finding that solitary branch vessel embolization often leads to inflow recruitment from less prominent branches, and the presence of a nidus whose ablation is critical. In retrospect, then, it is not surprising that treatment approaches consisting of single-vessel coiling, or simple embolization of the nidus without concomitant treatment of all feeding branches, failed to produce the desired result. The aggressiveness of early T2EL embolization procedures may have been tempered by the potential for visceral and spinal cord complications.^5,6 However, current midterm outcomes data suggest that predictable and durable success in T2EL treatment will require complete nidus ablation and occlusion of all arterial branches of the sac.

How can we pursue this more aggressive goal while maintaining an appropriate safety profile? In several instances, we have pursued this objective via staged interventions: initial angiographic coil/glue deployment, followed by laparoscopic clipping of persistent feeding vessels. The use of Onyx^® (EV3-Covidien), as championed by Abularrage and Bosiers,^7,8 offers the potential to achieve full treatment with a single intervention.

Advantages of Onyx include predictable polymerization times and lack of adhesion to the delivery catheter. These features permit deliberate and complete obliteration of the nidus, with intentional extension of the polymerizing mixture into the feeding vessels.

T2EL intervention has thus completed its first iteration. The value of routine angiographic examination is clear, particularly as regards the detection of occult type I and III endoleaks. Failure analysis of first-generation T2EL interventions suggests that incomplete obliteration of the endoleak complex (nidus and all feeding branches) sets the stage for vessel recruitment and reestablishment of sac flow. Promising alternative therapies have been identified, and we await their thorough evaluation.

Dr. Geraghty is an associate professor, surgery and radiology, in the division of general surgery, vascular surgery section at Washington University School of Medicine, St. Louis, Mo., and co-director of the Washington University Limb Preservation Center.

1. J Vasc Surg, 2012. 55(5): p. 1263-7.

2. J Vasc Interv Radiol, 2012. 23(7): p. 866-72; quiz 872.

3. J Endovasc Ther, 2012. 19(2): p. 182-92.

4. J Vasc Surg, 2012. 55(1): p. 33-40.

5. Ann Vasc Surg, 2012. 26(6): p. 860 e1-7.

6. J Vasc Interv Radiol, 2013. 24(1): p. 49-55.

7. J Vasc Surg, 2012. 56(3): p. 630-6.

8. J Cardiovasc Surg (Torino), 2013.

A call for a prospective randomized trial

While I agree with Dr. Geraghty’s comments concerning the initial poor results reported for the percutaneous treatment of Type II endoleaks,¹ I disagree with comments made in April 2013 at the Charing Cross meeting by Dr. Hence Verhagen that there is "no need to worry about Type II endoleaks since they are low pressure."²

Early on in our experience we began measuring sac pressures after trans- lumbar catheterization and have found that some aneurysm sacs may in fact have systolic arterial pressures of 8-90 mm HG from large lumbar or IMA collaterals. Furthermore, we and others have described the treatment of patients with ruptured AAA after EVAR who upon open exploration where found to have large patent lumbar arteries as the sole etiology of the ruptured AAA.

Dr. Geraghty and Dr. Sarac at Cleveland Clinic have also described the important observation that these Type II endoleaks may be associated with a Type I or III endoleaks and thus put patients at even higher risk of rupture.³ The extent of these leaks may not be completely elucidated until the time of angiography, again emphasizing the importance of a more aggressive approach to diagnosis and treatment in patients with an enlarging aneurysm sac.

These authors have also appropriately pointed out that overall treatment success rates are low with persistence of type II endoleaks on long–term follow-up. While we initially described an overall success rate of 30%, our approach has changed over time to include direct access to the endoleak nidus with the injection of a flow directed glue (Onyx) to obliterate the flow channel and feeding vessels.

We have found this approach to be more successful than attempting to cannulate each of the feeding lumbar vessels or coil embolization of the aneurysm sac, and can be performed via either a translumbar or transarterial approach using SMA to IMA collaterals. While our success rate using this technique has improved to nearly 80%, several words of caution should be noted. 1) Onyx glue is approved for use in the treatment of intracerebral vascular malformations and does not have a peripheral indication at this time. 2) It is critically important that the interventionalist obtains access into the nidus/flow channel to allow the embolic agent to flow. Otherwise you are injecting glue directly into the sac thrombus and wasting time and an expensive embolic agent. 3) There are often multiple levels of lumbar vessels involved and we have found that we often have to go back several times at different levels to treat extensive Type II endoleaks. All of these observations emphasize the need to further study the treatment of Type II endoleaks and the need for a prospective randomized trial to better identify the best treatment options.

Dr. Kwolek is the director of the vascular and endovascular training program at Massachusetts General Hospital, Boston, and the chief of vascular surgery at Newton Wellesley Hospital.

1. J Vasc Surg, 2012. 55(5): p. 1263-7.

2. Management of Type II endoleaks divides the experts at CX 35. Vascular News International,58, May 2012, BIBA publishing.

3. J Vasc Surg, 2012. 55(1): p. 33-40.

4. J Vasc Surg, 2012. 56(3): p. 630-6.

The management of Type II endoleaks remains controversial. At the Charing Cross meeting this year Jean- Pierre Becquemin and Hence Vehagen debated whether Type II endoleaks should be treated. Dr. Verhagen suggested that results of endoleak treatment are so poor and the natural history of Type II endoleaks so benign that perhaps we shouldn’t even try to treat them. Dr. Becquemin felt that an attempt at treatment for some endoleaks was still necessary. This prompted our editors to suggest a U.S. version of the debate. As you will see both Dr. Geraghty and Dr. Kwolek feel that there is merit in pursuing treatment but with certain caveats. We appreciate their insight into this important subject.

– Dr. Russell Samson is the medical editor of Vascular Specialist.

A slow start can be salvaged

Our group recently published the midterm outcomes of our series of percutaneous glue and /or coil embolizations to treat type II endoleaks (T2EL) accompanied by continued aneurysm sac growth.¹ Painstaking retrospective data collection, augmented by blinded review of all follow-up CT scans, demonstrated that at 23 months post intervention, T2EL had persisted or recurred in 72% of patients. Furthermore, the rate of aneurysm sac growth was not altered by the percutaneous intervention.

Other institutions have also reported significant rates of T2EL persistence/recurrence following embolization, and in the Cleveland Clinic experience, continued sac growth in excess of 5 mm in diameter was documented in 56% of patients who had undergone an attempt at T2EL ablation.^2-4 In light of this data, one might logically question why I continue to support intervention in this setting.

The midterm reappraisals of T2EL interventions are certainly sobering. We can no longer accept apparent procedural success as a guarantee that these endoleaks will remain clinically and radiographically dormant. Yet these studies were not without their bright spots. In our series, diagnostic angiography (via transfemoral and translumbar approaches) detected occult type I or type III endoleaks in 21% of patients, prompting definitive repair by additional endograft placement. Similar angiographic elucidation of type I and III endoleaks was confirmed by the University of Chicago experience, with a 16% detection rate.² The diagnosis and treatment of these highly pressurized leaks likely contributed to the low incidence of aneurysm rupture and aneurysm-related mortality seen in most of these series.

Bright spots aside, current midterm results for T2EL intervention leave much to be desired. I would contend, however, that these interventions should be refined, not abandoned. We now appreciate that T2EL mimic the behavior of complex arteriovenous malformations in several ways: the presence of multiple feeding and draining branches, the finding that solitary branch vessel embolization often leads to inflow recruitment from less prominent branches, and the presence of a nidus whose ablation is critical. In retrospect, then, it is not surprising that treatment approaches consisting of single-vessel coiling, or simple embolization of the nidus without concomitant treatment of all feeding branches, failed to produce the desired result. The aggressiveness of early T2EL embolization procedures may have been tempered by the potential for visceral and spinal cord complications.^5,6 However, current midterm outcomes data suggest that predictable and durable success in T2EL treatment will require complete nidus ablation and occlusion of all arterial branches of the sac.

How can we pursue this more aggressive goal while maintaining an appropriate safety profile? In several instances, we have pursued this objective via staged interventions: initial angiographic coil/glue deployment, followed by laparoscopic clipping of persistent feeding vessels. The use of Onyx^® (EV3-Covidien), as championed by Abularrage and Bosiers,^7,8 offers the potential to achieve full treatment with a single intervention.

Advantages of Onyx include predictable polymerization times and lack of adhesion to the delivery catheter. These features permit deliberate and complete obliteration of the nidus, with intentional extension of the polymerizing mixture into the feeding vessels.

T2EL intervention has thus completed its first iteration. The value of routine angiographic examination is clear, particularly as regards the detection of occult type I and III endoleaks. Failure analysis of first-generation T2EL interventions suggests that incomplete obliteration of the endoleak complex (nidus and all feeding branches) sets the stage for vessel recruitment and reestablishment of sac flow. Promising alternative therapies have been identified, and we await their thorough evaluation.

Dr. Geraghty is an associate professor, surgery and radiology, in the division of general surgery, vascular surgery section at Washington University School of Medicine, St. Louis, Mo., and co-director of the Washington University Limb Preservation Center.

1. J Vasc Surg, 2012. 55(5): p. 1263-7.

2. J Vasc Interv Radiol, 2012. 23(7): p. 866-72; quiz 872.

3. J Endovasc Ther, 2012. 19(2): p. 182-92.

4. J Vasc Surg, 2012. 55(1): p. 33-40.

5. Ann Vasc Surg, 2012. 26(6): p. 860 e1-7.

6. J Vasc Interv Radiol, 2013. 24(1): p. 49-55.

7. J Vasc Surg, 2012. 56(3): p. 630-6.

8. J Cardiovasc Surg (Torino), 2013.

A call for a prospective randomized trial

While I agree with Dr. Geraghty’s comments concerning the initial poor results reported for the percutaneous treatment of Type II endoleaks,¹ I disagree with comments made in April 2013 at the Charing Cross meeting by Dr. Hence Verhagen that there is "no need to worry about Type II endoleaks since they are low pressure."²

Early on in our experience we began measuring sac pressures after trans- lumbar catheterization and have found that some aneurysm sacs may in fact have systolic arterial pressures of 8-90 mm HG from large lumbar or IMA collaterals. Furthermore, we and others have described the treatment of patients with ruptured AAA after EVAR who upon open exploration where found to have large patent lumbar arteries as the sole etiology of the ruptured AAA.

Dr. Geraghty and Dr. Sarac at Cleveland Clinic have also described the important observation that these Type II endoleaks may be associated with a Type I or III endoleaks and thus put patients at even higher risk of rupture.³ The extent of these leaks may not be completely elucidated until the time of angiography, again emphasizing the importance of a more aggressive approach to diagnosis and treatment in patients with an enlarging aneurysm sac.

These authors have also appropriately pointed out that overall treatment success rates are low with persistence of type II endoleaks on long–term follow-up. While we initially described an overall success rate of 30%, our approach has changed over time to include direct access to the endoleak nidus with the injection of a flow directed glue (Onyx) to obliterate the flow channel and feeding vessels.

We have found this approach to be more successful than attempting to cannulate each of the feeding lumbar vessels or coil embolization of the aneurysm sac, and can be performed via either a translumbar or transarterial approach using SMA to IMA collaterals. While our success rate using this technique has improved to nearly 80%, several words of caution should be noted. 1) Onyx glue is approved for use in the treatment of intracerebral vascular malformations and does not have a peripheral indication at this time. 2) It is critically important that the interventionalist obtains access into the nidus/flow channel to allow the embolic agent to flow. Otherwise you are injecting glue directly into the sac thrombus and wasting time and an expensive embolic agent. 3) There are often multiple levels of lumbar vessels involved and we have found that we often have to go back several times at different levels to treat extensive Type II endoleaks. All of these observations emphasize the need to further study the treatment of Type II endoleaks and the need for a prospective randomized trial to better identify the best treatment options.

Dr. Kwolek is the director of the vascular and endovascular training program at Massachusetts General Hospital, Boston, and the chief of vascular surgery at Newton Wellesley Hospital.

1. J Vasc Surg, 2012. 55(5): p. 1263-7.

2. Management of Type II endoleaks divides the experts at CX 35. Vascular News International,58, May 2012, BIBA publishing.

3. J Vasc Surg, 2012. 55(1): p. 33-40.

4. J Vasc Surg, 2012. 56(3): p. 630-6.

The management of Type II endoleaks remains controversial. At the Charing Cross meeting this year Jean- Pierre Becquemin and Hence Vehagen debated whether Type II endoleaks should be treated. Dr. Verhagen suggested that results of endoleak treatment are so poor and the natural history of Type II endoleaks so benign that perhaps we shouldn’t even try to treat them. Dr. Becquemin felt that an attempt at treatment for some endoleaks was still necessary. This prompted our editors to suggest a U.S. version of the debate. As you will see both Dr. Geraghty and Dr. Kwolek feel that there is merit in pursuing treatment but with certain caveats. We appreciate their insight into this important subject.

– Dr. Russell Samson is the medical editor of Vascular Specialist.

A slow start can be salvaged

Our group recently published the midterm outcomes of our series of percutaneous glue and /or coil embolizations to treat type II endoleaks (T2EL) accompanied by continued aneurysm sac growth.¹ Painstaking retrospective data collection, augmented by blinded review of all follow-up CT scans, demonstrated that at 23 months post intervention, T2EL had persisted or recurred in 72% of patients. Furthermore, the rate of aneurysm sac growth was not altered by the percutaneous intervention.

Other institutions have also reported significant rates of T2EL persistence/recurrence following embolization, and in the Cleveland Clinic experience, continued sac growth in excess of 5 mm in diameter was documented in 56% of patients who had undergone an attempt at T2EL ablation.^2-4 In light of this data, one might logically question why I continue to support intervention in this setting.

The midterm reappraisals of T2EL interventions are certainly sobering. We can no longer accept apparent procedural success as a guarantee that these endoleaks will remain clinically and radiographically dormant. Yet these studies were not without their bright spots. In our series, diagnostic angiography (via transfemoral and translumbar approaches) detected occult type I or type III endoleaks in 21% of patients, prompting definitive repair by additional endograft placement. Similar angiographic elucidation of type I and III endoleaks was confirmed by the University of Chicago experience, with a 16% detection rate.² The diagnosis and treatment of these highly pressurized leaks likely contributed to the low incidence of aneurysm rupture and aneurysm-related mortality seen in most of these series.

Bright spots aside, current midterm results for T2EL intervention leave much to be desired. I would contend, however, that these interventions should be refined, not abandoned. We now appreciate that T2EL mimic the behavior of complex arteriovenous malformations in several ways: the presence of multiple feeding and draining branches, the finding that solitary branch vessel embolization often leads to inflow recruitment from less prominent branches, and the presence of a nidus whose ablation is critical. In retrospect, then, it is not surprising that treatment approaches consisting of single-vessel coiling, or simple embolization of the nidus without concomitant treatment of all feeding branches, failed to produce the desired result. The aggressiveness of early T2EL embolization procedures may have been tempered by the potential for visceral and spinal cord complications.^5,6 However, current midterm outcomes data suggest that predictable and durable success in T2EL treatment will require complete nidus ablation and occlusion of all arterial branches of the sac.

How can we pursue this more aggressive goal while maintaining an appropriate safety profile? In several instances, we have pursued this objective via staged interventions: initial angiographic coil/glue deployment, followed by laparoscopic clipping of persistent feeding vessels. The use of Onyx^® (EV3-Covidien), as championed by Abularrage and Bosiers,^7,8 offers the potential to achieve full treatment with a single intervention.

Advantages of Onyx include predictable polymerization times and lack of adhesion to the delivery catheter. These features permit deliberate and complete obliteration of the nidus, with intentional extension of the polymerizing mixture into the feeding vessels.

T2EL intervention has thus completed its first iteration. The value of routine angiographic examination is clear, particularly as regards the detection of occult type I and III endoleaks. Failure analysis of first-generation T2EL interventions suggests that incomplete obliteration of the endoleak complex (nidus and all feeding branches) sets the stage for vessel recruitment and reestablishment of sac flow. Promising alternative therapies have been identified, and we await their thorough evaluation.

Dr. Geraghty is an associate professor, surgery and radiology, in the division of general surgery, vascular surgery section at Washington University School of Medicine, St. Louis, Mo., and co-director of the Washington University Limb Preservation Center.

1. J Vasc Surg, 2012. 55(5): p. 1263-7.

2. J Vasc Interv Radiol, 2012. 23(7): p. 866-72; quiz 872.

3. J Endovasc Ther, 2012. 19(2): p. 182-92.

4. J Vasc Surg, 2012. 55(1): p. 33-40.

5. Ann Vasc Surg, 2012. 26(6): p. 860 e1-7.

6. J Vasc Interv Radiol, 2013. 24(1): p. 49-55.

7. J Vasc Surg, 2012. 56(3): p. 630-6.

8. J Cardiovasc Surg (Torino), 2013.

A call for a prospective randomized trial

While I agree with Dr. Geraghty’s comments concerning the initial poor results reported for the percutaneous treatment of Type II endoleaks,¹ I disagree with comments made in April 2013 at the Charing Cross meeting by Dr. Hence Verhagen that there is "no need to worry about Type II endoleaks since they are low pressure."²

Early on in our experience we began measuring sac pressures after trans- lumbar catheterization and have found that some aneurysm sacs may in fact have systolic arterial pressures of 8-90 mm HG from large lumbar or IMA collaterals. Furthermore, we and others have described the treatment of patients with ruptured AAA after EVAR who upon open exploration where found to have large patent lumbar arteries as the sole etiology of the ruptured AAA.

Dr. Geraghty and Dr. Sarac at Cleveland Clinic have also described the important observation that these Type II endoleaks may be associated with a Type I or III endoleaks and thus put patients at even higher risk of rupture.³ The extent of these leaks may not be completely elucidated until the time of angiography, again emphasizing the importance of a more aggressive approach to diagnosis and treatment in patients with an enlarging aneurysm sac.

These authors have also appropriately pointed out that overall treatment success rates are low with persistence of type II endoleaks on long–term follow-up. While we initially described an overall success rate of 30%, our approach has changed over time to include direct access to the endoleak nidus with the injection of a flow directed glue (Onyx) to obliterate the flow channel and feeding vessels.

We have found this approach to be more successful than attempting to cannulate each of the feeding lumbar vessels or coil embolization of the aneurysm sac, and can be performed via either a translumbar or transarterial approach using SMA to IMA collaterals. While our success rate using this technique has improved to nearly 80%, several words of caution should be noted. 1) Onyx glue is approved for use in the treatment of intracerebral vascular malformations and does not have a peripheral indication at this time. 2) It is critically important that the interventionalist obtains access into the nidus/flow channel to allow the embolic agent to flow. Otherwise you are injecting glue directly into the sac thrombus and wasting time and an expensive embolic agent. 3) There are often multiple levels of lumbar vessels involved and we have found that we often have to go back several times at different levels to treat extensive Type II endoleaks. All of these observations emphasize the need to further study the treatment of Type II endoleaks and the need for a prospective randomized trial to better identify the best treatment options.

Dr. Kwolek is the director of the vascular and endovascular training program at Massachusetts General Hospital, Boston, and the chief of vascular surgery at Newton Wellesley Hospital.

1. J Vasc Surg, 2012. 55(5): p. 1263-7.

2. Management of Type II endoleaks divides the experts at CX 35. Vascular News International,58, May 2012, BIBA publishing.

3. J Vasc Surg, 2012. 55(1): p. 33-40.

4. J Vasc Surg, 2012. 56(3): p. 630-6.