Accepted Manuscript Nonvisualized type III endoleak masquerading as endotension: A case report Akihiro Yoshitake, Takashi Hachiya, Takahito Itoh, Hiroto Kitahara, Mio Kasai, Shinji Kawaguchi, Hideyuki Shimizu PII:
S0890-5096(15)00025-4
DOI:
10.1016/j.avsg.2014.10.039
Reference:
AVSG 2233
To appear in:
Annals of Vascular Surgery
Received Date: 21 August 2014 Revised Date:
9 October 2014
Accepted Date: 22 October 2014
Please cite this article as: Yoshitake A, Hachiya T, Itoh T, Kitahara H, Kasai M, Kawaguchi S, Shimizu H, Nonvisualized type III endoleak masquerading as endotension: A case report, Annals of Vascular Surgery (2015), doi: 10.1016/j.avsg.2014.10.039. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
ACCEPTED MANUSCRIPT
RI PT
Nonvisualized type III endoleak masquerading as endotension: A case report
Akihiro Yoshitake, Takashi Hachiya, Takahito Itoh, Hiroto Kitahara, Mio Kasai, Shinji
SC
Kawaguchi, Hideyuki Shimizu
M AN U
Department of Cardiovascular Surgery, Keio University School of Medicine, Tokyo, Japan
TE D
Address for correspondence: Dr. Akihiro Yoshitake, Department of Cardiovascular
Japan.
81-3-3353-1211.
Fax:
81-3-5379-3034.
AC C
Phone:
EP
Surgery, Keio University School of Medicine, 35 Shinanomachi, Shinjuku, Tokyo,
[email protected]
1
e-mail
address:
ACCEPTED MANUSCRIPT
Abstract
RI PT
Here, we describe a case of nonvisualized type III endoleak masquerading as endotension that was diagnosed by opening the aneurysm sac during surgery and
successfully treated surgically. A 79-year-old man underwent endovascular aneurysm
SC
repair (EVAR) 4 years previously for an aneurysm that had enlarged gradually without
M AN U
endoleak. An open surgical operation was performed. The sac pressure was 132 mmHg—similar to the preoperative systolic blood pressure—and nonpulsatile. After the aneurysm sac was opened without clamping the aorta, a type III endoleak from the
TE D
suture point of the prosthetic endograft was detected. The prosthetic graft was successfully replaced with a Y-graft. The current findings suggest that nonvisualized
AC C
EP
type III endoleaks may be a potential cause of endotension.
2
ACCEPTED MANUSCRIPT
Introduction
RI PT
Endovascular abdominal aortic aneurysm repair (EVAR) has been performed since 1990.1 The most common complications associated with EVAR are endoleaks, which
SC
occur in up to 45% of patients.2-5 Even in the absence of endoleaks, the abdominal aortic aneurysm (AAA) may continue to enlarge after endovascular repair. White and
M AN U
colleagues6 defined endotension as a phenomenon in which postoperative high sac pressure occurs in the absence of continuous perfusion of the aneurysm sac. Endotension may be caused by graft porosity,7 intrasaccular hygroma,8,9 graft
TE D
infection,10,11 etc.; however, controversy exists about the etiology and clinical
EP
consequences of endotension.
AC C
Materials and Methods
A 79-year-old man was suffering from diabetes, hypertension, and hypercholesterolemia. He had an asymptomatic 56 mm × 52 mm AAA, which had been treated with a Cook R of 26 mm by 88 mm main body endoprosthesis with an ipsilateral leg of 14 Zenith○ mm by 54 mm and a contralateral leg of 14 mm by 54 mm (Cook, Japan). After EVAR,
3
ACCEPTED MANUSCRIPT
computed tomography (CT) was performed annually. The CT angiography, both with
RI PT
arterial phase and delayed acquisitions, and color-flow duplex ultrasound scans showed that there were no endoleaks and the aneurysm sac had enlarged gradually. Four years after the surgery, the size of the aneurysm sac had increased to 67 mm × 61 mm (Fig.1).
SC
He had hypertension, which was controlled at 120–140/50–70 mmHg following
M AN U
treatment with calcium blockers, β-blockers, and angiotensin receptor blockers. Moreover, he had diabetes, which was controlled with oral hypoglycemic agents, and
TE D
had hypercholesterolemia, which was treated with statins.
The patient was diagnosed with endotension, and an operation was performed. A
EP
median laparotomy was performed. Umbilical tapes were passed around the supra celiac
AC C
abdominal aorta and bilateral common iliac arteries. The sac pressure was measured by putting a 23-gauge needle into the intrasac; the pressure was 132 mmHg—compared with a systemic pressure of 70/45 mmHg. The sac pressure waveform was pulseless. After systemic heparinization, the aortic sac was opened without clamping the aorta. The thrombosis and blood was contained in the aortic sac. After carefully removing the
4
ACCEPTED MANUSCRIPT
thrombosis, minimal oozing was detected from 3 suture points in the graft (Fig.2). An
RI PT
umbilical tape was passed around the aorta below the bilateral renal arteries and was cross-clamped with the stent-graft. As the proximal stent-graft was impossible to remove, the proximal side of the stent-graft had to be cut and a proximal anastomosis
SC
was performed by incorporating the native artery and the endograft. The distal
M AN U
stent-graft was removed completely and Y-grafting with a 22 mm × 11 mm bifurcated
Discussion
TE D
Dacron graft was performed (Fig.3). The postoperative course was uneventful.
Our report is notable because it showed that the visualization of the nonvisualized
EP
endoleak was possible after opening the sac and removing the thrombus in a patient
AC C
with endotension after endovascular repair. Moreover, we have demonstrated the increasing sac pressure in a patient with endotension. The exact mechanism of the persistent sac pressurization without an endoleak remains unclear. Some authors12-14 suggest that the endotension is a result of direct pressure transmission through the endograft wall, through the branch vessels, or from fluid accumulation due to graft
5
ACCEPTED MANUSCRIPT
infection or hygroma. An endoleak was detected at the suture point that anchors the
RI PT
fabric to the nitinol stent. In the present case, the mechanism of the sac enlargement was considered to be a type III endoleak from the suture points. The sac pressure was similar to the systolic blood pressure and remained unchanged, which we suspect was caused
SC
by the endoleak channel being sealed by a thrombus or having a very low flow,
M AN U
resulting in the non-bilateral endoleak channel—a one-way channel. Thus, after the systemic pressure dropped under general anesthesia during the procedure, the sac pressure remained similar to the preoperative systemic pressure. As usual, the blood
TE D
flow did not exist when the systolic blood pressure remained unchanged, making it difficult to identify the endoleak. However, following an increase in blood pressure
EP
increase or decrease in the sac pressure, a persistent blood flow through the suture
AC C
points occurred. Thus, the endoleak was visualized when the sac was opened and the sac pressure decreased.
There are several treatment options for endotension. Some authors have reported successful treatment by endovascular repair,15,16 open replacement of the graft, or wrapping of the endograft with a new graft. In such patients where the mechanism of
6
ACCEPTED MANUSCRIPT
endoleak is known, relining with another endograft could serve as an alternate treatment.
RI PT
Moreover, we did not apply any stitches at the bleeding site, as the endograft was considered to be too thin to close the suture points completely. We selected open surgery for several reasons. First, if the endotension had occurred through the prosthetic graft
SC
previously implanted, it would have been difficult to determine the point of the
M AN U
endoleak and to completely cover it by endovascular repair from the inside. Second, if the endotension had occurred by pressure transmission or fluid accumulation from the
Conclusion
EP
useless.
TE D
branch vessels, endovascular repair of the graft’s interior surface would have been
AC C
Our report describes a case of nonvisualized type III endoleak masquerading as endotension after EVAR. Our findings suggest that nonvisualized type III endoleaks are among the potential causes for endotension.
7
ACCEPTED MANUSCRIPT
Acknowledgments
AC C
EP
TE D
M AN U
SC
RI PT
There was no external source of funding or any study sponsors.
8
ACCEPTED MANUSCRIPT
References
RI PT
1. Parodi JC, Palmaz JC, Barone HD. Transfemoral intraluminal graft implantation for abdominal aortic aneurysms. Ann Vasc Surg 1991 Nov;5(6):491-9.
2. Stolzmann P, Frauenfelder T, Pfammatter T, et al. Endoleaks after endovascular
SC
abdominal aortic aneurysm repair: detection with dual-energy dual-source CT.
M AN U
Radiology 2008;249(2):682-91.
3. Alsac JM, Desgranges P, Kobeiter H, et al. Emergency endovascular repair for ruptured abdominal aortic aneurysms: feasibility and comparison of early results with
TE D
conventional open repair. Eur J Vasc Endovasc Surg 2005;30(6):632-9. 4. Golzarian J, Valenti D. Endoleakage after endovascular treatment of abdominal aortic
EP
aneurysms: diagnosis, significance and treatment. Eur Radiol 2006;16(12):2849-57.
AC C
5. Görich J, Rilinger N, Sokiranski R, et al. Endoleaks after endovascular repair of aortic aneurysm: are they predictable?-initial results. Radiology 2001;218(2):477-80. 6. White GH, May J. How should endotension be defined? History of a concept and evolution of a new term. J Endovasc Ther 2000; 7: 435-8.
9
ACCEPTED MANUSCRIPT
7. Thoo CH, Bourke BM, May J. Symptomatic sac enlargement and rupture due to
RI PT
seroma after open abdominal aortic aneurysm repair with polytetrafluoroethylene graft: implications for endovascular repair and endotension. J Vasc Surg 2004;40:1089-94.
SC
8. Gawenda M, Jaschke G, Winter ST, et al. Endotension as a result of pressure
transmission through the graft following endovascular aneurysm repair—an in vitro
M AN U
study. Eur J Vasc Endovasc Surg 2003;26:501-5.
9. Risberg B, Delle M, Eriksson E, et al. Aneurysm sac hygroma: a cause of
TE D
endotension. J Endovasc Ther 2001;8:447-53.
10. White GH. What are the causes of endotension? J Endovasc Ther 2001;8:454-6.
EP
11. Kar B, Dougherty K, Reul GJ, et al. Aortic stent-graft infection due to a presumed aortoenteric fistula. J Endovasc Ther 2002;9:901-6.
AC C
12. White GH, May J, Petrasek P, et al. Endotension: an explanation for continued AAA growth after successful endoluminal repair. J Endovasc Surg 1999;6:308-15.
13. Meier GH, Parker FM, Godziachvili V, et al. Endotension after endovascular aneurysm repair: the Ancure experience. J Vasc Surg 2001;34:421-6; discussion 426-7.
10
ACCEPTED MANUSCRIPT
14. Parodi JC, Berguer R, Ferreira LM, et al. Intra-aneurysmal pressure after incomplete
RI PT
endovascular exclusion. J Vasc Surg 2001;34:909-14.
15. Kougias P, Lin PH, Dardik A, et al. Successful treatment of endotension and
SC
aneurysm sac enlargement with endovascular stent graft reinforcement. J Vasc Surg
M AN U
2007;46:124-7.
16. Goodney PP, Fillinger MF. The effect of endograft relining on sac expansion after endovascular aneurysm repair with the original-permeability Gore Excluder abdominal
AC C
EP
TE D
aortic aneurysm endoprosthesis. J Vasc Surg 2007;45:686-93.
11
ACCEPTED MANUSCRIPT
Figure legends
abdominal aortic aneurysm and no endoleak.
RI PT
Figure 1. Computed tomography angiography (CTA; axial images) showing the
SC
Figure 2. Intraoperative view showing oozing from 3 suture parts of the graft (arrows).
M AN U
Figure 3. Post-operative 3-dimensional reconstruction of the computed tomography
AC C
EP
TE D
angiography (CTA) showing Y-grafting.
12
AC C
EP
TE D
M AN U
SC
RI PT
ACCEPTED MANUSCRIPT
AC C
EP
TE D
M AN U
SC
RI PT
ACCEPTED MANUSCRIPT
AC C
EP
TE D
M AN U
SC
RI PT
ACCEPTED MANUSCRIPT
S0890-5096(15)00025-4
DOI:
10.1016/j.avsg.2014.10.039
Reference:
AVSG 2233
To appear in:
Annals of Vascular Surgery
Received Date: 21 August 2014 Revised Date:
9 October 2014
Accepted Date: 22 October 2014
Please cite this article as: Yoshitake A, Hachiya T, Itoh T, Kitahara H, Kasai M, Kawaguchi S, Shimizu H, Nonvisualized type III endoleak masquerading as endotension: A case report, Annals of Vascular Surgery (2015), doi: 10.1016/j.avsg.2014.10.039. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
ACCEPTED MANUSCRIPT
RI PT
Nonvisualized type III endoleak masquerading as endotension: A case report
Akihiro Yoshitake, Takashi Hachiya, Takahito Itoh, Hiroto Kitahara, Mio Kasai, Shinji
SC
Kawaguchi, Hideyuki Shimizu
M AN U
Department of Cardiovascular Surgery, Keio University School of Medicine, Tokyo, Japan
TE D
Address for correspondence: Dr. Akihiro Yoshitake, Department of Cardiovascular
Japan.
81-3-3353-1211.
Fax:
81-3-5379-3034.
AC C
Phone:
EP
Surgery, Keio University School of Medicine, 35 Shinanomachi, Shinjuku, Tokyo,
[email protected]
1
address:
ACCEPTED MANUSCRIPT
Abstract
RI PT
Here, we describe a case of nonvisualized type III endoleak masquerading as endotension that was diagnosed by opening the aneurysm sac during surgery and
successfully treated surgically. A 79-year-old man underwent endovascular aneurysm
SC
repair (EVAR) 4 years previously for an aneurysm that had enlarged gradually without
M AN U
endoleak. An open surgical operation was performed. The sac pressure was 132 mmHg—similar to the preoperative systolic blood pressure—and nonpulsatile. After the aneurysm sac was opened without clamping the aorta, a type III endoleak from the
TE D
suture point of the prosthetic endograft was detected. The prosthetic graft was successfully replaced with a Y-graft. The current findings suggest that nonvisualized
AC C
EP
type III endoleaks may be a potential cause of endotension.
2
ACCEPTED MANUSCRIPT
Introduction
RI PT
Endovascular abdominal aortic aneurysm repair (EVAR) has been performed since 1990.1 The most common complications associated with EVAR are endoleaks, which
SC
occur in up to 45% of patients.2-5 Even in the absence of endoleaks, the abdominal aortic aneurysm (AAA) may continue to enlarge after endovascular repair. White and
M AN U
colleagues6 defined endotension as a phenomenon in which postoperative high sac pressure occurs in the absence of continuous perfusion of the aneurysm sac. Endotension may be caused by graft porosity,7 intrasaccular hygroma,8,9 graft
TE D
infection,10,11 etc.; however, controversy exists about the etiology and clinical
EP
consequences of endotension.
AC C
Materials and Methods
A 79-year-old man was suffering from diabetes, hypertension, and hypercholesterolemia. He had an asymptomatic 56 mm × 52 mm AAA, which had been treated with a Cook R of 26 mm by 88 mm main body endoprosthesis with an ipsilateral leg of 14 Zenith○ mm by 54 mm and a contralateral leg of 14 mm by 54 mm (Cook, Japan). After EVAR,
3
ACCEPTED MANUSCRIPT
computed tomography (CT) was performed annually. The CT angiography, both with
RI PT
arterial phase and delayed acquisitions, and color-flow duplex ultrasound scans showed that there were no endoleaks and the aneurysm sac had enlarged gradually. Four years after the surgery, the size of the aneurysm sac had increased to 67 mm × 61 mm (Fig.1).
SC
He had hypertension, which was controlled at 120–140/50–70 mmHg following
M AN U
treatment with calcium blockers, β-blockers, and angiotensin receptor blockers. Moreover, he had diabetes, which was controlled with oral hypoglycemic agents, and
TE D
had hypercholesterolemia, which was treated with statins.
The patient was diagnosed with endotension, and an operation was performed. A
EP
median laparotomy was performed. Umbilical tapes were passed around the supra celiac
AC C
abdominal aorta and bilateral common iliac arteries. The sac pressure was measured by putting a 23-gauge needle into the intrasac; the pressure was 132 mmHg—compared with a systemic pressure of 70/45 mmHg. The sac pressure waveform was pulseless. After systemic heparinization, the aortic sac was opened without clamping the aorta. The thrombosis and blood was contained in the aortic sac. After carefully removing the
4
ACCEPTED MANUSCRIPT
thrombosis, minimal oozing was detected from 3 suture points in the graft (Fig.2). An
RI PT
umbilical tape was passed around the aorta below the bilateral renal arteries and was cross-clamped with the stent-graft. As the proximal stent-graft was impossible to remove, the proximal side of the stent-graft had to be cut and a proximal anastomosis
SC
was performed by incorporating the native artery and the endograft. The distal
M AN U
stent-graft was removed completely and Y-grafting with a 22 mm × 11 mm bifurcated
Discussion
TE D
Dacron graft was performed (Fig.3). The postoperative course was uneventful.
Our report is notable because it showed that the visualization of the nonvisualized
EP
endoleak was possible after opening the sac and removing the thrombus in a patient
AC C
with endotension after endovascular repair. Moreover, we have demonstrated the increasing sac pressure in a patient with endotension. The exact mechanism of the persistent sac pressurization without an endoleak remains unclear. Some authors12-14 suggest that the endotension is a result of direct pressure transmission through the endograft wall, through the branch vessels, or from fluid accumulation due to graft
5
ACCEPTED MANUSCRIPT
infection or hygroma. An endoleak was detected at the suture point that anchors the
RI PT
fabric to the nitinol stent. In the present case, the mechanism of the sac enlargement was considered to be a type III endoleak from the suture points. The sac pressure was similar to the systolic blood pressure and remained unchanged, which we suspect was caused
SC
by the endoleak channel being sealed by a thrombus or having a very low flow,
M AN U
resulting in the non-bilateral endoleak channel—a one-way channel. Thus, after the systemic pressure dropped under general anesthesia during the procedure, the sac pressure remained similar to the preoperative systemic pressure. As usual, the blood
TE D
flow did not exist when the systolic blood pressure remained unchanged, making it difficult to identify the endoleak. However, following an increase in blood pressure
EP
increase or decrease in the sac pressure, a persistent blood flow through the suture
AC C
points occurred. Thus, the endoleak was visualized when the sac was opened and the sac pressure decreased.
There are several treatment options for endotension. Some authors have reported successful treatment by endovascular repair,15,16 open replacement of the graft, or wrapping of the endograft with a new graft. In such patients where the mechanism of
6
ACCEPTED MANUSCRIPT
endoleak is known, relining with another endograft could serve as an alternate treatment.
RI PT
Moreover, we did not apply any stitches at the bleeding site, as the endograft was considered to be too thin to close the suture points completely. We selected open surgery for several reasons. First, if the endotension had occurred through the prosthetic graft
SC
previously implanted, it would have been difficult to determine the point of the
M AN U
endoleak and to completely cover it by endovascular repair from the inside. Second, if the endotension had occurred by pressure transmission or fluid accumulation from the
Conclusion
EP
useless.
TE D
branch vessels, endovascular repair of the graft’s interior surface would have been
AC C
Our report describes a case of nonvisualized type III endoleak masquerading as endotension after EVAR. Our findings suggest that nonvisualized type III endoleaks are among the potential causes for endotension.
7
ACCEPTED MANUSCRIPT
Acknowledgments
AC C
EP
TE D
M AN U
SC
RI PT
There was no external source of funding or any study sponsors.
8
ACCEPTED MANUSCRIPT
References
RI PT
1. Parodi JC, Palmaz JC, Barone HD. Transfemoral intraluminal graft implantation for abdominal aortic aneurysms. Ann Vasc Surg 1991 Nov;5(6):491-9.
2. Stolzmann P, Frauenfelder T, Pfammatter T, et al. Endoleaks after endovascular
SC
abdominal aortic aneurysm repair: detection with dual-energy dual-source CT.
M AN U
Radiology 2008;249(2):682-91.
3. Alsac JM, Desgranges P, Kobeiter H, et al. Emergency endovascular repair for ruptured abdominal aortic aneurysms: feasibility and comparison of early results with
TE D
conventional open repair. Eur J Vasc Endovasc Surg 2005;30(6):632-9. 4. Golzarian J, Valenti D. Endoleakage after endovascular treatment of abdominal aortic
EP
aneurysms: diagnosis, significance and treatment. Eur Radiol 2006;16(12):2849-57.
AC C
5. Görich J, Rilinger N, Sokiranski R, et al. Endoleaks after endovascular repair of aortic aneurysm: are they predictable?-initial results. Radiology 2001;218(2):477-80. 6. White GH, May J. How should endotension be defined? History of a concept and evolution of a new term. J Endovasc Ther 2000; 7: 435-8.
9
ACCEPTED MANUSCRIPT
7. Thoo CH, Bourke BM, May J. Symptomatic sac enlargement and rupture due to
RI PT
seroma after open abdominal aortic aneurysm repair with polytetrafluoroethylene graft: implications for endovascular repair and endotension. J Vasc Surg 2004;40:1089-94.
SC
8. Gawenda M, Jaschke G, Winter ST, et al. Endotension as a result of pressure
transmission through the graft following endovascular aneurysm repair—an in vitro
M AN U
study. Eur J Vasc Endovasc Surg 2003;26:501-5.
9. Risberg B, Delle M, Eriksson E, et al. Aneurysm sac hygroma: a cause of
TE D
endotension. J Endovasc Ther 2001;8:447-53.
10. White GH. What are the causes of endotension? J Endovasc Ther 2001;8:454-6.
EP
11. Kar B, Dougherty K, Reul GJ, et al. Aortic stent-graft infection due to a presumed aortoenteric fistula. J Endovasc Ther 2002;9:901-6.
AC C
12. White GH, May J, Petrasek P, et al. Endotension: an explanation for continued AAA growth after successful endoluminal repair. J Endovasc Surg 1999;6:308-15.
13. Meier GH, Parker FM, Godziachvili V, et al. Endotension after endovascular aneurysm repair: the Ancure experience. J Vasc Surg 2001;34:421-6; discussion 426-7.
10
ACCEPTED MANUSCRIPT
14. Parodi JC, Berguer R, Ferreira LM, et al. Intra-aneurysmal pressure after incomplete
RI PT
endovascular exclusion. J Vasc Surg 2001;34:909-14.
15. Kougias P, Lin PH, Dardik A, et al. Successful treatment of endotension and
SC
aneurysm sac enlargement with endovascular stent graft reinforcement. J Vasc Surg
M AN U
2007;46:124-7.
16. Goodney PP, Fillinger MF. The effect of endograft relining on sac expansion after endovascular aneurysm repair with the original-permeability Gore Excluder abdominal
AC C
EP
TE D
aortic aneurysm endoprosthesis. J Vasc Surg 2007;45:686-93.
11
ACCEPTED MANUSCRIPT
Figure legends
abdominal aortic aneurysm and no endoleak.
RI PT
Figure 1. Computed tomography angiography (CTA; axial images) showing the
SC
Figure 2. Intraoperative view showing oozing from 3 suture parts of the graft (arrows).
M AN U
Figure 3. Post-operative 3-dimensional reconstruction of the computed tomography
AC C
EP
TE D
angiography (CTA) showing Y-grafting.
12
AC C
EP
TE D
M AN U
SC
RI PT
ACCEPTED MANUSCRIPT
AC C
EP
TE D
M AN U
SC
RI PT
ACCEPTED MANUSCRIPT
AC C
EP
TE D
M AN U
SC
RI PT
ACCEPTED MANUSCRIPT
