endoleak, is a major drawback which less covered by a beginner centre. But, it way moy trouble if come the hand of even an axperience surgeon.

1. Complications after Endovascular
Aneurysm Repair
Dicky A.Wartono ,MD
Aortic Endovascular Surgery 2013

2. • Common complications during or after EVAR
• Endoleak
• Surgical complication
• Systemic complications,
• Ischemic complications
• Infection complications

3. Cardiovasc Intervent Radiol (2006) 29:935–946

4. Cardiovasc Intervent Radiol (2006) 29:935–946

5. Surgical Complications
•LOCAL WOUND COMPLICATIONS (1-10%)
– groin hematoma, infection, or lymphocele
•ACCESS ARTERY INJURY (1-11%)
– Arterial thrombosis, dissection, or pseudoaneurysm
– correct surgical skills,
– Preoperative CT evaluation of the access artery

6. Interventional Cardiology, 2010;5:81–5
Transfemoral access should be avoided in the following cases:
• previous aorto-femoral bypass;
• bulky aortic atherosclerosis (severe atheroma with mobile element
>5mm);
• a minimal luminal diameter smaller than the external diameter
of the introducer sheath;
• severe vessel angulations (minimal angle <40°); and • circumferential and
extensive vascular calcifications.
•Surgical Complications

7. J Vasc Surg 2009;50:1293-300
•Surgical Complications

8. Ischemic Complications after EVAR
– clot formation or clot embolization into aortic side
branches and include colonic, renal, and pelvic
ischemia.
– misplacement of the stent graft,

9. • COLONIC ISCHEMIA 1 to 3% of cases
– mortality rate of 50% within 1 month
– thrombotic deposits and atheroma in the suprarenal aorta
– multifocal patchy ischemia
• SPINAL CORD ISCHEMIA 0.21%
– variable anatomy of the artery of Adamkiewicz
– cerebrospinal fluid drainage and, if indicated, recanalization of occluded
collateral arteries
• RENAL ARTERY OCCLUSION 5%
– imaging technology for guiding the EVAR procedure and a learning curve
– stent placement in the renal artery with slight protrusion of the stent over the
proximal part of the stent
• Limb Occlusion 40% and 5% (2nd
gen)
Ischemic Complications

11. The Vertebrobasilar System
The vertebral arteries originate from
the subclavian artery,
and ascend through the transverse
foramen of the upper six cervical
vertebra. At the upper margin of the
Axis (C2) it moves outward and
upward to the transverse foramen of the
Atlas (C1). It then moves backwards
along the articular process of atlas into
a deep groove, passes beneath the
atlanto-occipital ligament and enters the
foramen magnum. The arteries then run
forward and unite at the caudal border
of the pons to form the basilar artery.
Ischemic Complications

12. Ann Thorac Surg 2011;92:568–70
Preoperative MRA showed
-connection type A (82%),
-an interrupted right vertebral artery in (11%),
-an interrupted left vertebral artery in (7%)
Ischemic Complications

13. Spinal Cord Blood Supply
The spinal cord lacks adequate collateral supply in some areas, making
these regions prone to ischemia after vascular occlusions. The upper
Thorasic (T1-T4) and first lumbar segments are the most vulnerable regions
of the cord.
Ischemic Complications

14. Blood supply of Spinal Cord
-anterior spinal artery
-- posterior spinal artery (right and left)
-Artery of Adamkiewicz
from the left in 80% of the population
- T5-T8 in 15%,
- T9-T12 in 75%, and
- L1-L2 in 10% [14].
Adamkiewicz artery
great radicular artery
major anterior segmental medullary artery
artery of the lumbar enlargement
great anterior radiculomedullary artery
great anterior segmental medullary artery
Ischemic Complications

15. J Vasc Surg 2009;49:1594-601.
risk of neurologic complications after TEVAR is increased when the LSA is
covered. Preemptive revascular- ization appears not protect against CVA but may
reduce the incidence of SCI.
Ischemic Complications

16. Ann Thorac Surg 2007;84:1201–5)
E. Weigang et al. / European Journal of Cardio-thoracic Surgery 40 (2011) 858—
868

17. J Vasc Surg 2004;40:698-702.)
The circulation after ligature of the internal iliac
artery is carried on by the anastomoses of:
-the middle rectal artery and the superior rectal
artery
-the iliolumbar artery with the last lumbar artery
-the lateral sacral arteries with the median sacral
artery
Ischemic Complications

18. Ischemic Complications

19. J Vasc Surg 2004;40:698-702.)
Ischemic Complications

20. IIA occlusion
-CIA problems
(short/ectasia/tort/cal
c/trombus)
-Type II endoleak
(embolized)
-Complication
- Buttock Cl
- Colitis Ischenia
- SCI
- Pelvic Inschemia
Ischemic Complications

21. Patient Selection
- >4.5cm IIA
- >1cm landing zone
- <10mm IIA diameter
Ischemic Complications

22. • Early and Late Limb Occlusion , EVAR 40% and 5% (2nd
gen)
– mural thrombotic deposits ,
• first- (20%) and second-generation (17 to 33%)
– first 2 months untill long after EVAR
– kinking of the unsupported endograft
– small-diameter stent graft into the external iliac artery
– migration and dislocation of an endograft >> turbulence of
hemodynamics and limb or entire stent-graft thrombosis
Ischemic Complications

24. Systemic
• Complications of Anticoagulation
– Bleeding
– Trombosis
• Contrast Toxicity (CIN)
– Screening .
• 3% <1.5mg/dl
• 4.1% >1.5mg/dl
• 12% >1.5mg/dl + DM
– CM selection ,type & volume
– Hydration

25. • Infection Complications 0.5 to 1%,
• Endograft contamination , periprocedural
contamination
• Secondary infection
• a kidney stone 1 year after EVAR procedure
• aortoenteric fistula
• Air bubbles can be seen within sac
• An additional puncture (sample)
• After intravenous administration of
antibiotics, resection of the endograft and
aneurismal sac, graft replacement

26. presented most commonly in the first postoperative year, and was
similar among patients undergoing open AAA repair and EAVR.
Patients with nosocomial infection had an earlier onset of AGI.
AGI was significantly higher in patients who had blood stream
septicemia and surgical site infection in the periprocedural
hospitalization. ( J Vasc Surg 2008;47:264-9.)

27. • 16.9% had endoleak identified on one-month post
EVAR scan
• late endoleak will occur in 12-15%
• endoleaks in 20 to 25% of patients (survilance 5
years)
• associated with aneurysm expansion and even
rupture
• Treatment of early and late Type II endoleaks
accounted for 2/3 of all secondary interventions
J Vasc Surg 2006;43:896-902
ENDOLEAK

28. • Aneurysm sac enlargement is more often seen in
patients with endoleak compared with those without
an endoleak
• Sac enlargement has been found in 20% of patients
with type I/III endoleak compared with 10% of
patients with type II endoleak and 5% of patients
with no endoleak
• have been reports on patients with shrinking
aneurysms with no endoleaks with aneurysm rupture
Natural history of aneurysms with endoleak
ENDOLEAK

29. Circ Cardiovasc Intervent. 2009;2:105-112.)
(J Vasc Surg 2003;37:1155-61.)

30. ENDOLEAK

31. ENDOLEAK

33. • Short or angulated infrarenal aortic necks & neck
length less <20mm are the most significant
preoperative risk factors for a type I endoleak
• Large-diameter aortic necks (>28 mm) can lead to an
endograft migration and endoleak
• Smaller amounts of mural thrombus in the aneurysm
sac also have been found to correlate with device-
related endoleaks
Risk factors and prevention

34. Risk factors and prevention
• infrarenal necks longer than 15 mm, a common iliac
artery diameter smaller than 18 mm, with minimum
continuous length of 15 mm.
• neck angulation, tortuousity and transmural
calcification, and thrombus
• Type I/III endoleak can sometimes occur after
mechanical trauma
• Paraplegia, colonic necrosis, and ischemic colitis
subsequent to embolotherapy for type II leaks
ENDOLEAK

35. ENDOLEAK

36. • Type 1 endoleak ( 2 – 12% / 10% req re intervension)
• Most common
• after TEVAR
• complex arterial anatomy
• Prox : Short, angulated, ulcerated, trapezoidal, and thrombus-containing necks
• Dist : dilated, irregular, and tortuous
• direct communication with the systemic blood flow
• immediate repair always repaired when they are detected
• Repair : angioplasty of the affected attachment site,a bare
metal stent.
• at the proximal docking site, more technically challenging,
as they typically arise just distal to the takeoff of the renal arteries,
and open repair can be required.
• type 1 endoleaks that were embolized using N-butyl-2-cyanoacrylate
(n-BCA)
• Th graft extension, baloon expdbl stent, embolization.. Long term?
ENDOLEAK

37. (A) Type I endoleak. An arteriogram
demonstrates a type I endoleak arising from
the right iliac limb of an Endologix stent graft
(Endologix, Inc., Irvine, CA). (B) A balloon
expandable stent was used to treated the type
I endoleak seen at the right distal limb of the
endograft. (C) Post–stent deployment. After a
Palmaz stent was deployed within the right
distal limb of the endograft, there was
complete resolution of the endoleak
ENDOLEAK

38. • Type II endoleaks . 10 to 25%. most common type of endoleak
encountered after endovascular repair of abdominal aortic
aneurysms (esp IMA origin)
• Low risk of rupture if sac not enlarge
• Can thrombose. immediate intervention is not needed, or rupture
• Others authors treat type II endoleaks more aggressively, as the
collateral vessels can transmit arterial pressures into the sac,
which may increase the chance of aneurysm expansion and
rupture.
• Repair : via a transarterial or translumbar approach >> single-
vessel embolization of the feeding artery.
• Success rates : 80% of type II endoleaks recurred after embolization.
• The etiology of the failure these endoleaks are not fed by a single
• The next step to further refine the transarterial approach is to
feed the microcatheter into the aneurysm sac,
ENDOLEAK

39. Staged algorithm of evaluation and treatment
of suspected type II endoleaks. www.jvir.org.)
ENDOLEAK

40. (A) Type II endoleak after endovascular
aneurysm repair. A postoperative computed
tomographic (CT) angiogram performed
approximately a year and half after the initial
placement of the endograft demonstrates
contrast within the aneurysm sac. The
aneurysm had increased in size since the
prior CT performed a year earlier. (B) Type II
endoleak angiogram. Selective
catheterization of the superior mesenteric
artery demonstrates filling of the type II
endoleak. (C) Arteriogram of the endoleak sac
was performed from a microcatheter that has
been used to select the inferior mesenteric
artery (IMA) endoleak via the superior
mesenteric artery. (D) Postembolization
image shows coils in endoleak sac and IMA
ENDOLEAK

41. • Other techniques to treat type II endoleaks.
• Lin et al reported a case of robotic ligation no recanalization of the
endoleak at the 3-month follow-up.
• Ling et al describe deployment of an endovascular graft with simultaneous
operative extraperitoneal dissection and Onyx to treat a type II endoleak.
• Zhou et al used a similar combined endovascular and laparoscopic
approach to repair a type II endoleak. Laparoscopy was used to identify
the distal IMA, which was surgically clipped.
– no further filling of the endoleak
• Mansueto et al have described a transcatheter transcaval technique for
endoleak embolization
– 1 year that are comparable to translumbar embolization.
ENDOLEAK

42. J Vasc Surg 2010;52:19-24
ENDOLEAK

43. Interactive CardioVascular and Thoracic
Surgery 0 (2012) 1–5 BEST EVIDENCE TOPIC
doi:10.1093/icvts/ivs201
ENDOLEAK

44. ENDOLEAK

45. ENDOLEAK
ENDOLEAK LONGTERM
TREATMENT
CONSERVATIVE

46. • Type III endoleaks
• defect within the graft material or
• structural failures causing separation between the
components
• inadequate overlap.
• require immediate repair because there is direct
communication
• Repair : placement of a new stent-graft
component across the defect or junctional
separation.
• This is often followed by further angioplasty to
remold the structural components of the stent
graft.
ENDOLEAK

47. • Type IV endoleaks
• caused by stent-graft porosity.
• immediate postdeployment aortogram, as the patient
is fully anticoagulated with heparin perioperatively.
• “blush” seen on the immediate postimplantation
angiogram, when patients are fully anticoagulated.
• no specific intervention other than normalization of
the coagulation profile.
• self-limited and resolve as the patients coagulation
returns to baseline.
ENDOLEAK

48. • Type V endoleaks (1-8%)
• enlarging aneurysm sac without a visible endoleak. (occult type I,II,III ?)
• Endotension can require conversion to open repair.
• Mennander et al describe a nonoperative approach to endotension in five
patients. Three of these patients had a rupture of the aneurysm sac but
did not have retroperitoneal bleeding or hematoma.
• A small case series out of Vienna described two cases of type V endoleaks
in patients who had undergone endovascular repair of thoracic aortic
aneurysms. These endoleaks were treated by redoing the stent-graft
placement, which had good results in both cases.
• Another group reported three cases of type V endoleaks in patients who
underwent EVAR for AAA. The authors' technique for repair of the
endoleak was to reinforce the indwelling stent graft by placing iliac or
aortic cuff extenders, which had good results.
ENDOLEAK

49. CONCLUSION
• EVAR is a widely used alternative to open repair of AAAs.
• The complication profile for EVAR differs substantially from that for open
surgical AAA repair.
• Most access-related complications can be avoided with close preoperative
examination of the patient and CT scan
• Endoleaks are one of the unique complications to endovascular repair of
aneurysms and can lead to aneurysm expansion and rupture if not
repaired.
• Accurate endoleak classification is critical prior to endoleak treatment; an
endoleak arteriogram is often necessary to ensure proper endoleak
classification.
• Lifelong imaging surveillance is necessary for a patient undergoing
endovascular aortic aneurysm repair.

50. Thank You

51. • REFERENCES
• Schermerhorn M L, O'Malley A J, Jhaveri A, Cotterill P, Pomposelli F, Landon B E. Endovascular vs. open repair of abdominal aortic aneurysms in the Medicare population. N Engl J Med.
2008;358:464–474. [PubMed]
• Hellinger J C. Endovascular repair of thoracic and abdominal aortic aneurysms: pre- and postprocedural imaging. Tech Vasc Interv Radiol. 2005;8:2–15. [PubMed]
• Veith F J, Baum R A, Ohki T, et al. Nature and significance of endoleaks and endotension: summary of opinions expressed at international conference. J Vasc Surg. 2002;35:1029–1035. [
PubMed]
• Rosen R J, Green R M. Endoleak management following endovascular aneurysm repair. J Vasc Interv Radiol. 2008;19(suppl):S37–S43. [PubMed]
• Maldonado T S, Rosen R J, Rockman C B, et al. Initial successful management of type I endoleak after endovascular aortic aneurysm repair with n-butyl cyanoacrylate adhesive. J Vasc Surg.
2003;38:664–670. [PubMed]
• Gorich J, Rilinger N, Sokiranski R, et al. Leakages after endovascular repair of aortic aneurysms: classification based on findings at CT, angiography, and radiology. Radiology.
1999;213:767–772. [PubMed]
• Rozenblit A M, Patlas M, Rosenbaum A T, et al. Detection of endoleaks after endovascular repair of abdominal aortic aneurysm: value of unenhanced and delayed helical CT acquisitions.
Radiology. 2003;227:426–433. [PubMed]
• Stavropoulos S W, Clark T W, Carpenter J P, et al. Use of CT angiography to classify endoleaks after endovascular repair of abdominal aortic aneurysms. J Vasc Interv Radiol. 2005;16:663–
667. [PubMed]
• Biasi L, Ali T, Hinchliffe R, Morgan R, Loftus I, Thompson M. Intraoperative DynaCT detection and immediate correction of a type 1a endoleak following endovascular repair of abdominal
aortic aneurysm. Cardiovasc Intervent Radiol. 2008 July 26 (Epub ahead of print).
• Kim J K, Noll R E, Tonnessen B H, Sternbergh W C. A technique for increased accuracy in the placement of the “giant” Palmaz stent for treatment of type IA endoleak after endovascular
abdominal aneurysm repair. J Vasc Surg. 2008;48:755–757. [PubMed]
• Jones J E, Atkins M D, Brewster D C, et al. Persistent type 2 endoleak after endovascular repair of abdominal aortic aneurysm is associated with adverse late outcomes. J Vasc Surg.
2007;46:1–8. [PubMed]
• Silverberg D, Baril D T, Ellozy S H, et al. An 8-year experience with type II endoleaks: natural history suggests selective intervention is a safe approach. J Vasc Surg. 2006;44:453–459. [
PubMed]
• Schurink G W, Aarts N J, Wilde J, et al. Endoleakage after stent-graft treatment of abdominal aneurysm; implications on pressure and imaging-an in vitro study. J Vasc Surg. 1998;28:234–
241. [PubMed]
• Baum R A, Carpenter J P, Golden M A, et al. Treatment of type II endoleaks after endovascular repair of abdominal aortic aneurysms: comparison of transarterial and translumbar
techniques. J Vasc Surg. 2002;35:23–29. [PubMed]
• Park J, Carpenter J P, Fairman R M, Stavropoulos S W. Type 2 endoleak embolization comparison: translumbar embolization versus modified transarterial embolization. J Vasc Interv
Radiol. 2008;19:S18. [PubMed]
• Stavropoulos S W, Kim H, Clark T W, Fairman R M, Velazquez O, Carpenter J P. Embolization of type 2 endoleaks after endovascular repair of abdominal aortic aneurysms with use of
cyanoacrylate with or without coils. J Vasc Interv Radiol. 2005;16:857–861. [PubMed]
• Stavropoulos S W, Carpenter J C, Fairman R M, Golden M A, Baum R A. Inferior vena cava traversal for endoleak embolization after endovascular abdominal aortic aneurysm repair. J Vasc
Interv Radiol. 2003;14:1191–1194. [PubMed]
• Baum R A, Cope C, Fairman R M, Carpenter J P. Translumbar embolization of type 2 endoleaks after endovascular repair of abdominal aortic aneurysms. J Vasc Interv Radiol. 2001;12:111–
116. [PubMed]
• Lin J C, Eun D, Shrivastava A, Shepard A D, Reddy D J. Total robotic ligation of inferior mesenteric artery for type II endoleak after endovascular aneurysm repair. Ann Vasc Surg. 2008 April
12 (Epub ahead of print).
• Ling A J, Pathak R, Garbowski M, Nadkarni S. Treatment of a large type II endoleak via extraperitoneal dissection and embolization of collateral vessel using ethylene vinyl alcohol
copolymer (Onyx) J Vasc Interv Radiol. 2007;18:659–662. [PubMed]
• Zhou W, Lumsden A B, Li J. IMA clipping for a type II endoleak: combined laparoscopic and endovascular approach. Surg Laparosc Endosc Percutan Tech. 2006;16:272–275. [PubMed]
• Mansueto G, Cenzi D, Scuro A, et al. Treatment of type II endoleak with a transcatheter transcaval approach: results at 1-year follow-up. J Vasc Surg. 2007;45:1120–1127. [PubMed]
• Mennander A, Pimenoff G, Heikkinen M, Partio R, Zeitlin R, Salenius J P. Nonoperative approach to endotension. J Vasc Surg. 2005;42:194–199. [PubMed]
• Zimpfer D, Schoder M, Gottardi R, et al. Treatment of type V endoleaks by endovascular redo-stent graft placement. Ann Thorac Surg. 2007;83:664–666. [PubMed]
• Kougias P, Lin P H, Dardik A, Lee W A, El Sayed H F, Zhou W. Successful treatment of endotension and aneurysm sac enlargement with endovascular stent graft reinforcement. J Vasc Surg.
2007;46:124–127. [PubMed]

52. • Type II Endoleaks After EVAR: A Continuing Dilemma
• Tue, 8/11/09 - 10:06am
• 0 Comments
• 6535 reads
• 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.

53. CT angiograms of type I endoleak in 78-year-old man. (a, b) Transverse
images during arterial phase and (c) oblique sagittal maximum intensity
projection show contrast material (arrow) flowing around the superior
fixation of stent-graft.

54. CT angiograms of type I endoleak in 78-year-
old man. (a, b) Transverse images during
arterial phase and (c) oblique sagittal
maximum intensity projection show contrast
material (arrow) flowing around the superior
fixation of stent-graft

55. CT angiograms of type I endoleak in 78-year-
old man. (a, b) Transverse images during
arterial phase and (c) oblique sagittal
maximum intensity projection show contrast
material (arrow) flowing around the superior
fixation of stent-graft.

56. Type II endoleak with supply from lumbar artery in 77-year-old man. Delayed
transverse postgadolinium fat-suppressed two-dimensional gradient-echo MR
angiogram (repetition time msec/echo time msec, 250/1.4; 7-mm section
thickness; 512 × 128 matrix, 42-cm field of view) shows contrast material
accumulation in aneurysm sac (arrows).

57. a) Frontal flush aortogram shows type III
endoleak (arrow) in a patient with aortouniiliac
stent-graft. (b) Arteriogram shows type III
endoleak (arrow); the defect has been selected
with a catheter.

58. (a) Frontal flush aortogram shows type
III endoleak (arrow) in a patient with
aortouniiliac stent-graft. (b) Arteriogram
shows type III endoleak (arrow); the
defect has been selected with a
catheter.

60. 1 year after endovascular aneurysm repair.
Axial images from CT angiogram show
peripheral contrast enhancement within
aneurysm sac (arrowheads), with no
connection to stent-graft. At angiography, this
finding was shown to be type II endoleak
originating from left lumbar artery
lower abdominal pain 18 months after
endovascular aneurysm repair. Digital
subtraction angiogram shows leakage of
contrast material adjacent to right iliac artery
attachment site (arrowheads), consistent with
type IB endoleak

61. 88-year-old man who presented with tearing
mid abdominal pain 4 months after
endovascular aneurysm repair. Unenhanced
coronal (A) and axial (B) spoiled gradient-
recalled echo images show large hematoma
within aneurysm sac (arrowheads) adjacent to
and contacting stent-graft, suggestive of high-
pressure endoleak
88-year-old man who presented with tearing
mid abdominal pain 4 months after
endovascular aneurysm repair. Digital
subtraction angiogram with marking catheter
shows saccular area of contrast leakage from
midportion of one of legs of stent-graft
(arrowheads). This is type III endoleak.

62. vessels
Circ Cardiovasc Intervent. 2009;2:105-112.)

63. Circ Cardiovasc Intervent. 2009;2:105-112.)

64. • Iinsidense per endoleak
• Incidense complication per pathology
– Dissection ac/chr
– IMH/PAU/Trauma
– Aneurysm
– Marfan
• Incidence per device n generation

65. • The available evidence suggests that the majority of isolated
type II endoleaks are innocuous and will seal spontaneously
during the long-term follow-up, even when they persist for
more than 6 months, and the vast majority of studies have
not demonstrated an association with the increased risk of
rupture or aneurysm-related mortality. However, if a type II
endoleak is associated with a significant sac enlargement (i.e.
>5 mm over a 6-month period), intervention is indicated,
usually in the form of a percutaneous embolization of the
feeding vessels. The caveat is that there is no randomized
data and that most studies had a mean follow-up period of
approximately 3 years longer follow- up in patients with type
II endoleak is lacking.

66. • Sarac TP, Gibbons C, Vargas L, Liu J, Srivastava
S, Bena J. Long term follow-up of type II
endoleak embolisation reveals the need for
close surveillance. J Vasc Surg 2012;55:33–40.
• Wyss TR, Brown LC, Powell JT, Greenhalgh
RM. Rate and predictability of graft rupture
after endovascular and open abdominal aortic
aneurysm repair: data from the EVAR Trials.
Ann Surg 2010;252:805–12.

72. Semin Intervent Radiol. 2009 March; 26(1): 33–38.
doi: 10.1055/s-0029-1208381
PMCID: PMC3036461
Aortic Stent Grafts
Guest Editor S. William Stavropoulos M.D.
Management of Endoleaks following Endovascular Aneurysm Repair

73. • Complication
– Endoleak
– Surgical Exposure
– Systemic
– Ischemic
– Infection
– Excluded aneurysml sac
- Definition & Class
- Incidense
- Mechanism
- Management

74. Arterial SupplyArterial Supply
- Spinal Arteries- Spinal Arteries
Anterior (1) & Posterior (2) Spinal ArteryAnterior (1) & Posterior (2) Spinal Artery
fromfrom Vertebral arteryVertebral artery
- Radicular Arteries ----- Segmental arteries- Radicular Arteries ----- Segmental arteries
fromfrom Vertebral, Ascending Cervical, Intercostal andVertebral, Ascending Cervical, Intercostal and
Lumbar ArteryLumbar Artery
Venous DrainageVenous Drainage
-- Longitudinal & Radicular VeinsLongitudinal & Radicular Veins
toto Intervertebral veinsIntervertebral veins ---- to---- to Internal Vertebral Venous PlexusInternal Vertebral Venous Plexus
toto external vertebral venous plexusexternal vertebral venous plexus ---- to---- to segmental veinssegmental veins
Arterial SupplyArterial Supply
- Spinal Arteries- Spinal Arteries
Anterior (1) & Posterior (2) Spinal ArteryAnterior (1) & Posterior (2) Spinal Artery
fromfrom Vertebral arteryVertebral artery
- Radicular Arteries ----- Segmental arteries- Radicular Arteries ----- Segmental arteries
fromfrom Vertebral, Ascending Cervical, Intercostal andVertebral, Ascending Cervical, Intercostal and
Lumbar ArteryLumbar Artery
Venous DrainageVenous Drainage
-- Longitudinal & Radicular VeinsLongitudinal & Radicular Veins
toto Intervertebral veinsIntervertebral veins ---- to---- to Internal Vertebral Venous PlexusInternal Vertebral Venous Plexus
toto external vertebral venous plexusexternal vertebral venous plexus ---- to---- to segmental veinssegmental veins
Spinal CordSpinal Cord Vascular SupplyVascular SupplySpinal CordSpinal Cord Vascular SupplyVascular Supply

75. anterior spinal arteryanterior spinal artery segmental arteriessegmental arteries
5. Adamkiwicz artery5. Adamkiwicz artery

76. The brain is one of the most
metabolically active organs
in the body, receiving 17% of
the total cardiac output and
about 20% of the oxygen available
in the body.
The brain receives it’s blood from
two pairs of arteries, the carotid and
vertebral. About 80% of the brain’s
blood supply comes from the carotid,
and the remaining 20% from the vertebral.
Blood Supply to the
Spinal Cord and Brain Stem

77. The Vertebrobasilar System
The vertebral arteries originate from
the subclavian artery,
and ascend through the transverse
foramen of the upper six cervical
vertebra. At the upper margin of the
Axis (C2) it moves outward and
upward to the transverse foramen of the
Atlas (C1). It then moves backwards
along the articular process of atlas into
a deep groove, passes beneath the
atlanto-occipital ligament and enters the
foramen magnum. The arteries then run
forward and unite at the caudal border
of the pons to form the basilar artery.

78. Blood Supply to the Spinal Cord
and Brainstem
The Spinal Cord receives its blood supply from two major sources;
1. Branches of the vertebral arteries, the major source of blood supply,
via the anterior spinal and posterior spinal arteries.
2. Multiple radicular arteries, derives sporadically from segmental
arteries
The Medulla, Pons and Midbrain areas receive their major sources of blood
supply from several important branches of the Basilar artery

79. Branches of the Vertebral Artery
1. Posterior Inferior Cerebellar Artery
(PICA), the largest branch of the
vertebral, arises at the caudal end of the
medulla on each side.
Runs a course winding between the
medulla and cerebellum
Distribution:
a. posterior part of cerebellar
hemisphere
b. inferior vermis
c. central nuclei of cerebellum
d. choroid plexus of 4th ventricle
e. medullary branches to dorsolateralmedullary branches to dorsolateral
medullamedulla

80. Branches of the Vertebral Artery
2. Anterior Spinal Artery, formed from a
Y-shaped union of a branch
from each vertebral artery.
Runs down the ventral median fissure
the length of the cord.
Distribution:
a. supplies the ventral 2/3 of the spinal
cord.

81. Branches of the Vertebral Artery
3. Posterior Spinal Arteries (2),
originate from each vertebral artery
or Posterior Inferior Cerebellar on
each side of the Medulla.
Descends along the dorsolateral sulcus.
Distribution:
supplies the dorsal 1/3 of the cord
of each side.

82. 4. Posterior meningeal, one or two branches that originate
from the vertebral opposite the foramen magnum. This branch
moves into the dura matter of the cranium
5. Bulbar branches, composed of several smaller arteries which
originate from the vertebral and it’s branches. These branches
head for the pons, medulla and cerebellum
Branches of the Vertebral Artery

83. Spinal Cord Blood Supply
Ventral Dorsal

84. Spinal Cord Blood Supply
Anterior Spinal
Artery, provides
sulcal branches
which penetrate the
ventral median
fissure and supply
the ventral 2/3 of
the spinal cord.
Posterior Spinal
Arteries, each
descends along the
dorsolateral surface
of the spinal cord
and supplies the
dorsal 1/3.

85. Radicular arteries,
originating from
segmental arteries at
various levels, which
divide into anterior and
posterior radicular
arteries as they move
along ventral and dorsal
roots to reach the spinal
cord. Here they reinforce
spinal arteries and
anastomose with their
branches.
Spinal Cord Blood Supply
From these varied sources of blood supply, a series of circumferential anastomotic
channels are formed around the spinal cord, called the arterial vasocorona, from
which short branches penetrate and supply the lateral parts of the cord

86. Spinal Cord Blood Supply
The radicular arteries provide the
main blood supply to the cord at
the thorasic, lumbar and sacral
segments. There are a greater
number on the posterior (10-23)
than anterior (6-10 only) side of
the cord.
One radicular artery, noticeably larger than the others, is called the
artery of Adamkiewicz, or the artery of the lumbar enlargement. Usually
located with the lower thorasic or upper lumbar spinal segment on the left
side of the spinal cord

87. Spinal Cord Blood Supply
The spinal cord lacks adequate collateral supply in some areas, making
these regions prone to ischemia after vascular occlusions. The upper
Thorasic (T1-T4) and first lumbar segments are the most vulnerable regions
of the cord.

88. Spinal Cord Blood Supply
There are several arteries that reinforce the
spinal cord blood supply and are termed
segmental arteries
1. The Vertebral arteries, spinal branches
which are present in the upper cervical
(~C3-C5) levels
2. Ascending Cervical arteries, present in the
lower cervical areas
3. Posterior Intercostal, present in the
mid-thorasic region
4. First Lumbar arteries, present in the
mid-lumbar regions

89. The spinal veins arranged in
an irregular pattern.
The anterior spinal veins run
along the midline and the
ventral roots. The posterior
spinal veins run along the
midline and the dorsal roots.
These are drained by the
anterior and posterior
radicular veins. These in turn
empty into an epidural venous
plexus which connects into an
external vertebral venous
plexus, the vertebral,
intercostal and lumbar veins.
Spinal Cord Blood Supply

90. Spinal Cord Blood Supply
Occlusion of the anterior spinal artery may lead to the anterioranterior
cord syndromecord syndrome, characterized by;
1. Loss of ipsilateral motor function, due to damage to ventral gray matter
and the ventral corticospinal tract.
2. Loss of contralateral pain and temperature sensation, due to damage to
the spinothalamic pathway

91. Spinal Cord Blood Supply
Occlusion of the posterior spinal arteries may lead to the rare
posterior cord syndromeposterior cord syndrome, characterized by;
1. Ipsilateral motor deficits, due to damage to corticospinal tract
2. Ipsilateral loss of tactile discrimination, position sense, vibratory sense,
due to damage to the dorsal columns

92. Blood Supply to the Brain Stem
The brain stem (medulla, pons
midbrain) receives the bulk of its
blood supply from the
vertebrobasilar system. Except
for the labyrynthine branch,
all other branches supply the
brain stem and cerebellum
The posterior cerebral has only
a small contribution, its main
target being the posterior
cerebral hemispheres

93. Branches of the Basilar Artery
1. Anterior Inferior Cerebellar Arteries
(AICA), originates near the lower border
of the Pons just past the union of the
vertebral arteries.
Distribution:
a. supplies anterior inferior surface and
underlying white matter of cerebellum
b. contributes to supply of central
cerebellar nuclei
c. also contributes to upper medullaalso contributes to upper medulla
and lower pontine areasand lower pontine areas

94. Branches of the Basilar Artery
2. Pontine arteries, numerous smaller
branches that can be subdivided into
Paramedian and Circumferential pontine
arteries. The Circumferential can be
further subdivided into Long and Short
pontine arteries.
Distribution:
a. paramedian pontine - basal pons
b. circumferential pontine - lateral pons
and middle cerebellar peduncle, floor
of fourth ventricle and pontine tegmentum

95. Branches of the Basilar Artery
3. Superior Cerebellar arteries, originates
near the end of the Basilar artery,
close to the Pons-Midbrain junction.
Runs along dorsal surface of cerebellum
Distribution:
a. cerebellar cortex, white matter and
central nuclei
b. Additional contribution to rostralAdditional contribution to rostral
pontine tegmentum, superior cerebellarpontine tegmentum, superior cerebellar
peduncle and inferior colliculuspeduncle and inferior colliculus

96. Branches of the Basilar Artery
4. Posterior cerebral arteries, the terminal
branches of the Basilar artery. They
appear as a bifurcation of the Basilar,
just past the Superior Cerebellar arteries
and the oculomotor nerve.
Curves around the midbrain and reaches
the medial surface of the cerebral
hemisphere beneath the splenium of the
corpus callosum
Distribution:
a. mainly neocortex and diencephalon
b. some contribution to interpeduncularsome contribution to interpeduncular
plexusplexus

97. Branches of the Basilar Artery
5. Labyrynthine arteries, may branch
from the basilar, but variable in its
origin. Supplies the region of the inner
ear

98. Blood Supply to the Medulla
The Medulla is supplied by the;
1. Anterior spinal artery, sends blood to the paramedian region of the caudal
medulla.
2. Posterior spinal artery, supplies rostral areas, including the gracile and
cuneate fasiculi and nuclei, along with dorsal areas of the inferior cerebellar
peduncle.
3. Vertebral artery, bulbar branches supply areas of both the caudal and rostral
medulla.
4. Posterior inferior cerebellar artery, supplies lateral medullary areas.

99. Blood Supply to the Medulla

100. Blood Supply to the Medulla
Occlusion of branches of the anterior spinal artery will produce
a inferior alternating hemiplegia (aka medial medullary syndromemedial medullary syndrome),
characterized by;
1. A contralateral hemiplegia of the limbs, due to damage to the
pyramids or the corticospinal fibers
2. A contralateral loss of position sense, vibratory sense and
discriminative touch, due to damage to the medial leminiscus
3. An ipsilateral deviation and paralysis of the tongue, due to
damage to the hypoglossal nucleus or nerve
Occasionally, these symptoms will develop after occlusion of the
vertebral artery before gives off its branches to the anterior spinal
artery

102. Blood Supply to the Medulla
TheThe posterior spinal arteriesposterior spinal arteries
supply thesupply the
gracile and cuneate fasiculi andgracile and cuneate fasiculi and
nuclei,nuclei,
spinal trigeminal tract andspinal trigeminal tract and
nucleus,nucleus,
portions of theportions of the
inferior cerebellar peduncleinferior cerebellar peduncle

103. Blood Supply to the Medulla
TheThe vertebral arteriesvertebral arteries supplysupply
the pyramids at the level of the Pons,the pyramids at the level of the Pons,
the inferior olive complex,the inferior olive complex,
the medullary reticular formation,the medullary reticular formation,
solitary motor nucleussolitary motor nucleus
dorsal motor nucleus of the Vagusdorsal motor nucleus of the Vagus
(cranial nerve X),(cranial nerve X),
hypoglossal nucleushypoglossal nucleus
(cranial nerve XII).(cranial nerve XII).
spinal trigeminal tract,spinal trigeminal tract,
spinothalamic tractspinothalamic tract
spinocerebellar tractspinocerebellar tract

104. Blood Supply to the Medulla
TheThe posterior inferiorposterior inferior
cerebellar arteriescerebellar arteries (PICA)(PICA)
supplysupply
spinothalamic tract,spinothalamic tract,
spinal trigeminal nucleus andspinal trigeminal nucleus and
tract,tract,
fibers from the nucleusfibers from the nucleus
ambiguous,ambiguous,
dorsal motor nucleus of thedorsal motor nucleus of the
Vagus (cranial nerve X)Vagus (cranial nerve X)
inferior cerebellar peduncleinferior cerebellar peduncle

105. Blood Supply to the Medulla
Occlusion of the posterior inferior cerebellar artery (or contributing
vertebral) will produce a lateral medullary syndromelateral medullary syndrome or Wallenberg’s syndromeWallenberg’s syndrome,
characterized by;
1. A contralateral loss of pain and temperature sense, due to
damage to the anterolateral system (spinothalamic tract)
2. An ipsilateral loss of pain and temperature sense on the face, due
to damage to the spinal trigeminal nucleus and tract
3. Vertigo, nausea and vomiting, due to damage to the vestibular nuclei
4. Hornor’s syndrome, (miosis [contraction of the pupil],
ptosis [sinking of the eyelid], decreased sweating), due to
damage to the descending hypothalamolspinal tract

107. Blood Supply to the Pons
The Pons is supplied by the;
1. The Basilar artery, contributions of this main artery can be further
subdivided;
a. paramedian branches, to medial pontine region
b. short circumferential branches, supply anterolateral pons
c. long circumferential branches, run laterally over the anterior
surface of the Pons to anastomose with branches of the anterior inferior
cerebellar artery (AICA).
2. Some reinforcing contributions by the anterior inferior cerebellar and
superior cerebellar arteries

108. Blood Supply to the PonsAdditional branches of the
Basilar artery can be found
branching off within the
region of the Pons;
1. Anterior Inferior Cerebellar
Arteries (AICA), originates near
the lower border
of the Pons just past the union
of the vertebral arteries.
Distribution:
a. supplies anterior inferior
surface and underlying white
matter of cerebellum
b. contributes to supply of
central cerebellar nuclei
c. also contributes to upperalso contributes to upper
medulla and lower pontine areasmedulla and lower pontine areas

109. Blood Supply to the Pons
2. Superior Cerebellar arteries,
originates near the end of the Basilar
artery, close to the
Pons-Midbrain junction.
Runs along dorsal surface of
cerebellum
Distribution:
a. cerebellar cortex, white matter and
central nuclei
b. Additional contribution to rostralAdditional contribution to rostral
pontine tegmentum, superiorpontine tegmentum, superior
cerebellar peduncle and inferiorcerebellar peduncle and inferior
colliculuscolliculus

110. Blood Supply to the Pons2. Labyrynthine arteries, may
branch from the basilar, but
variable in its origin. Supplies
the region of the inner ear.
Divides into two branches;
a. anterior vestibular
b. common cochlear
The labyrinthine has a variable
origin, according to a study done
by Wende et. al., 1975, (sample
size of 238) the artery originated
from;
1. Basilar (16%)
2. AICA (45%)
3. Superior cerebellar (25%)
4. PICA (5%)
5. Remaining 9% were of duplicate
origin

111. Blood Supply to the Pons
The paramedian branches of the Basilar artery supplies the paramedian
regions of the Pons, this includes corticospinal fibers (basis pedunculi),
the medial leminiscus, abducens nerve and nucleus (cranial nerve VI) ,
pontine reticular area, and periaquaductal gray areas

112. Blood Supply to the Pons
TheThe paramedian branchesparamedian branches
of the Basilar arteryof the Basilar artery
supplysupply
corticospinal fibers,corticospinal fibers,
the medial leminiscus,the medial leminiscus,
abducens nerve andabducens nerve and
nucleus (cranial nervenucleus (cranial nerve
VI) ,VI) ,
pontine reticular area,pontine reticular area,
periaquaductal gray areasperiaquaductal gray areas

113. Blood Supply to the Pons
Obstruction of the paramedian pontine arteries will produce a
middle alternating hemiplegia (also termed medial pontine syndrome)
which is characterized by;
1. Hemiplegia of the contralateral arm and leg, due to damage to the
corticospinal tracts
2. Contralateral loss of tactile discrimination, vibratory and position
sense, due to damage to the medial leminiscus
3. Ipsilateral lateral rectus muscle paralysis, due to damage to the
abducens nerve or tract (can cause diplopia “double vision”)

114. Blood Supply to the Pons
TheThe short circumferential branchesshort circumferential branches
supply,supply,
pontine nuclei,pontine nuclei,
pontocerebellar fibers,pontocerebellar fibers,
medial leminiscusmedial leminiscus
the anterolateral system (spinothalamicthe anterolateral system (spinothalamic
fibers)fibers)

115. Blood Supply to the Pons
TheThe long circumferential brancheslong circumferential branches supply,supply,
along with thealong with the anterior inferior cerebellaranterior inferior cerebellar (caudally),(caudally),
andand superior cerebellar arterysuperior cerebellar artery (rostrally).(rostrally).
middle and superior cerebellar peduncles,middle and superior cerebellar peduncles,
vestibular and cochlear nerves and nuclei,vestibular and cochlear nerves and nuclei,
facial motor nucleus (cranial nerve VII)facial motor nucleus (cranial nerve VII)
trigeminal nucleus (cranial nerve V)trigeminal nucleus (cranial nerve V)
spinal trigeminal nucleus and tract (cranial nerve V),spinal trigeminal nucleus and tract (cranial nerve V),
hypothalamospinal fibers,hypothalamospinal fibers,
the anterolateral system (spinothalamic)the anterolateral system (spinothalamic)
pontine reticular nuclei.pontine reticular nuclei.

116. Blood Supply to the Pons
Occlusions of long branches circumferential branches of the basilar
artery produce a lateral pontine syndrome, characterized by;
1. Ataxia, due to damage to the cerebral peduncles (middle and superior)
2. Vertigo, nausea, nystagmus, deafness, tinitus, vomiting, due to
damage to vestibular and cochlear nuclei and nerves
3. Ipsilateral pain and temperature deficits from face, due to damage to
the spinal trigeminal nucleus and tract
4. Contralateral loss of pain and temperature sense from the body,
due to damage to the anterolateral system (spinothalamic)
5. Ipsilateral paralysis of facial muscles and masticatory muscles, due
to damage to the facial and trigeminal motor nuclei (cranial nerves
VII and V)

121. Blood Supply to the Midbrain
The major blood supply to the midbrain is derived from branches
of the basilar artery;
1. Posterior cerebral artery, forms a plexus with the posterior
communicating arteries in the interpeduncular fossa, branches from this
plexus supply a wide area if the midbrain
2. Superior cerebellar artery, supplies dorsal areas around the
central gray and inferior colliculus with support from branches of
the posterior cerebral artery.
3. Quadrigeminal, (some posterior choroidal) a branch of the posterior
cerebral, provides support for the tectum (superior and inferior colliculi)
4. Posterior communicating artery, derived from the internal carotid,
joins the posterior cerebral to form portions of the circle of Willis
(arterial circle). Contributes to the interpeduncular plexus
5. Branches of these arteries are best understood when grouped into
paramedian, short circumferential and long circumferential

122. Blood Supply to the Midbrain
The paramedian arteries, derived from the posterior communicating and
posterior cerebral, form a plexus in the interpeduncular fossa, enter the
through the posterior perforated substance, this system supplies
raphe region,raphe region,
oculomotor complex,oculomotor complex,
medial longitudinal fasiculus,medial longitudinal fasiculus,
red nucleusred nucleus
substantia nigrasubstantia nigra
crus cerebricrus cerebri

123. Blood Supply to the Midbrain
Occlusion of midbrain paramedian branches produces a medial
midbrain or superior alternating hemiplegia (or Weber’s syndrome)
characterized by;
1. Contralateral hemiplegia of the limbs, and contralateral face
and tongue due to damage to the descending motor tracts
(crus cerebri).
2. Ipsilateral deficits in eye motor activity, caused by damage to the
oculomotor nerve

124. Blood Supply to the Midbrain
The short circumferential arteries originate from the interpeduncular
plexus and portions of the posterior cerebral and superior cerebellar
arteries, this system supplies
crus cerebri,crus cerebri,
substantia nigrasubstantia nigra
midbrain tegmentummidbrain tegmentum

125. Blood Supply to the Midbrain
The long circumferential branches originate mainly from the posterior
cerebral artery, one important branch, the quadrigeminal (collicular
artery) supplies the superior and inferior colliculi.

126. Blood Supply to the Midbrain
The posterior choroidal arteries
originate near the basilar
bifurcation into the posterior
cerebral arteries. In addition
to providing reinforement to
the midbrain short and long
circumferential arteries they
move forward to supply portions
of the diencephalon and the
choroid plexus of the third
and lateral ventricles

129. Other Clinical Points
Substantial infarcts within the Pons are generally rapidly fatal,
due to failure of central control of respiration
Infarcts within the ventral portion of the Pons can produce
paralysis of all movements except the eyes. Patient is conscious
but can communicate only with eyes. LOCKED-IN-SYNDROME

130. Vascular Medicine 17(3) 168–173

131. J Vasc Surg 2004;40:703-10
• Pelvic ischemic complications after open
infrarenal aor- tic reconstruction occur in 1%
to 2% of patients, with an associated mortality
rate greater than 40%.
• Likewise, lower extremity ischemia after
aortic reconstructions, often referred to as
“trash foot” is a well-recognized result of
atheroemboli, and occurs in 1% to 5% of
patients.

132. • Case Reports in Medicine
• Volume 2011 (2011), Article ID 954572, 4
pages
• doi:10.1155/2011/954572
• The Adamkiewicz artery (AKA) supplies most
of the blood to the anterior spinal artery,
which perfuses the anterior two thirds of the
spinal cord. AKA originates variably between
T5 and L3 and from the left side in 75% of
cases [11]. In 7.5% of cases also it arises from

133. The spinal veins arranged in
an irregular pattern.
The anterior spinal veins run
along the midline and the
ventral roots. The posterior
spinal veins run along the
midline and the dorsal roots.
These are drained by the
anterior and posterior
radicular veins. These in turn
empty into an epidural venous
plexus which connects into an
external vertebral venous
plexus, the vertebral,
intercostal and lumbar veins.
Spinal Cord Blood Supply