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Endoleak

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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.

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.

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  • Common, non-endoleak-related complications during or after EVAR can be categorized as complications owing to Excluded aneurysmal sac.
    surgical exposure of the cannulated arteries,
    systemic complications,
    ischemic complications owing to
    intentional or inadvertent clot embolization or
    covering of an aortic side branch,
    stenosis or occlusion of astent-graft limb, and
    infection complications of the stent graft and
    excluded aneurysmal sac.
  • The real benefit of EVAR over open surgery is the decreased rate of systemic complications, especially in the periopera- tive period [5]. However, systemic complications are the most common complication during the first 30 postoperative days.
    Cardiovasc Intervent Radiol (2006) 29:935–946
  • usually results in procedure abandonment or surgical con- version. A multicenter study concluded that an aneurysm diameter greater than or equal to 60 mm was the most important risk factor for failure to complete the procedure [8]. There are other risk factors for deployment failure and these include difficult access anatomy, tortuous arteries, and a short proximal neck
    Risk factors for AAA rupture include proximal type I endoleak, midgraft type III endoleak, graft migration, and postoperative kinking of the endograft
  • Although clinical surveillance with or without medical treatment or surgical repair are mostly enough for definitive treatment, ultrasound (US) or computed tomography (CT) evaluation can be needed to evaluate the extent of the lesion.
    The stiff and large-catheter system of the stent graft (commonly between 20- and 24-French) potentially cannot be introduced within the aortic aneurysm, especially in the presence of small and heavily calcified iliofemoral access arteries, resulting in abortion of the EVAR procedure or conversion to an iliac conduit. Finally, the introduction of the large-catheter system can induce vessel wall dissection or even perforation. In case of a postsurgical groin pseudoaneurysm (Fig. 1), US-guided thrombin injection is not always successful as the pseudoaneurysmal neck can be too large, making surgical repair the only definitive treat- ment option.
    Correct positioning and deployment of the stent graft strictly needs high-quality fluoroscopy and digital subtraction angiography imaging using injection of iodi- nized contrast medium. Commonly, an average amount of
    Surgical Complications
    LOCAL WOUND COMPLICATIONS IN THE GROIN
    Local wound complications include groin hematoma, infection, or lymphocele, and the incidence is 1 to 10%.3
    ACCESS ARTERY INJURY
    Arterial thrombosis, dissection, or pseudoaneurysm formation can occur in up to 3% of EVAR procedures.
    correct surgical skills,
    preoperative US or CT evaluation of the common femoral and iliac arteries with special attention to access vessel diameter, tortuosity, and degree of calcification is mandatory.
    Contrast Nephropathy
    50 to 100 mL of dye is needed for an EVAR procedure.
    6.7% of cases,
    carbon dioxide (CO2) can be used as an alternative contrast agent.
    injected through the stent- graft delivery catheter, making the placement of a pigtail catheter in the aorta unnecessary.8
  • • 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
  • Guidant Ancure ..Clinical use of this technique was unacceptable: it had not been evaluated by the FDA, nor had doctors been appropriately trained to perform it
    Device failure n cant retranct.. Have to open
  • clot formation or clot embolization into aortic side branches and include colonic, renal, and pelvic ischemia.
    thereby partially or completely covering an aortic or iliac side branch, can result in renal or pelvic ischemia.
  • COLONIC ISCHEMIA
    Bowel ischemia occurs in 1 to 3% of cases after open aortic aneurysm repair, and the incidence seems to be in the same as for EVAR.9,10 Postoperative bowel ischemia after aortic aneurysm repair still remains a serious com- plication with a mortality rate of 50% within 1 month.9 However, the pathophysiological mechanism of colonic ischemia in open versus endovascular repair is most probably different. Whereas interruption of the inferior mesenteric or iliac arteries has been suggested to be the cause of bowel ischemia in open procedures, the same mechanism does not seem to be important for EVAR. Zhang et al11 presume that the presence of thrombotic deposits and atheroma in the suprarenal aorta may be responsible for major bowel ischemia in EVAR proce- dures. These thrombotic and atheromatous deposits can be dislodged while the proximal part of the endograft is being positioned and deployed just below the renal arteries or when the proximal part of the endograft is balloon-dilated. These maneuvers can induce upstream flushing of mural clot material or atherosclerotic debris into the superior mesenteric artery. These microemboli may also migrate into the renal, inferior mesenteric, internal iliac, and lower-limb circulation resulting in segmental, skipped, or patchy ischemia of the embolized areas. This mechanism of microemboli embolization also explains why bowel ischemia after EVAR mostly presents as multifocal patchy ischemia. This type of bowel ischemia is not seen after open repair, most probably because suprarenal aortic and ostial inferior mesenteric arterial clamping during open repair makes distal microembolization unlikely. Finally, these obser- vations also stress the importance of careful preoperative analysis of the proximal aneurysmal neck to identify thrombus or atheroma, making these patients poor candidates for EVAR.
    SPINAL CORD ISCHEMIA
    Spinal cord ischemia after EVAR for AAA is very rare, and the EUROSTAR database found an incidence of 0.21% in 2862 patients.12 The mechanism is not com- pletely understood, but atheromatous embolization and interruption of collateral circulation from lumbar and internal iliac arteries together with a variable anatomy of the artery of Adamkiewicz seem to be the most contributing factors. The treatment is the same as for paraplegia after thoracoabdominal EVAR or open repair and consists in cerebrospinal fluid drainage13–16 and, if indicated, recanalization of occluded collateral arteries like the internal iliac artery.17
    RENAL ARTERY OCCLUSION (STENTING AND RETRIEVAL OF THE STENT GRAFT)Inadvertent stent-graft placement with partial or total coverage of one or both renal arteries occurs in less than 5% of cases18 and is potentially associated with the lack of high-quality imaging technology for guiding the EVAR procedure and a learning curve of the endovas- cular team. In their early experience with aortic stent grafting, Kalliafas et al18 described renal artery occlusion in 5 of 204 patients, resulting in renal failure with chronic hemodialysis need in two of them. If misplace- ment is detected during EVAR, then an attempt can be made, using a pull-down maneuver with an inflated angioplasty balloon or by tugging caudally on a guide wire placed across the endograft bifurcation and exteri- orized from both femoral arteries. Using this technique, Go ̈rich et al19 could move the stent graft from 5 to
    27 mm more distally. Importantly, these authors did not perform this procedure on stent grafts with barbs at the proximal part of the suprarenal stent.
    Finally, in case of partial coverage of one renal artery, stent placement in the renal artery with slight protrusion of the stent over the proximal part of the stent graft into the aorta can also solve the problem.20
    Early and Late Limb Occlusion after EVAR
    Limb thrombosis in abdominal aortic stent grafts is a known complication, especially in unsupported endog- rafts, in which it can occur in as many as 40% of cases.21,22 The underlying mechanism is most fre- quently limb kinking of the unsupported endograft limb. Second-generation supported stent grafts per- form better than unsupported endografts with regard to avoidance of limb thrombosis, and these second- generation stent grafts are all associated with varying rates of limb occlusion ranging between 0% and 5%.23 Most of the thrombotic events occur within the first 2 months after EVAR, and the underlying causes of limb thrombosis are stent-graft kinking (Fig. 2) and extension of the small-diameter stent graft into the external iliac artery.24,25 Recently, it has been demon- strated that limb occlusion can also occur long after EVAR. The pathophysiological mechanism of late (after 4 to 5 years of follow-up) limb occlusion can be migration and dislocation of an endograft component causing major turbulence of hemodynamics and even- tually limb or entire stent-graft thrombosis.23 Treat- ment of limb occlusion includes various surgical and endovascular revascularization techniques; the best treatment option depends on the patient’s general
    status as well as on local anatomic changes of the stent graft and excluded aneurysm.
    In contrast to limb thrombosis after EVAR, incidentally found mural thrombotic deposits are much more frequent in both first- (20%) and second-gener- ation (17 to 33%) supported endografts.26 This circum- ferential layer of thrombotic material (Fig. 3) is observed more in Zenith stent grafts (Cook Medical, Blooming- ton, IN) than in Excluder stent grafts (W.L. Gore and Associates, Flagstaff, AZ), but they are clinically silent and are not associated with potential stent-graft throm- bosis or distal embolization. Additionally, there is no difference in survival among patients presenting with mural deposits in their endograft compared with patients without this thrombotic layer. Based on these observa- tions, additional treatment in the form of relining the endograft with another endograft or administering any type of anticoagulant therapy cannot be recommended to these patients.
  • Patients with an interrupted right vertebral artery had a high risk of malperfusion of the vertebrobasilar system due to occlusion of the LSA. Some patients with an interrupted left vertebral artery carry a high risk of malperfusion of the cerebellum because of a terminal posterior inferior cerebellar artery (PICA). In patients with a terminal PICA, the vertebral artery is not con- nected to the basilar artery and ends in the PICA (Fig 2). A normal PICA branches off before the left and right vertebral arteries join the basilar artery. In patients with a left terminal PICA, the left vertebral artery is not connect to the basilar artery and ends in the PICA. Ischemia of the region around the PICA can be caused by occlusion of the left subclavian artery. An interrupted left vertebral artery includes a left terminal PICA, but it is difficult to accurately diagnose a terminal PICA on MRA.
    The LSA occlusion without revascularization in patients undergoing TEVAR is associated with increased risks of subsequent subclavian steal syndrome, watershed poste- rior circulation strokes, and spinal cord ischemia
    The LSA occlusion without revascularization in patients undergoing TEVAR is associated with increased risks of subsequent subclavian steal syndrome, watershed poste- rior circulation strokes, and spinal cord ischemia [6]. In study 2 we evaluated the patients with distal arch or proximal descending aneurysm which have slight risk of spinal cord ischemia, so we did not evaluate spinal cord ischemia. Botta and colleagues [6] reported that intentional closure of the LSA caused a cerebellar stroke in a 22-year- old patient, despite no alterations of the circle of Willis. Görich and colleagues [7] reported that among 4 patients with incomplete LSA overstenting and 19 with complete occlusion of the LSA, 3 patients (13.6%) had ischemic arm symptoms but none showed persistent signs of vertebro- basilary insufficiency. In the series of Tiesenhausen and colleagues [8], 3 (37.5%) of 8 patients with partial or com- plete occlusion of the LSA had vertebrobasilar symptoms. Criado and colleagues [9] reported that occlusion of one vertebral artery caused vertebrobasilary ischemia resulting in cerebellar infarction in 2.7% of patients. Bilateral verte- bral artery occlusion (by overstenting of the LSA and an additional pathologic right vertebral artery) caused persis- tent neurologic deficits in 23% of patients [10].
    herefore, we do not recommend prophylactic LSA transposition or LCCA- LSA bypass for all patients who undergo LSA occlusion with a stent graft because most patients with subclavian steal syndrome are asymptomatic. However, LCCA-LSA bypass or LSA transposition should be performed in patients with a high risk of malperfusion of the vertebro- basilar system due to occlusion of the left subclavian artery as assessed by preoperative MRA.
    In conclusion, 11% of patients who underwent surgery for thoracic aortic aneurysms were considered to have a high risk of vertebrobasilar system malperfusion owing to the presence of LSA occlusion on preoperative MRA. Preoperative MRA is considered very useful for identify- ing patients at high risk for vertebrobasilar system malp- erfusion due to LSA occlusion.
  • Blood supply of Spinal Cord
    - anterior spinal artery q
    - primary blood supply of anterior 2/3 of spinal cord, including both the lateral coricospinal tract and ventral corticospinal tract
    - posterior spinal artery (right and left)
    primary blood supply to the dorsal sensory columns
    - Artery of Adamkiewicz
    the largest anterior segmental artery
    typically arises from left posterior intercostal artery, which branches from the aorta, and supplies the lower two thirds of the spinal cord via the anterior spinal artery
    significant variation exists
    from the left in 80% of the population
    - T5-T8 in 15%,
    - T9-T12 in 75%, and
    - L1-L2 in 10% [14].
  • segment of aorta often encroaches upon or involves the aortic arch vessels. Recent series suggest that involvement of zones 0 to 2 of the arch occurs in 􏰄40% of TEVAR cases.8,9 It is well established that if covering zones 0 or 1 with an endograft is anticipated, preoperative revasculariza- tion is a necessary adjunct to prevent significant complica- tions. The management of patients in whom zone 2 is involved, where left subclavian artery (LSA) coverage is expected, has been more controversial. Early concerns were predominantly for upper limb ischemia or vertebrobasilar syndrome; however, these proved to be rare complications that did not warrant routine preoperative revasculariza- tion.10 More recently, several series and reviews have iden- tified an increased risk of neurologic complications, spe- cifically cerebrovascular accident (CVA) and spinal cord ischemia (SCI), after coverage of the LSA.11
    The etiology behind CVA is unclear. The suggested mechanisms include atheroembolization from instrumen- tation of the aortic arch and hypoperfusion of the posterior circulation. If the former were true, one might expect prolonged procedure times and evidence of more athero- matous disease in the aortic arch in those patients who sustained a stroke. The latter is, of course, thought to be secondary to reduced vertebral blood flow, after occlusion of the LSA. With this in mind, patients with a dominant
    left vertebral artery, or those with an incomplete posterior circulation, should prove more vulnerable. A dominant left vertebral artery is, however, reported to be present in as many as 60% of individuals, which would make revascular- ization a serious consideration in 􏰄50%.8
    however, involve the ante- rior circulation alone or the anterior circulation in conjunc- tion with the posterior circulation. The interpretation of these findings may be that CVA has multiple causes and, therefore, revascularization is not exclusively protective
    The anatomic basis of SCI after LSA coverage during TEVAR is thought to be secondary to reduced anterior spinal and costocervical arterial blood flow.13 These vessels may prove more critical to spinal cord perfusion when numerous intercostals vessels are covered by the stent graft. Although the increased risk of SCI is evident from our results, the protective role of revascularization is, again, much less clear. This is perhaps due to the very small number of studies reporting this complication in this co- hort (1 SCI in 13 studies), therefore introducing bias. Regardless, SCI is also strongly associated with the extent of coverage of the thoracic aorta and, more specifically, with coverage of the distal thoracic aorta near the artery of Adamkiewicz. This is evident from studies that report an increased incidence of SCI associated with both an in- creased length of thoracic aorta covered and the use of multiple stents (suggesting greater aortic cover- age).4,11,37,42,43 Indeed, Appoo et al43 found that in 80% of patients with SCI, the entire thoracic aorta was covered. Furthermore, some series have shown a correlation be- tween concomitant or previous abdominal aortic aneurysm repair and SCI.11,33 This finding is not universal, how- ever.37,49 Lastly, the contribution of cerebrospinal fluid drainage is also unclear from the data. This is due to significant variations in its use; whether routine or selective in high-risk patients or in limited reporting in the series we reviewed.
    The reason for a potentially increased rate of SCI after LSA coverage cannot be identified from our results and the series we reviewed. Because the effect of preoperative revas- cularization is inconclusive, it remains unclear whether LSA coverage itself results in critical spinal ischemia or whether it is merely a surrogate marker for more extensive aortic disease requiring more extensive coverage and, therefore, more extensive intercostals vessel occlusion. Furthermore, it is unclear whether revascularization is protective.
    In the absence of this information, we can conclude that the 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.
  • However, there are reports of delayed onset of verteb- robasilary insufficiency and arm ischaemia [21,22], following LSA covering with ESGs. Insufficient blood supply to the posterior cerebral circulation may evolve in the presence of hypoplasia of the right vertebral artery (VA) and/or posterior communicating arteries (PCOMAs) exits [23]. Surgical transposition of the LSA to the left common carotid artery (LCCA) or LCCA-to-LSA bypass prior to TEVAR with LSA covering may preserve blood flow to the brain stem and spinal cord [1,12]. Alternatively, a branched ESG approach can be implemented [24,25].
    In the current review, we outline various strategies that have been advocated to manage and treat patients requiring covering of the LSA with ESG.
    ESG placement in the proximal part of the descending aorta often requires covering the LSA ostium to extend the proximal landing zone with a minimum of 2 cm of normal aortic wall. Covering the LSA can lead to vascular and neurological complications and to type-II endoleak by retrograde perfusion from the LSA into the aneurysm sac or the dissection’s false lumen in certain patients. Several authors [6,29,32,33,38], therefore, recommend prophylactic revascularisation of the LSA before coverage in high-risk patients. Others [48,50,51] criticise every additional surgical procedure by suggesting that they add to the invasiveness and overall treatment of TAA or dissection patients [50]. In addition, they draw attention to the 1—5% mortality rates described in association with LSA-to-LCCA bypass or LSA transposition [50], although these data refer to occlusive atherosclerotic lesions of the LSA and not to LSA coverage by ESGs. Another argument in favour of a procedure without prophylactic LSA revascularisation is that LSA coverage is a well-tolerated procedure in patients with normal (no apparent angiographic lesions) supra-aortic branches [30,50]. When collateral blood flow from the muscular arterial branches in the neck and shoulder girdle [17] and via the contralateral VA [50] is adequate, most patients with subclavian steal syndrome are asymptomatic [50]. This may be difficult to maintain for incipient aortic conditions, for instance, in acute aortic dissection or some traumatic transections. After systematically probing the literature to analyse whether the hypothesis that the putative absence of a collateral network in acute aortic conditions leads to a higher frequency of neurological events with coverage of the LSA ostium is true, we found that unequivocal information on this paradigm is lacking. This is due to low patient numbers and few specifics by the authors in differentiating emer- gency, acute, chronic and elective cases and in reporting (neurologic) complications. However, recent data [34,45,49] reveal that a high percentage of patients undergoing TEVAR with LSA coverage need conditional prophylactic LSA transposition or LSA-to- LCCA bypass surgery due to abnormal supra-aortic vascular anatomy or existing supra-aortic pathology. Moreover, the same studies report a significant incidence of devastating neurologic complications in the remaining non-revascu- larised group.
    The reported incidence of stroke varies from 2% to 15% [15,18,34,38,45,46,48], whereby the causes seem multi- factorial. Although a significant number of strokes occur in the posterior circulation and can be attributed to localised anatomical vascular malformations or vascular pathology directly linked to LSA coverage, still another significant number does occur in other parts of the brain and has other aetiology, for instance, hypoperfusion or emboli. It is generally known that LSA covering without prophylactic revascularisation leads to a significant higher incidence of stroke compared with LSA covering with prophylactic revascularisation. Nevertheless, a substantial part of all presenting strokes do occur in patients with TEVAR without LSA coverage, and even in some with LSA covering with prophylactic revascularisation. TEVAR patients, therefore, still present an elevated risk of perioperative stroke (due to guidewire manipulations and ESG deployment during the procedure).
    SCI is another serious potential complication of TEVAR with an incidence of between 0% and 5%, although few data are available. Proposed pathophysiologic mechanisms include, for instance, LSA coverage leading to reduced blood flow to the VA and thus to the spinal cord via the spinal artery and/or to reduced anterior spinal and costocervical blood flow by coverage of intercostal vessels by one or more stent grafts. Further suggested risk factors for compromised spinal cord perfusion in TEVAR are the occlusion of intercostal arteries by the stent grafts at the T8-12 level, previous abdominal aortic surgery, occlusion of internal iliac arteries and renal failure. Overall, the risk of SCI after TEVAR is significant and is not to be underestimated because of the condition’s severity.
    Unfortunately, many of these neurological conditions do not resolve after secondary revascularisation. It thus may be necessary to perform prophylactic LSA transposition or LSA- to-LCCA bypass surgery in elective patients scheduled for TEVAR with LSA coverage, also because their additional surgical risk is low as they are usually free of occlusive atherosclerotic lesions of the LSA.
    Subclavian steal syndrome is common after TEVAR with LSA coverage, with an incidence of 5—37.5%. Most of these patients are asymptomatic due to the flow inversion from the VA and the presence of collaterals in the neck and shoulder girdle, as symptoms, if they occur, tend to be mild and transient.
    The incidence of left-arm ischaemia is reported between 0% and 36%. Symptoms are mostly transient and consist of a cooler hand, exercise-induced paraesthesias of the left arm and hand, claudication and rest pain or even distal digital trophic changes. Prophylactic revascularisation prevents such symptoms.
    Overall, left-upper-extremity symptoms occur in about 20% of patients, who undergo TEVAR and LSA coverage without prior revascularisation. When one considers the high frequency of this complication together with the substantial threat of severe neurologic sequela (i.e., stroke or SCI after TEVAR with LSA coverage and without prophylactic revascu- larisation), a prophylactic revascularisation is strongly recommended.
    By contrast, covering of the LSA without prophylactic revascularisation of the LSA is justified in acute unstable patients (e.g., patients with aortic rupture) because of the shortage of time to perform prophylactic LSA transposition or LSA-to-LCCA bypass surgery. As we anticipate the absence of a patent collateral network in those conditions, secondary revascularisation of the LSA is indicated after the emergency situation.
    The LSA-to-LCCA bypass or LSA transposition procedure may itself be hazardous and there are few reports that document cases that do not proceed to TEVAR because of complications related to the preparatory LSA revascularisa- tion. Future studies are necessary to distinguish whether the morbidity of TEVAR without prophylactic revascularisation is significantly greater than the combined morbidity of TEVAR with prophylactic revascularisation. Until databases and reports include all patients on an intention-to-treat basis, definitive evidence that one approach is superior to another is difficult to acquire. Nevertheless, such pathology-based rather than procedure-based databases would incorporate the added complication rate of the prophylactic surgical procedure in the total equation.
    Finally, prophylactic LSA transposition or LSA-to-LCCA bypass surgery and TEVAR is recommended for elderly and high-risk patients not suitable for conventional open surgery. This is based on the fact that, so far, long-term results regarding integrity and durability of the stent-graft device are missing [53]. However, in traumatic aortic rupture, descending aneurysm rupture and in acute aortic dissection type-B patients with complications, where conventional surgery exhibits high mortality and morbidity rates, TEVAR is recommended as first-line therapy.
  • We strive to preserve pelvic blood flow whenever pos- sible, particularly in patients who have had previous pelvic procedures that might have interrupted hypogastric artery collateral vessels, sustained hypotension, and possible distal pelvic embolization. Like others,26,27 we attempt to save 1 or both hypogastric arteries, and have even reimplanted the hypogastric artery into the external iliac artery or performed endovascular external iliac to internal iliac artery bypass. However, we have found this to be a cumbersome proce- dure, particularly in patients who are obese or have calcified
    iliac arteries. Other adjunctive procedures, including place- ment of larger “aortic cuffs” or flared iliac limbs to accom- modate ectatic iliac arteries, are beneficial in preserving pelvic blood flow. However, their use is somewhat limited to ectatic iliac arteries less than 2.5 cm in maximum diam- eter. Our results suggest that bilateral hypogastric artery interruption is relatively safe in patients with complex aor- toiliac aneurysms, particularly when pelvic collateral circu- lation from the external iliac and femoral arteries is pre- served.
  • We strive to preserve pelvic blood flow whenever pos- sible, particularly in patients who have had previous pelvic procedures that might have interrupted hypogastric artery collateral vessels, sustained hypotension, and possible distal pelvic embolization. Like others,26,27 we attempt to save 1 or both hypogastric arteries, and have even reimplanted the hypogastric artery into the external iliac artery or performed endovascular external iliac to internal iliac artery bypass. However, we have found this to be a cumbersome proce- dure, particularly in patients who are obese or have calcified
    iliac arteries. Other adjunctive procedures, including place- ment of larger “aortic cuffs” or flared iliac limbs to accom- modate ectatic iliac arteries, are beneficial in preserving pelvic blood flow. However, their use is somewhat limited to ectatic iliac arteries less than 2.5 cm in maximum diam- eter. Our results suggest that bilateral hypogastric artery interruption is relatively safe in patients with complex aor- toiliac aneurysms, particularly when pelvic collateral circu- lation from the external iliac and femoral arteries is pre- served.
  • Early and Late Limb Occlusion after EVAR 40% / 0% and 5% (2nd gen)
    mural thrombotic deposits are much more frequent in both first- (20%) and second-gener- ation (17 to 33%) supported endografts.
    first 2 months after EVAR,
    kinking of the unsupported endograft
    small-diameter stent graft into the external iliac artery
    also occur long after EVAR
    migration and dislocation of an endograft component causing major turbulence of hemodynamics and even- tually limb or entire stent-graft thrombosis
    best treatment option depends on the patient’s general status as well as on local anatomic changes of the stent graft and excluded aneurysm
    endograft with another endograft or administering any type of anticoagulant therapy cannot be recommended to these patients
    Lower extremity ischemic complications. A sum- mary of lower extremity ischemic complications is pre- sented in Table I. Of 21 patients with lower extremity ischemia, this complication was the result of limb occlusion in 15 patients (71%), atheroembolization in 3 patients (14.7%), and common femoral artery thrombosis in 3 pa- tients (14.7%).
    Limb occlusions manifested with pain and parasthesia (n 􏰂 5), rest pain alone (n 􏰂 4), intermittent claudication (n 􏰂 5), and decreased femoral pulse as the sole finding (n 􏰂 1). No patient had motor deficits. Limb occlusions were managed according to surgeon preference, as follows: 4 patients underwent thrombectomy and stent placement, 7 patients underwent femorofemoral bypass, 1 graft was eventually explanted because of persistent type I endoleak, and 3 patients were managed expectantly. The 3 patients managed expectantly all had intermittent claudication, which has subsequently improved. In 14 of 15 patients with limb occlusions unsupported endografts (Ancure) were implanted. Five limb occlusions in patients with Ancure devices in place had been stented a priori, because of kinked or stenosed limbs noted at the initial EVAR. One patient with a supported endograft (AneuRx) had limb occlusion at 6 months post-EVAR. In 4 of 15 occluded limbs (26.7%) devices were deployed in the external iliac artery (P 􏰂 .206). Average limb diameter of the 15 occluded limbs was 13.2 mm.
    In summary, ischemic complications after EVAR oc- curred in 9% of patients in our series. Pelvic ischemia often results from atheroembolization, despite preservation of hypogastric arterial circulation. The overall ischemic com- plications after interruption of hypogastric arteries before EVAR was 16.3%, compared with 8% in intact hypogastric arteries (P 􏰂 .091). This approaches statistical significance, and is likely due to limb deployment in the external iliac artery in those patients with coiled hypogastric arteries. Colonic and spinal ischemia are associated with the highest morbidity and mortality. Limb ischemia is most often a result of limb occlusion, and can be successfully managed with standard interventions.
  • pseudoaneurysm formation, bleeding around the sheath, bleeding at the treatment site, and bleeding from remote sites including retroperitoneal hemorrhage and stroke.
    Inadequate anticoagulation may also lead to complications such as thrombosis at the treatment site, embolization of clot formed on the catheters and guidewires,
    50 to 100 mL of dye is needed for an EVAR procedure.
    6.7% of cases,
    carbon dioxide (CO2) can be used as an alternative contrast agent.
    injected through the stent- graft delivery catheter, making the placement of a pigtail catheter in the aorta unnecessary
    Pretreatment: 3 days before procedure, aspirin 100 mg and clopidogrel 75 mg
    Intraprocedural: Heparin bolus 5000 U, than 1000 U/l continously, with control of ACT ~200
    Posttreatment: dual-therapy for one year, with aspirin to be continued indefinitely thereafter The clinical course of CIN depends on baseline renal function, coexisting risk factors, degree of hydration, and other factors. The usual course of CIN is a transient asymptomatic elevation in serum creatinine. Serum creatinine usually begins to rise within 24 hours of intravascular iodinated contrast medium administration, peaks within 4 days, and often returns to baseline within 7 to 10 days. It is unusual for patients to develop permanent renal dysfunction. When chronic renal failure develops, it is usually in the setting of multiple risk factors and associated with lifelong morbidity.
    Several studies have shown that patients with transient CIN tend to have longer hospital stays, higher mortality, and higher incidences of cardiac and neurologic events than contrast-receiving patients whose kidney function remains stable. These observations have led to widespread hesitance in the use of intravascular iodinated contrast medium when the risk of CIN is felt to be high. However, many studies investigating CIN and its consequences following intravascular iodinated contrast medium administration have failed to include a control group of patients not receiving contrast medium; therefore, it is possible that much of the morbidity and mortality previously attributed to CIN in the literature may in fact be due to other etiologies. Larger studies with proper control groups and longitudinal outcomes data are needed.
    CIN.. Non ionik low molecular contrass.. Max 100cc… cin>20% if >100cc dye… gfr <30cc… 30 cc dye.. Cin
    Hydration 0.9 saline 6 – 12j before after
  • Infection Complications after EVAR
    The incidence of aortic stent-graft infection is 0.5 to 1%, and untreated stent-graft infection can result in general- ized sepsis and death.27 There are multiple causes of endograft infection. Endograft contamination during EVAR procedure seems to be the source of early infection. Secondary infection from a remote source is another pathophysiological mechanism of graft contam- ination: van den Berg et al28 reported a stent-graft infection following septic complication of a kidney stone 1 year after EVAR procedure. Another case of stent-graft
    infection after EVAR is shown in Fig. 4. In this case, the patient underwent an appendectomy for appendicitis and periappendicular abscess formation 1 month prior to EVAR. The cause of stent-graft infection can be peri- procedural contamination, but also contamination from the appendicitis-induced peritonitis. A third cause of infection is an aortoenteric fistula (Fig. 5). Multiple mechanisms of aortoenteric fistula creation are already described and include stent-graft migration, erosion of the aorta and duodenum by embolization coils, fabric rupture, inflammatory nature of the aneurysm, and bac- terial aortitis with chronic duodenal erosion
    Little is known of the true incidence of AGI or contrib- uting factors that may increase risk. This study demon- strates that the rate of AGI is low, is significantly associated with BSI and SSI, and has a 1-year mortality rate of 28%. This low rate of infection and high mortality has been similarly reported in previous small series
  • Endovascular aneurysm repair (EVAR) is a minimally invasive technique to repair abdominal aortic aneurysms (AAAs) that has emerged as an alternative to open aneurysm repair.1 EVAR, however, is complicated by endoleaks in 20 to 25% of patients.2,3 There are five different types of endoleaks, which are classified based by the source of vessels that causes the inflow into the aneurysm sac. Type I endoleaks are leaks at the proximal or distal attachment sites. Type II endoleaks are caused by retrograde flow through collateral vessels into the aneurysm sac. Type III endoleaks are holes, defects, or separations in the stent-graft material. Type IV endoleaks represent porous graft walls. Type V endoleaks have been described as being due to endotension with an enlarging aneurysm sac without a visible endoleak.4
    Patients who have had EVAR undergo lifelong surveillance to evaluate for the presence of aneurysm expansion and endoleaks. Detection of endoleaks is essential, as endoleaks are associated with aneurysm expansion and even rupture.5 Triphasic computed tomographic angiography (CTA) is the most commonly utilized imaging modality to evaluate postoperative EVAR and is highly sensitive and specific at detecting endoleaks.6,7 Other techniques commonly utilized for detection of endoleaks are magnetic resonance and duplex ultrasonography. Once an endoleak has been detected on CTA, patients at our institution are referred for digital subtraction angiography (DSA) to classify the endoleak. DSA is more accurate than CTA in classifying endoleaks because the direction of blood flow can be seen during DSA. Endoleak repair is then performed following the DSA exam
    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]
  • Type I and type III endoleaks represent direct communication with the systemic blood flow and the aneurysm sac and require immediate repair. Type I endoleaks occur at either the proximal (Ia) or distal (Ib) attachment sites and can be seen during insertion of the initial stent graft or during a follow-up surveillance imaging exam. Because as many as 10% of patients require reintervention due to type I endoleaks seen on 30-day surveillance CTAs, optimizing intraoperative imaging is under investigation. Initial studies have demonstrated that using Dyna CT, axial CT images that are reconstructed from fluoroscopic data, improves intraoperative detection of type I endoleaks.9 Type I endoleaks are always repaired when they are detected. Initial attempt at repair involves angioplasty of the affected attachment site. If this is not successful, a bare metal stent can be placed over the attachment site. This is usually done with a balloon expandable stent because of the need for large stent sizes with strong radial force. If this is not successful, insertion of an overlapping stent graft in the nonadherent portion of the stent graft can be performed.10 Fig. ​Fig.11 demonstrates a type Ib endoleak in a patient with a stent graft that was placed ~8 months earlier. The endoleak arises from the right distal limb of the endograft. Initial attempts were made to seal the leak with angioplasty alone, which were unsuccessful. Therefore, a Palmaz stent (Cordis Corporation, Miami Lakes, FL) was placed (Fig. 1B) and post–stent deployment DSA demonstrated resolution of the endoleak (Fig. 1C). Type I endoleaks occurring at the proximal docking site, however, can be more technically challenging, as they typically arise just distal to the takeoff of the renal arteries, and open repair can be required. Maldonado et al described a series of type 1 endoleaks that were embolized using N-butyl-2-cyanoacrylate (n-BCA). The endoleaks were accessed using a reverse-curve catheter at the proximal attachment site. A microcatheter was then advanced into the sac, and n-BCA was used to embolize the endoleaks.5
    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]
    more common in patients with complex arterial anatomy. Short, angulated, ulcerated, trapezoidal, and thrombus-containing necks pose a challenge in constructing a seal between the stent-graft and the native aorta. Likewise, dilated, irregular, and tortuous iliac arteries present a problem for the distal attachment site in patients with abdominal aortic aneurysms.
    Type Ic endoleaks occur in patients with abdominal aortic aneurysms in whom aortouniiliac stent-grafts were placed in conjunction with a femoral-femoral bypass. To prevent retrograde perfusion of the aneurysm, the contralateral common iliac artery is occluded either with coils or with a specially designed occluder device.
    Type Ic endoleaks occur when the common iliac artery occlusion is not complete and back-filling of the aneurysm occurs. Treatment of type Ic endoleaks involves further embolization of the common iliac artery.
  • The management of type II endoleaks continues to be the topic of debate, and type II endoleak rates are as high as 10 to 25%.3 Type II endoleaks arise from branch vessels that were excluded from the aneurysm sac during the initial stent-graft placement. These vessels then feed into the aneurysm sac via retrograde flow and most commonly arise from the inferior mesenteric artery (IMA) or lumbar artery. Increased blood flow into the aneurysm can cause enlargement of the aneurysm sac, which can increase pressure and can cause rupture.11 It has been shown that type II endoleaks can spontaneously thrombose. Recent work has shown that if a type II endoleak is present without an associated increase in size of the aneurysm sac, immediate intervention is not needed, as this endoleak can spontaneously thrombose. It has been shown that with increased time, the rate of spontaneous resolution increases.12 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.13
    Repair of type II endoleaks is routinely done via a transarterial or translumbar approach. Initially, type II endoleaks were treated by doing single-vessel embolization of the feeding artery. Using a microcatheter, the collateral branch vessel supplying the endoleak was selectively embolized with coils near the aneurysm sac. Success rates of the single-vessel transarterial approach, however, were poor, and in one study as many as 80% of type II endoleaks recurred after transarterial embolization.14 The etiology of the failure of embolization to repair the endoleak stems from the idea that these endoleaks are not fed by a single vessel but rather a network of vessels. When one artery supplying the endoleak is embolized, other vessels communicating with the endoleak will continue to supply the endoleak sac. The next step to further refine the transarterial approach is to feed the microcatheter into the aneurysm sac, and coil embolize the sac itself and then embolize the feeding vessels as the microcatheter is withdrawn, thereby treating the nidus or sac of the endoleak as well as the major feeding artery. This technique has shown results comparable to translumbar endoleak embolization discussed below.15 Fig. ​Fig.22 demonstrates a type II endoleak discovered on CTA nearly a year and half after the initial placement of a aorto-uni-iliac endograft. DSA demonstrated the endoleak receiving inflow from branches arising from the IMA (Fig. 2). Postembolization DSA demonstrated complete resolution of the endoleak with coils in place (Fig. 2D).
  • A second approach to repairing type II endoleaks is via a translumbar approach. This technique involves embolizing the endoleak sac nidus, which breaks the communication between the multiple arteries that supply the endoleak, leading to more durable results.14 The endoleak sac is accessed by using set landmarks as determined by prior CTA and/or flush aortography done in a supine position. Translumbar embolization is usually done from the left (as the inferior vena cava need not be traversed), but it is also safe to perform right-sided translumbar (transcaval) embolization.16,17 The patient is placed prone, and the endoleak is accessed via a direct puncture under fluoroscopic guidance. A sheath needle (Translumbar Access needle, Boston Scientific, Natwick, MA) is directed toward the anterolateral aspect of the vertebral body until the needle enters into the aneurysm sac. When the endoleak cavity is accessed, blood return will be seen coming from the catheter. Contrast injection can confirm needle placement into the sac and will often demonstrate the feeding vessels. Coils can then be used to embolize the endoleak sac. There are two main types of coils that can be used for embolization: stainless steel or platinum coils. Stainless steel coils provide fewer artifacts on follow-up CTA, which will be important in further surveillance, but are stiffer than platinum coils. The platinum coils, however, form a tighter nest in the endoleak. N-BCA (Trufill, Cordis, Miami, FL) “glue” or Onyx (ev3, Plymouth, MN) can also be directly injected into the sac. Care must be taken not to reflux liquid embolics into the feeding vessels, as colonic ischemia or paralysis can result. For this reason, endoleak embolization with thrombin or small particles is not recommended. From a translumbar approach, the feeding vessels can be directly accessed using a microcatheter. The feeding arteries can then be embolized using coils prior to embolization of the endoleak sac. Translumbar embolization has been shown to be more durable than single-vessel transarterial endoleak embolization.14,18
    Other techniques have been attempted to treat type II endoleaks. Lin et al reported a case of robotic ligation of the IMA using the da Vinci Surgical System with no recanalization of the endoleak at the 3-month follow-up.19 Ling et al describe deployment of an endovascular graft with simultaneous operative extraperitoneal dissection and Onyx to treat a type II endoleak.20 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. Angiography was then performed to determine whether there was persistent filling of the endoleak. In this case report, there was persistent filling of the aneurysm sac and further laparoscopic dissection was performed until a branch of the left colic was found and clipped. Completion angiography demonstrated no further filling of the endoleak.21 Mansueto et al have described a transcatheter transcaval technique for endoleak embolization with results at 1 year that are comparable to translumbar embolization.22
  • Other techniques have been attempted to treat type II endoleaks.
    Lin et al reported a case of robotic ligation of the IMA using the da Vinci Surgical System with no recanalization of the endoleak at the 3-month follow-up.19
    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. Angiography was then performed to determine whether there was persistent filling of the endoleak. Laparoscopic dissection was performed until a branch of the left colic was found and clipped. Completion angiography demonstrated no further filling of the endoleak.21
    Mansueto et al have described a transcatheter transcaval technique for endoleak embolization with results at 1 year that are comparable to translumbar embolization.22
  • Type III endoleaks are usually caused by a defect within the graft material or are due to structural failures causing separation between the components or inadequate overlap. These endoleaks require immediate repair because there is direct communication between the systemic circulation and the aneurysm sac. Repair of type 3 endoleaks involves 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.
  • Type IV endoleaks are generally seen on the immediate postdeployment aortogram, as the patient is fully anticoagulated with heparin perioperatively. These endoleaks are self-limited and resolve as the patients coagulation returns to baseline.
  • Type V endoleaks are classified as an enlarging aneurysm sac without a visible endoleak. 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.23 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.24 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.25
    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]
  • Type I endoleaks have blood flow that originates from a stent-graft attachment site. Further categorization of type I endoleaks as proximal (type Ia) and distal (type Ib) has been described (18). With either type, separation occurs between the stent-graft and the native arterial wall, creating direct communication between the aneurysm sac and the systemic arterial circulation (Fig 1). Type I endoleaks are the most common to occur after endovascular repair of thoracic aortic aneurysms (27). In addition, type I endoleaks are more common in patients with complex arterial anatomy. Short, angulated, ulcerated, trapezoidal, and thrombus-containing necks pose a challenge in constructing a seal between the stent-graft and the native aorta. Likewise, dilated, irregular, and tortuous iliac arteries present a problem for the distal attachment site in patients with abdominal aortic aneurysms. Type Ic endoleaks occur in patients with abdominal aortic aneurysms in whom aortouniiliac stent-grafts were placed in conjunction with a femoral-femoral bypass. To prevent retrograde perfusion of the aneurysm, the contralateral common iliac artery is occluded either with coils or with a specially designed occluder device. Type Ic endoleaks occur when the common iliac artery occlusion is not complete and back-filling of the aneurysm occurs. Treatment of type Ic endoleaks involves further embolization of the common iliac artery.
  • Type II endoleaks represent retrograde blood flow through aortic branch vessels into the aneurysm sac. Type II endoleaks occur when blood travels through the branches from the portion of the aorta that has not received a stent or iliac arteries that anastomose with vessels in direct communication with the aneurysm sac. Typical sources include the inferior mesenteric and lumbar arteries (Fig 2). As is the case with type I endoleaks, a direct communication from the systemic arterial circulation to the aneurysm sac is established. Type II endoleaks are the most common type of endoleak encountered after endovascular repair of abdominal aortic aneurysms. The number of patent branch vessels and the amount of thrombus in the aneurysm sac preoperatively appear to correlate with the risk of endoleak development (28).
  • Type III endoleaks occur when there is a structural failure of the stent-graft. This includes stent-graft fractures, holes that develop in the fabric of the device, or junctional separations seen with modular devices (Fig 3). Repetitive stresses that are placed on the grafts from arterial pulsations can cause these types of leaks. In addition, as the aneurysm sac shrinks, over time additional forces are applied to the grafts that can result in graft failure. Although type III endoleaks are currently fairly unusual, they will likely become more prevalent as long-term follow-up data are accrued on the existing population of patients with stent-grafts.
  • Transcript

    • 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
    • 10. 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
    • 11. 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
    • 12. 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
    • 13. 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
    • 14. 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
    • 15. Ann Thorac Surg 2007;84:1201–5) E. Weigang et al. / European Journal of Cardio-thoracic Surgery 40 (2011) 858— 868
    • 16. 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
    • 17. Ischemic Complications
    • 18. J Vasc Surg 2004;40:698-702.) Ischemic Complications
    • 19. IIA occlusion -CIA problems (short/ectasia/tort/cal c/trombus) -Type II endoleak (embolized) -Complication - Buttock Cl - Colitis Ischenia - SCI - Pelvic Inschemia Ischemic Complications
    • 20. Patient Selection - >4.5cm IIA - >1cm landing zone - <10mm IIA diameter Ischemic Complications
    • 21. • 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
    • 22. 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
    • 23. • 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
    • 24. 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.)
    • 25. • 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
    • 26. • 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
    • 27. Circ Cardiovasc Intervent. 2009;2:105-112.) (J Vasc Surg 2003;37:1155-61.)
    • 28. ENDOLEAK
    • 29. ENDOLEAK
    • 30. • 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
    • 31. 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
    • 32. ENDOLEAK
    • 33. • 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
    • 34. (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
    • 35. • 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
    • 36. Staged algorithm of evaluation and treatment of suspected type II endoleaks. www.jvir.org.) ENDOLEAK
    • 37. (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
    • 38. • 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
    • 39. J Vasc Surg 2010;52:19-24 ENDOLEAK
    • 40. Interactive CardioVascular and Thoracic Surgery 0 (2012) 1–5 BEST EVIDENCE TOPIC doi:10.1093/icvts/ivs201 ENDOLEAK
    • 41. ENDOLEAK
    • 42. ENDOLEAK ENDOLEAK LONGTERM TREATMENT CONSERVATIVE
    • 43. • 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
    • 44. • 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
    • 45. • 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
    • 46. 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.
    • 47. Thank You
    • 48. • 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]
    • 49. • 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.
    • 50. 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.
    • 51. 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
    • 52. 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.
    • 53. 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).
    • 54. 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.
    • 55. (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.
    • 56. 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
    • 57. 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.
    • 58. vessels Circ Cardiovasc Intervent. 2009;2:105-112.)
    • 59. Circ Cardiovasc Intervent. 2009;2:105-112.)
    • 60. • Iinsidense per endoleak • Incidense complication per pathology – Dissection ac/chr – IMH/PAU/Trauma – Aneurysm – Marfan • Incidence per device n generation
    • 61. • 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.
    • 62. • 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.
    • 63. 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
    • 64. • Complication – Endoleak – Surgical Exposure – Systemic – Ischemic – Infection – Excluded aneurysml sac - Definition & Class - Incidense - Mechanism - Management
    • 65. 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
    • 66. anterior spinal arteryanterior spinal artery segmental arteriessegmental arteries 5. Adamkiwicz artery5. Adamkiwicz artery
    • 67. 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
    • 68. 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.
    • 69. 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
    • 70. 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
    • 71. 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.
    • 72. 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.
    • 73. 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
    • 74. Spinal Cord Blood Supply Ventral Dorsal
    • 75. 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.
    • 76. 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
    • 77. 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
    • 78. 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.
    • 79. 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
    • 80. 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
    • 81. 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
    • 82. 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
    • 83. 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
    • 84. 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
    • 85. 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
    • 86. 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
    • 87. 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
    • 88. 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
    • 89. 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.
    • 90. Blood Supply to the Medulla
    • 91. 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
    • 92. 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
    • 93. 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
    • 94. 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
    • 95. 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
    • 96. 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
    • 97. 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
    • 98. 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
    • 99. 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
    • 100. 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
    • 101. 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
    • 102. 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”)
    • 103. 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)
    • 104. 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.
    • 105. 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)
    • 106. 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
    • 107. 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
    • 108. 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
    • 109. 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
    • 110. 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.
    • 111. 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
    • 112. 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
    • 113. Vascular Medicine 17(3) 168–173
    • 114. 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.
    • 115. • 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
    • 116. 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