Endoluminal aneurysm repair (EVAR) has rapidly evolved since its introduction by Parodi et al [1] in 1991 as an alternative to open surgery for abdominal aortic aneurysms (AAA), and with the continuous updating of endoluminal techniques and devices its range of indications is expanding, and the current intermediate results are satisfactory [2], but there are still questions about the long-term stability of EVAR, and the most common factor affecting long-term The most common factor affecting long-term outcomes is endoleak, i.e., the persistent presence of blood flow in the tumor cavity. Endoleak is a common complication specific to endoluminal repair and refers to the presence of active blood flow outside the lumen of the graft, within the lumen of the tumor and adjacent vessels after stent-type vessel placement. In recent years, it has also been suggested that the persistence and or growth of intraluminal pressure (Endotension) also falls under the definition of endoleaks [3-5]. According to the time of occurrence endoleaks can be divided into primary (occurring intraoperatively or within 30 d after surgery) and secondary (occurring after 30 d after surgery), where primary endoleaks include both transient and persistent (lasting until after 30 d) types. There are four types of endoleaks according to the source of blood leakage, type I: endoleaks are formed because the stent type vessel and the autologous vessel cannot fit closely together, including the proximal and distal interfaces. Type II: The leakage comes from the reflux of blood from collateral vessels, including the lumbar artery, inferior mesenteric artery, middle sacral artery, and internal iliac artery. Type III: Endoleaks due to the inability of the stent-type vessel’s own interface to tightly fit or the rupture of the artificial vessel. Type IV: Leakage formed through the woven seam of the stent-covered artificial vessel. Type II endoleaks include two subtypes, IIa refers to blood flow with inflow channels without outflow channels, and IIb refers to blood flow with inflow channels and outflow channels. The endotension proposed in recent years has been classified as type V endoleaks, and some scholars have divided type V endoleaks into four subcategories, including invisible pressure conduction, incompletely healed endoleaks, occult type I and III endoleaks, and occult type II endoleaks [3-5]. However, the author believes that subcategory III should be classified as type I and III endoleaks, and the main causes of the so-called endotension are (1) occult regurgitation of blood in the visceral artery or collateral vessels, which has a low pressure and may not always be visualized on CTA or ultrasonography; (2) equal pressure of blood flow in the visceral artery or collateral vessels with the pressure in the tumor lumen, and although there is no regurgitation of blood into the tumor lumen, this equal pressure Although there is no return blood into the tumor lumen, this equal pressure causes fluidization of the thrombus in the tumor lumen, which results in continuous pressure transmission. Therefore, in some ways, type V endoleaks are similar in scope to type II endoleaks. Among all types of endoleaks, type II endoleaks are the most common, and there is a clear consensus on the management of type I and III endoleaks, whereas the management of type II endoleaks is controversial [6]. Diagnosis of type II endoleaks CTA is still the main means of diagnosing type II endoleaks with high sensitivity and specificity [7-9], and the controversy mainly lies in the way of obtaining the original CT data, with some scholars suggesting that the images should be obtained in the delayed phase (delayed by 60-120 seconds, or even 300 seconds) [10-11]. Our experience suggests that most type II leaks may not be visualized in the arterial phase, and if we can continuously scan the late arterial phase, venous phase, and delayed venous phase to observe the whole process of endoleaks appearance, it will not only improve the diagnostic rate, but also help greatly to assist in determining the origin of the leak [12]. In fact Doppler ultrasound is able to visualize very clearly, accurately and in real time in most cases a regurgitant endoleak from the inferior mesenteric artery, internal iliac artery or lumbar artery. However, ultrasound findings may be influenced by patient conditions such as obesity, pneumatization of the intestinal canal, and operator experience. For primary endoleaks, it has been suggested that a contrast catheter is left in the aneurysmal lumen and intra-arterial angiography is performed through the catheter to check for the presence of type II endoleaks after the stent-type vessel has been released, or arteriography can be performed after the stent-type vessel has been released with delayed image acquisition, which also helps to detect primary type II endoleaks [13]. Sometimes it needs to be shown under selective branch arteriography. III. Clinical prognosis of type II endoleaks Type II endoleaks can account for approximately 40% of all endoleaks diagnosed. Its diagnostic rate can be 10-25% at day 30 postoperatively, 18.9% at 1 year, and 10% after 1 year [14]. Despite its low-flow type of endoleaks, there is still a potential risk of continued growth of the tumor lumen leading to tumor rupture. This type of endoleak is not directly related to the design and material of the stent-type vessel, but rather to the condition of the individual patient’s visceral arteries; thicker, patent submesenteric arteries; and patent and well-communicating bilateral internal iliac arteries are all high-risk factors for type II endoleaks. In addition, Andre Marchiori and colleagues [15] studied the risk factors associated with type II endoleaks and found that type II endoleaks occurred in 28 of 195 patients, with an incidence of 13.4%. All of these cases had greater than or equal to four patent lumbar arteries with a mean diameter greater than 2.3 mm, 10 spontaneously healed lumbar arteries with a diameter less than 2 mm, and 18 non-spontaneously healed lumbar artery leaks, all with a diameter of 2.7 mm. This suggests that at least one lumbar artery with a diameter greater than 2 mm is responsible for the persistence of endoleaks. The natural prognosis of type II endoleaks has important implications for the development of treatment strategies.Daniel Silverberg and colleagues [16] followed all AAA patients after EVAR in a single center from 1997-2005 and analyzed the natural regression of type II leaks over an 8-year period and found that the incidence of type II endoleaks was 16% (154 of 965) with a mean The follow-up period was 2 months (1 to 72 months) and 35.7% of patients healed spontaneously (55 cases) with a mean healing time of 14.5 months. approximately 75% healed spontaneously within 5 years; 19 patients required treatment (12.3%) at 19.9 months postoperatively. In 13 of these patients (8.4%), the tumor grew more than 5 mm in diameter, whereas in about 80% of patients, even with type II endoleaks, the tumor did not grow more than 5 mm in diameter within 4 years, and no patient had tumor rupture or required conversion to open surgical treatment. This suggests that the natural regression of type II endoleaks is at least mild. When to intervene in type II endoleaks is a complex and controversial issue. There are reports in the literature that type II endoleaks can lead to late rupture of abdominal aortic aneurysms [17-18] and can increase the risk of rupture by transmitting systemic blood pressure into the aneurysmal cavity [19]; in contrast, there are reports confirming that type II endoleaks do not lead to rupture of the aneurysm and only require follow-up monitoring. Based on these debates, there are currently two voices regarding the management of type II endoleaks: one advocates immediate intervention; the other recommends intervention only if the aneurysm grows significantly or persists for >6 or 12 months [20-21], not only because persistent type II endoleaks are more likely to lead to aneurysm growth, but also because studies claim that late rupture of the aneurysm [22]. In our experience, the best indicator of the need for intervention is based on follow-up after endoluminal repair: if the aneurysm continues to grow, it is likely to rupture at a later stage with high intraluminal pressure; if the aneurysm is stable or even shrinking, then the risk of rupture at a later stage is correspondingly low. Most scholars choose CTA as a monitoring tool to measure the maximum diameter of the tumor at the same site to determine whether type II leak requires intervention, and generally consider a continuous growth of tumor diameter >5 mm as a signal for intervention, while Bargellini et al [23] believe that the early effect of type II endoleaks on the tumor is mainly manifested in the change of tumor volume, and therefore advocate monitoring the tumor volume to assist in determining the effect of type II leak on patients, but volume monitoring is time-consuming and laborious, and its popularity is difficult. V. Treatment of type II endoleaks 1. Prophylactic intervention There is a consensus on the embolization of the internal iliac artery to prevent type II endoleaks, but there are still different views on the prophylactic embolization of the inferior mesenteric artery and the lumbar artery. Usually, embolization of one internal iliac artery is safer to avoid the occurrence of gluteal muscle necrosis or claudication, and for cases where stent-type vessels need to cover both internal iliac arteries, branch vessel products are now also available to help reconstruct at least one internal iliac artery. carl et al [25] conducted a study of 69 patients with a strategy to prevent type II endoleaks by preembolizing the inferior mesenteric artery, after the release of the stent graft, through The results were not statistically significant, although the incidence of endoleaks was slightly lower in the prevention group than in the control group, and two patients died of colonic necrosis (3%). Salvatore et al [26] applied the same design of intraluminal spring coil embolization combined with fibrin glue injection (2.5-5 ml) pretreatment, and the results suggested that the incidence of type II endoleaks was 2.2% vs. 15.2% in the pretreatment and control groups (P<0.05), the incidence of iliac branch thrombosis was 1.6% in the pretreatment group, one patient required open intervention for renal artery embolization, and one case of colonic necrosis Partial bowel resection was performed. Selective embolization of the inferior mesenteric artery is not only technically challenging, but also has the risk of causing distal embolism, while selective embolization of the lumbar artery has a lower success rate because of the higher technical requirements, and the more commonly used embolization materials include steel rings, thrombin, gelatin, Onyx (ethylene vinyl alcohol polymer), and biogel. Moreover, theoretically, liquid embolization materials have the potential to cause paraplegia due to non-selective embolization of the lumbosacral follower artery and anterior spinal artery [27,28]. Overall, although these preoperative or intraoperative embolization techniques appear to be highly attractive, there is controversy as to whether preoperative preembolization of aortic visceral vessels is effective in reducing the incidence of type II endoleaks [29-32]. The vast majority of patients with patent aortic visceral vessels do not develop type II endoleaks, so prophylactic management instead poses an unnecessary risk to many patients [33] 2. Postoperative reintervention Current treatment options for type II endoleaks include transarterial embolization, transumbilical puncture embolization, transvenous embolization, direct thrombin injection, lumpectomy ligation of the lumbar and mesenteric arteries, and open surgery. The literature reports [25] that type II endoleaks are more common in the lumbar artery than in the inferior mesenteric artery, with an incidence of up to 19%, while the incidence of type II endoleaks associated with the inferior mesenteric artery is approximately 3.6% . The internal iliac artery is also involved in the formation of type II endoleaks in our center's cases. Due to the specific anatomical location of the lumbar artery after EVAR, the success rate of direct embolization of it was low, only about 33%, in agreement with our results. In the cases where direct embolization was successful, most of them were via internal iliac artery access, and some scholars [34] directly entered the luminal cavity via vena cava to directly embolize the lumbar artery, with a technical success rate of 92% (1 failure) and a mean intraluminal pressure of 75 ± 31.5 mmHg before treatment A mean pressure of 16.5 ± 12.2 mmHg after treatment, with a mean reduction in the maximum diameter of the tumor of 3 mm (2- 10 mm), with an overall success rate of 83% (10 vs 12). In cases where direct embolization is not possible, direct embolization by percutaneous puncture of the lumen or intraluminal injection of hemagglutinin and/or fibrin glue is possible. The principle is to activate the human coagulation cascade to form a fibrin clot, which produces a biodegradable adhesive tissue seal, thus acting by closing the blood flow in the lumen or preventing the transmission of fluid pressure. Embolization of the inferior mesenteric artery can mostly be accomplished through the superior mesenteric artery, via the Riolans arch, with a reported technical success rate of up to 80% [34]. Solis and colleagues [35] reported a high failure rate of transarterial treatment in 10 patients with type II endoleaks, six of whom still had persistent endoleaks.Chuter and colleagues [36] treated 11 primary type II endoleaks with a transarterial approach, and only one was found to be satisfactory at follow-up.Terhi and colleagues [37] also reported a success rate of only 20 %. It has been suggested [38] that the behavior of type II endoleaks resembles that of arteriovenous malformations, which is why embolization of one offender vessel alone is not very effective. This suggests that treatment should be aimed at complete embolization of the endoleak lumen; otherwise, embolization of one offender vessel alone may only result in regurgitation of blood from other adjacent vessels. Although the number of cases reported in the available studies was too small to complete a controlled count, the available data still suggest that the prognosis of patients undergoing transumbilical embolization is better than that of patients undergoing transarterial embolization. in another study by Baum and colleagues [39], a total of 20 cases underwent transarterial embolization of the IMA and 13 cases underwent direct transumbilical embolization, and it was observed that 16 cases failed in the former group and only 1 case failed in the latter group. It may be because trans-lumbar puncture embolization directly into the endoleak lumen makes it easier to cut off the communication between collateral vessels, thus making the embolization effect more certain. Retroperitoneal ligation with the application of a titanium clip to occlude the inferior mesenteric artery or the lumbar artery, an approach first proposed by Wisseliink [40], may be more appropriate in cases where the offender vessels are multiple sets of lumbar arteries, as these cases are difficult to resolve by endoluminal techniques. The difficulties are that the operator needs to be more skilled in lumpectomy and it is more invasive.