Endovascular Aneurysm Repair (EVAR) is the application of a stent-graft (SG) to isolate the aneurysm from the blood flow, thus reducing the risk of increasing size and rupture of the aneurysm by reducing the constant impact of high velocity blood flow on the aneurysm wall. Since 1991, when it was first performed by Parodi, this minimally invasive procedure has spread rapidly around the world, and its feasibility and good recent results are undeniable. The development of EVAR is hampered by the persistent increase in pressure, tumor enlargement and even rupture, which are often difficult to diagnose and treat. At present, the mechanism and significance of endoleaks are not completely clear, and there are controversies in diagnosis and treatment. 1.Definition and typing 1.1.Definition Endoleak is the presence of persistent blood flow visible on imaging outside the SG lumen and within the aneurysm lumen after EVAR(2-4) . 1.2, Fractionation There are various fractions of endoleaks, among which the most cited is the fractionation differentiated by the site of blood leakage proposed by White (2-3) It was endorsed by the Society for Vascular Surgery and the American Association for Vascular Surgery (SVS/AAVS) (4), and was partially modified by Veith et al. (1) in 2002. Type I endoleaks are SG attachment endoleaks. It is caused by the failure of complete closure between the proximal or distal end of the SG and the aneurysm neck, resulting in persistent flow of blood into the aneurysm lumen. There are three subtypes: type IA and type IB refer to proximal and distal endoleaks, respectively, and type IC refers to endoleaks caused by poorly closed iliac artery occlusion (Iliacoccluder) in AUI stents. Type II endoleaks are regurgitant endoleaks, which are caused by persistent regurgitation of blood flow in the lumbar artery, submesenteric artery, and other collateral arteries.Veith et al. (1) further divided type II endoleaks into: type IIA endoleaks, simple type, with a single inflow tract and no outflow tract; type IIB endoleaks, complex type, with multiple inflow and outflow tracts.Type III endoleaks are caused by structural disruption of the SG Internal leakage, including joint leakage, skeleton disconnection (IIIA); rupture of overlay (IIIB). Among them, type IIIB can be further divided into large breach (≥2mm) and small breach (<2mm) according to the size of the fissure. type IV endoleaks refer to those occurring within 30 days after EVAR and caused by SG structural integrity but excessive pore size, while those occurring after 30 days are not included. Endotension in a narrow sense refers to delayed enhancement CT scans after EVAR that do not detect endoleaks but have increased tension in the tumor cavity. In a broader sense, it refers to all cases of increased intratumoral tension, including all types of endoleaks and narrowly defined endotensions. The latter two types of endotension can only be confirmed during surgery, and it is advocated to treat endotension as V-type endoleaks. Endoleaks can be classified according to the temporal phase: endoleaks occurring within 30 days after surgery are called acute endoleaks; those occurring after 30 days are called delayed endoleaks; endoleaks that occur again after the endoleaks have closed on their own or after treatment are called recurrent endoleaks. 2. Etiology The etiology of endoleaks is not fully understood and may be related to many factors such as anatomy, type of grafts and operation level. Short, angular tumor necks, and thrombosis or ulcer formation in the tumor neck make it difficult to seal between the SG and the host vessel, which may easily produce type I endoleaks, while dilated, irregular, and excessively twisted iliac vessels may also cause poor distal apposition resulting in type IB endoleaks. The patient's age, the length of the proximal aneurysm neck, and the patency of branches such as the lumbar artery and submesenteric artery are associated with an increased incidence of type II endoleaks. A relatively low incidence of type II endoleaks has been found in patients with low preoperative A/BI and smoking, possibly because these patients are more atherosclerotic and more prone to occlusion; smoking increases blood coagulability and may also allow some small leaks to close on their own (5). The incidence of type II endoleaks is not significantly higher in patients on long-term anticoagulation therapy, but it can be detrimental to the self-closure of endoleaks and make reintervention more difficult. The mechanism of endotension is also unclear and may be due to the presence of a small endoleak not detected by imaging or to blood pressure conduction through the SG or thrombus, as well as to blood osmosis (6, 7). 3. incidence Walschot et al. (8) counted complications after EVAR in 39 publications (total 2387 patients) between 1995 and 1999, and the incidence of perioperative endoleaks of all types was 13.1%, and the rate of delayed endoleaks was 5.4%. Previously, Schurink et al. (9) did a similar study: in 23 publications (1189 EVAR cases), type I endoleaks accounted for 60% (24% proximal endoleaks and 36% distal endoleaks), type II endoleaks accounted for 19% (18% lumbar and submesenteric arteries and 1% internal iliac artery), type III and IV endoleaks together accounted for 18%, and the remaining 3% had unknown typing. In 2003, the European EUROSTAR Collaborative Group calculated data from 110 centers with EVAR: 8.9% (320/3595) for type II endoleaks, 12% (297/2462) for type I, III or mixed endoleaks, and 5.4% (5.4%) for endotension. incidence of 5.4% (5). However, these are mostly follow-up results within the mid-term period, and the incidence of endoleaks remains to be revealed by long-term results. 4. Diagnosis 4.1. Intraoperative diagnostic points Intraoperative contrast should be performed immediately after SG release in order to detect endoleaks in a timely manner. It is generally not difficult to determine the type of endoleak according to the site of leakage and the flow direction of the contrast agent, and placing the catheter at the proximal and distal attachment of the SG respectively can help determine the site of leakage. Some type I endoleaks may have outflow tracts from the lumbar artery or the inferior mesenteric artery, which can be easily confused with type II endoleaks, and the direction of blood flow can be carefully identified by playback: if the direction of blood flow from the lumbar artery or the inferior mesenteric artery is prograde, i.e., the blood flows to the tumor cavity from other parts rather than from branch vessels, it suggests a possible type I endoleak; if the direction of blood flow from the branches is retrograde If the direction of blood flow in the branches is retrograde, then it may be type II endoleak. 4.2. Postoperative follow-up Because of the unpredictability of endoleaks, close postoperative follow-up is necessary and key to the diagnosis and treatment of endoleaks. We advocate follow-up SCTA at 30 days, 6 months, 12 months, and 18 months after surgery, to be followed by annual review afterwards. The diagnostic tools for late endoleaks are variously reported by EUROSTAR as spiral CT ( 84%), arteriography ( 4%), MRI (3%), and Doppler ultrasound ( 8%) (5). Our practice shows that SCTA has a high detection rate for endoleaks, and a delayed SCTA-enhanced scan with 3 mm layer thickness is recommended. Changes in tumor neck diameter and length, tumor diameter and angulation should be noted during follow-up, and an increase in the maximum transverse diameter of the tumor of more than 8 mm should be considered as tumor expansion. However, CT has a certain leakage rate and sometimes it is not easy to determine the type of endoleaks (it is difficult to confirm the direction of blood flow), so other means, such as arteriography, are needed to identify the type of endoleaks. In contrast, Doppler ultrasound has the advantage of being noninvasive and easy to operate, and can dynamically show some type II endoleaks missed by CT with good sensitivity and specificity; the application of ultrasound contrast agents further increases the sensitivity of detection, but ultrasound examination can also be affected by patient size, intestinal pneumatization and other factors, and the level of the operator has a relatively large impact on the results. Measurement of pressure within the aneurysm lumen is a more sensitive and reliable indicator, but no noninvasive means of detection is currently available. Therefore, there is no absolutely reliable and effective means of detecting endoleaks, which should be used according to the patient's specific situation and available conditions. 5. Treatment Open surgery is the only treatment method that has a definite effect on endoleaks, but its surgical trauma also makes the original EVAR minimally invasive, and many patients choose intracavitary treatment precisely because they have contraindications to surgery, so it becomes urgent to explore effective and minimally invasive means of reintervention. 5.1. Timing of treatment There is still controversy regarding the timing of endoleak management. Approximately 50% to 60% of immediate postoperative endoleaks will close on their own one month postoperatively. The results of EUROSTAR (5) showed that both tumor and neck diameters were larger in patients with type I/III endoleaks than in those without endoleaks (P values 0.0001 and 0.009, respectively); the reintervention rate was 54% in the former and 6% in the latter (P = 0.001); 11% in the former and 0.8% in the latter (P = 0.0001); and the cumulative rupture rate within 2 years was 0.8% in the latter (P = 0.0001). The cumulative rupture rate within 2 years was higher in the former (4%) than in the latter (0.7%) (P = 0.0001). Therefore, it is believed that these SG-associated endoleaks should be managed promptly because types I and III endoleaks lead to direct communication between the tumor cavity and systemic blood flow and are high-risk factors for postoperative tumor rupture and conversion to open surgery. The management of type II endoleaks is more controversial: some authors argue that type II endoleaks have the potential for embolization of these branch or collateral vessels as long as the tumor lumen does not increase in size, and therefore close follow-up is sufficient as long as regular follow-up is performed, and the indication for reintervention is confirmation of tumor expansion (5, 13). There are also arguments for immediate management because branch vessels can transmit blood pressure to the tumor lumen, thereby increasing the risk of tumor rupture (14). Whether prophylactic embolization should be performed is also debated: some advocate aggressive embolization with or without tumor dilatation (15, 16). No significant difference in the incidence of postoperative endoleaks with or without embolization has also been reported (17), and there have been reports of aortic enterocutaneous fistulas due to spring-ring embolization (18). We believe that patients with early asymptomatic type II endoleaks can be followed up to 6 months postoperatively and managed if CT at 6 months postoperatively still shows endoleaks with dilated aneurysms. 5.2. Management The management of endoleaks should depend on their type. type I endoleaks can be corrected by balloon dilation, release of an extended graft (cuff), or bare stent (stent). It should be noted that balloon dilation should be moderate and should not be repeated for the sake of imaging perfection, which would result in SG deformation or even treatment failure. The use of extension grafts or stents should be based on anatomic conditions, and caution should be exercised if the proximal neck is short, angulated, or otherwise anatomically compromised. In addition, the use of spring-ring embolization or n-butyl cyanoacrylate n-BCA has been reported to be effective in treating type I endoleaks (19). If the endoleak is severe, the tumor is significantly dilated, and the anatomic conditions are not suitable for cuff or stent placement and no other means are available, open surgery should be considered to prevent tumor rupture, provided the patient is able to tolerate the surgery. The main methods of management of type II endoleaks are transcavitary or transumbilical access embolization (20). Endoluminal embolization is the embolization of the lumen of the tumor or the vessel directly causing the endoleak, usually the lumen of the lumbar or submesenteric artery, with a spring coil. However, there are questions about the long-term efficacy of this measure, and recurrence of type II endoleaks after embolization has been found (20), probably because some type IIB endoleaks have many input and output tracts, just like vascular malformations, and endoluminal embolization often only embolizes one of them, and blood will soon return through other side branches and form another endoleak. Another method is direct trans-lumbar puncture embolization. Before surgery, the relationship between the endoleak site and the location of SG is clarified, and appropriate bony markers are determined. The puncture site is selected under arteriography, and then a puncture needle is used to puncture from the lateral lumbar region through the guide sheath, which can embolize both the luminal cavity and the branches of the lumbar artery or the inferior mesenteric artery. Commonly used emboli are metal spring coils, and liquid emboli such as n-BCA can also be applied. Laparoscopic ligation of the endoleaks has also been advocated, although the need for prophylactic ligation is controversial and its effectiveness has yet to be proven. Type III endoleaks should be treated upon diagnosis because of the direct communication between the tumor cavity and the systemic bloodstream. Intraluminal treatment can be considered first by adding an extension graft or releasing another SG into the original SG cavity to cover the defect. This type of endoleak is more dangerous because of the rapid re-increase of pressure in the tumor cavity. Those who fail intracavitary treatment should be operated aggressively. Type IV endoleaks are uncommon in current SGs and mostly occur in patients with long-term anticoagulation when the SG is released immediately after imaging. This type of endoleak is generally self-limiting and does not require treatment as long as coagulation is good. As the Achilles heel of EVAR, the prevention and treatment of endoleaks are very important and must be addressed in the continued development of EVAR. At present, there are still many problems to be solved in the diagnosis and treatment of endoleaks, and the clarification of its mechanism and impact is still waiting for the results of medium and long-term follow-up, while the active prevention, clear diagnosis and effective management of endoleaks require unremitting research by scholars from various countries.