Endoleak is defined as persistent blood flow in the aneurysm sac after endovascular aneurysm repair (EVAR). Most of sac growth after EVAR could be originated from endoleak during long-term follow-up. The cause of type I endoleak may change with the period after EVAR. Endovascular treatment may be difficult for type Ia endoleak due to disease progression. Fenestrated/branched EVAR may be an alternative treatment to open conversion. Type II endoleak is not always benign. Large and late type II endoleak may lead to sac growth, and slow flow type II endoleak may be complex to treat. Treatment for type II endoleak with hostile neck aneurysm should be considered to prevent type I endoleak due to disease progression. Occult type I or III endoleak should be noted in patients with type II endoleak. The mortality is high in patients with ruptured aneurysm due to type III endoleak, while the perioperative mortality is low in patients with unruptured aneurysm with type III endoleak. Therefore, type III endoleak should be diagnosed before rupture. However, the diagnosis of type IIIb endoleak by imaging may be challenging.

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Endovascular aortic repair (EVAR) has been adopted worldwide as the treatment for abdominal aortic aneurysm (AAA). Endoleak is one of the specific complications after EVAR that we often face. The correct diagnosis of endoleak type is essential in order for us to perform proper reintervention procedures. This article covers the various imagings of endoleak based on the cases we experienced in our daily practice.

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Type II endoleak after EVAR or TEVAR in the treatment of aortic aneurysms is a growing concern since a substantial population shows sac enlargement due to type II endoleak and that compromises the durability of the treatments. There are miscellaneous approaches reported in the literature in the intervention to address these issues; however, we focus on transarterial or percutaneous approach in this review. We also address the limitation of endovascular treatment of type II endoleak after EVAR. Additionally, embolization of type II endoleak after TEVAR is discussed.

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Type II endoleak (EL2) is the most common graft-related complication after endovascular abdominal aortic aneurysm repair (EVAR), and is associated with aneurysmal enlargement, re-intervention and even rupture. Patent aortic side branches, i.e., the inferior mesenteric artery (IMA) or the lumbar artery (LA) are thought to be the independent risk factor for EL2. Some researchers proposed preoperative embolization for the prevention of EL2 such as aortic side branch embolization or sac embolization. However, the efficacy of these preventive methods is controversial because there has been little evidence to support it. Therefore, we have been starting prospective multi-center clinical trials of preoperative IMA and LA embolization. In this article, we reviewed previous research regarding preoperative embolization for EL2, and also outlined the early stages of our clinical trials.

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We describe the tips and tricks of prophylactic intraoperative abdominal aortic aneurysm (AAA) sac embolization during endovascular abdominal aortic aneurysm repair (EVAR) to prevent the occurrence of endoleak and aneurysm sac expansion. We performed prophylactic intraoperative AAA sac embolization for patients with an infrarenal neck angulation > 60° or AAA sac diameter > 60 mm. A 4F catheter was inserted into the AAA sac before EVAR. The aneurysm sac was embolized with n-butyl cyanoacrylate–lipiodol–ethanol (NLE) during proximal neck (PN) aortic balloon occlusion. PN aortic balloon occlusion decreases sac pressure and promotes retrograde blood flow into the sac from aortic branches. PN aortic balloon occlusion can prevent leakage of embolic materials into the aortic branches and allow safe injection of embolic materials into the AAA sac. The endoleak and AAA sac diameter were evaluated by subtraction enhanced MRI at 6 months and yearly after EVAR. It is impossible to identify an endoleak by enhanced CT owing to the presence of a high-density material (Lipiodol or coils) in the aneurysm sac. Intraoperative AAA sac embolization combined with inferior mesenteric artery (IMA) embolization is one of the safe available options. Prophylactic intraoperative AAA sac embolization using NLE during PN aortic balloon occlusion combined with aortic branch embolization is a safe and effective procedure to reduce the incidence of type II endoleaks and prevent sac expansion after EVAR.

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Endovascular aortic repair (EVAR) for abdominal aortic aneurysm has an early survival benefit but an inferior late survival compared with open repair. To improve results for late survival after EVAR it is necessary to prevent secondary aneurysm rupture. Significant risk factors for secondary rupture were type I A endoleak, type III endoleak, graft migration, and postoperative kinking of the endograft. Surgical treatment is necessary for some of these patients. The aim of this article is to introduce an overhaul concept - that is a treatment strategy for possible etiology of sac expansion with/without type II endoleaks-, and secondary endovascular treatment for late type 1 endoleak and IIIb endoleak.

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A total of 831 patients underwent EVAR for AAA between April, 2007 and October, 2018. Of these, late open reintervention for aneurysmal sac enlargement after EVAR was performed for 22 patients. All of them were discharged home with no significant complications during the hospitalization. Intraoperative findings at the time of exposing the aneurysmal cavity included various and multiple endoleaks, which could not be identified by enhanced CT. A variety of persistent endoleaks were considered to be one of the primary factors which could exacerbate clinical outcomes of additional endovascular treatments for sac enlargement after EVAR.

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A 50-year-old Japanese male experienced a rare true aneurysm in the distal splenic artery that showed spontaneous regression after embolization for the aneurysm in the proximal splenic artery. Abdominal contrast-enhanced CT incidentally demonstrated a saccular aneurysm in the main trunk of the splenic artery and a fusiform-type aneurysm at the splenic hilum. Because the aneurysm in the main trunk of the splenic artery showed a slight increase on follow-up CT performed 2 months post-discharge, we considered it a therapeutic indication. We performed coil embolization for the aneurysm in the main trunk of the splenic artery using the isolation and packing technique and chose not to treat the aneurysm in the splenic hilum. Observation by serial CT was performed over 1 year after treatment, and CT showed no recurrence of the treated aneurysm in the main splenic artery. On the other hand, the untreated splenic aneurysm at the splenic hilum gradually shrunk and eventually disappeared, with thrombus formation.

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RADPLAT is intensive targeted chemoradiation consisting of superselective intra-arterial cisplatin infusion concurrently with radiotherapy for advanced head and neck cancer. It was proposed by Dr.Robbins in 1992. In RADPLAT, surgery is performed only for salvage purpose.
Larynx preserving treatment has a social impact. Larynx preserving treatment avoiding radical laryngectomy is thought to be an ultimate frontier of RADPLAT. The main feeding artery of laryngeal carcinoma is the superior laryngeal artery, which is a branch of the superior thyroid artery. Most of the larynx is supplied by superior laryngeal artery, but some parts of the larynx are supplied by small arteries from glandular branches of the superior thyroid artery, penetrating through the thyroid cartilage. Generally speaking, super-selective infusion into the feeding artery is ideal. However, high dose cisplatin infusion into superior laryngeal artery may induce complications of laryngeal mucosal necrosis, laryngeal edema or nerve palsy. We should consider the larynx to be a more delicate organ than the maxillary or tongue. We infuse cisplatin at the point of the bifurcation of the superior laryngeal artery. Super-selective infusion of cisplatin into the superior laryngeal artery has risks of complications such as mucosal necrosis, laryngeal edema or laryngeal nerve palsy. We would emphasize that less frequent and milder adverse events were experienced in our series, unlike concurrent systemic chemoradiation therapy.

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Superselective transarterial infusion therapy of high-dose cisplatin with concomitant irradiation is to infuse cisplatin to tumor feeding arteries directly via a catheter. Sodium thiosulfate which is a neutralizer of cisplatin facilitates this method performed. Malignant head and neck tumors are a good indication for this method. In particular, maxillary cancer is particularly suitable indication. In this article, we describe the practice and efficacy of this method in detail.

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