经腔胶水栓塞 II 型内漏后感染支架移植物和严重主动脉炎:病例报告。

IF 0.7 Q3 MEDICINE, GENERAL & INTERNAL AME Case Reports Pub Date : 2024-05-30 eCollection Date: 2024-01-01 DOI:10.21037/acr-23-148
Nathaniel Robinson, Tiziano Tallarita, Jason Beckermann, Vinay Nijhawan, Jeremy McBride, Nishant Saran, Thomas Carmody, Joseph Wildenberg
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引用次数: 0

摘要

背景:II 型内漏很常见,如果需要治疗,通常会进行栓塞。虽然经动脉栓塞术很常见,但也有其他方法,包括经腔栓塞术。并发症可能发生,我们报告了一例感染病例,诊断和治疗都很困难。目前还没有数据表明,用 2-氰基丙烯酸正丁酯(n-BCA)胶水对 II 型内漏进行经腔栓塞后,主动脉支架移植物会发生感染:我们报告了一例罕见的病例,一名 71 岁的男性在使用线圈和 n-BCA 胶水经腔栓塞治疗 II 型内漏后感染了 Gore Excluder 肾下支架移植物。内漏导致囊肿迅速增大。支架移植是在 5 年前选择性植入的。内漏栓塞后不久,患者出现腹痛和不适。动脉瘤壁和邻近肠系膜出现了强烈的炎症反应。我们的鉴别标准包括栓塞后的正常炎症与感染,但这很难区分。正电子发射断层扫描和组织活检证实了感染。由于患者有广泛的心脏病史、冠状动脉搭桥术和组织二尖瓣置换术后状态、充血性心力衰竭且左心室射血分数残余 36%,因此被认为是手术的高风险患者。手术前,他接受了为期两周的优化治疗,包括纠正体液状况、静脉注射抗生素、营养咨询和膳食补充。手术通过经腹途径取出了移植物,并用低温保存的同种异体移植物重建了主动脉。有趣的是,小肠和大肠及其肠系膜被发现贴在动脉瘤囊上。除了一过性急性肾损伤在一周内缓解外,术后病程并无异常。6 个月后的随访计算机断层扫描显示旁路广泛通畅:结论:胶水栓塞会诱发炎症,促进动脉瘤囊内血栓形成。结论:胶水栓塞会诱发炎症,促进动脉瘤囊内血栓的形成。采用经腔途径进入动脉瘤囊,存在胶水渗出囊外以及器械污染移植物的风险。区分炎症和感染可能比较困难,组织活检可提供最确凿的诊断。风险最小化的注意事项包括:术前优化、经腹部入路、输尿管支架和吻合口组织加固。
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Infected stent graft and severe aortitis after transcaval glue embolization of type II endoleak: a case report.

Background: Type II endoleaks are common and embolization is often performed if treatment is necessary. Although transarterial embolization is common, other methods including trans-caval embolization are also utilized. Complications can occur and we report a case of infection that was challenging to diagnose and treat. There is no data regarding the risk of aortic stent graft infection after trans-caval embolization with n-butyl 2-cyanoacrylate (n-BCA) glue of a type II endoleak.

Case description: We report a rare case of infected, Gore Excluder infrarenal stent graft after transcaval embolization with coil and n-BCA glue to treat a type II endoleak in a 71-year-old male. The endoleak caused a rapid sac enlargement. The stent graft was placed 5 years earlier electively. Soon after the endoleak embolization, the patient experienced abdominal pain and malaise. There was an intense inflammatory reaction involving the aneurysm wall and the adjacent bowel mesentery. Our differential included normal inflammation after embolization vs. infection and this was difficult to distinguish. The infection was confirmed by positron emission tomography scan and tissue biopsy. The patient was deemed high-risk for surgery because of his extensive cardiac history, status post coronary bypass and tissue mitral valve replacement, congestive heart failure with residual left ventricular ejection fraction of 36%. He was optimized by correcting fluid status, administration of intravenous antibiotic, and nutrition consultation with dietary supplementation before surgery over the course of 2 weeks. The graft was explanted through a transabdominal approach, and the aorta was reconstructed with cryopreserved allograft. Interestingly, the small and large intestine with their mesentery were found to be plastered to the aneurysm sac. The post-operative course was unremarkable except for a transient acute kidney injury that resolved within 1 week. Follow-up computed tomography scan at 6 months showed widely patent bypass.

Conclusions: Glue embolization induces inflammation promoting thrombus formation inside the aneurysm sac. With a transcaval approach to the sac, there is the risk of extravasation of glue outside the sac as well as contamination of the graft with instrumentation. Differentiating between inflammation and infection can be difficult, and tissue biopsy provided the most conclusive diagnosis. Risk minimization considerations include, pre-operative optimization, a transabdominal approach, ureteral stenting, and tissue buttressing of anastomosis.

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