胃左动脉解剖变异致胃静脉曲张硬化治疗后脾梗死1例报告并文献复习。

IF 2.3 3区 医学 Q3 GASTROENTEROLOGY & HEPATOLOGY
Shuai Jie Qian, Zhi Yin Huang, Yang Tai, Cheng Wei Tang, Hao Wu
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The patient was prescribed with oral antibiotics and nonsteroidal anti-inflammatory drugs, and his symptoms gradually improved. The patient was followed up for 2 years, during which splenic infarction was improved, and he did not experience recurrence of variceal bleeding at the time of writing this letter.</p><p>Variceal bleeding is a serious complication associated with cirrhotic portal hypertension and non-cirrhotic portal vein thrombosis [<span>1, 3</span>]. Endoscopic sclerotherapy with cyanoacrylate has been regarded as an effective therapeutic option for gastric variceal bleeding [<span>1, 4</span>]. Ectopic embolization after cyanoacrylate injection, although rare, has been documented, which is described as thrombosis at different sites including lungs, cerebral and coronary arteries, renal vein, and portal or splenic veins [<span>2</span>]. Splenic infarction is most frequently caused by splenic vein occlusion related to the migration of the agent through a shunt. 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The patient was prescribed warfarin as the long-term anticoagulant therapy, although disease improvement was hardly observed, which was withdrawn 18 months later due to noncompliance of the patient. He was rushed to our Emergency Center due to massive hematemesis and hematochezia 8 months after cessation of treatment. At that admission, esophagogastroduodenoscopy (EGD) showed severe gastroesophageal varices (Figure 1b,c). And abdominal contrast-enhanced CT scan suggested a cavernous transformation of the portal vein (Figure 1a) and abundant collateral vessels. Considering the presence of prehepatic portal hypertension, two sessions of endoscopic band ligation combined with sclerotherapy were performed to treat hemorrhage and prevent rebleeding.</p><p>At admission, physical examination and laboratory tests of the patient revealed no remarkable abnormalities. The patient was then hospitalized for sclerotherapy to prevent rebleeding. During the procedure, severe gastric varices were observed (Figure 2a). Spurting hemorrhage occurred immediately after sclerosing agent cyanoacrylate (B. Braun, Melsungen, Germany) was injected (Figure 2b). Although emergency hemostasis was successfully performed by using a titanium clip (Figure 2c), the patient complained of persistent severe pain in the left upper quadrant of the abdomen and left waist accompanied by mild fever (37.4°C) at 30 h after the endoscopic treatment. Peripheral blood tests revealed an elevated white blood cell (WBC) count (15.5 × 10<sup>9</sup>/L; normal range 3.5–9.5 × 10<sup>9</sup>/L) and neutrophil percent (84.1%; normal range 40%–75%). A repeat abdominal contrast-enhanced CT scan revealed a large hypodense area of the spleen (Figure 2d). 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引用次数: 0

摘要

氰基丙烯酸酯的内镜硬化疗法已被推荐为胃静脉曲张急性出血的一线治疗选择。然而,内镜下注射氰基丙烯酸酯治疗胃静脉曲张可能导致脾梗死[2],其病因尚不清楚。我们在此报告一例24岁的男性患者,由于脾动脉闭塞和胃左动脉(LGA)伴侧支动脉代偿性扩张,经氰基丙烯酸酯内镜硬化治疗后出现脾梗死。一名24岁男性因遗传性血栓相关的门静脉海绵状变性引起胃静脉曲张出血而入院。患者在入院前3年被诊断为遗传性血栓病,诊断时腹部CT扫描显示广泛动脉血栓形成累及腹腔干及其分支,静脉血栓形成累及门静脉、肠系膜上静脉和脾静脉(图1a)。患者被开华法林作为长期抗凝治疗,但几乎没有观察到疾病的改善,18个月后由于患者的不遵守而停药。他在停止治疗8个月后因大量呕血和便血被紧急送往我们的急救中心。入院时,食管胃十二指肠镜(EGD)显示严重的胃食管静脉曲张(图1b,c)。腹部CT增强扫描显示门静脉海绵样转变(图1a)和丰富的侧支血管。考虑到肝前门静脉高压症的存在,我们进行了两次内镜下带状结扎联合硬化治疗,以治疗出血并防止再出血。入院时,体格检查和实验室检查未见明显异常。患者随后住院接受硬化治疗以防止再出血。手术过程中,观察到严重的胃静脉曲张(图2a)。注射硬化剂氰基丙烯酸酯(B. Braun, Melsungen, Germany)后立即发生喷射性出血(图2b)。虽然使用钛夹成功进行了紧急止血(图2c),但患者在内镜治疗后30 h仍主诉腹部左上腹和左腰持续剧烈疼痛,并伴有轻度发热(37.4℃)。外周血检查显示白细胞(WBC)计数升高(15.5 × 109/L;正常范围3.5 ~ 9.5 × 109/L),中性粒细胞百分比(84.1%;正常范围40%-75%)。重复腹部增强CT扫描显示脾脏大面积低密度区(图2d)。然后诊断为动脉栓塞引起的脾梗死。为了探讨该病例发生动脉异位栓塞的原因,我们进行了三维重建的计算机断层血管造影(CTA),显示位于胃底连接LGA和脾动脉的几条异常扩大的动脉。脾内供血异常动脉闭塞(图3a),表明硬化剂通过增大的LGA动脉分支进入脾内动脉(图3b,c),导致脾梗死。患者给予口服抗生素及非甾体类抗炎药,症状逐渐好转。患者随访2年,脾梗死改善,写此信时无静脉曲张出血复发。静脉曲张出血是肝硬化门静脉高压和非肝硬化门静脉血栓形成相关的严重并发症[1,3]。氰基丙烯酸酯内镜硬化疗法被认为是胃静脉曲张出血的有效治疗选择[1,4]。氰基丙烯酸酯注射后异位栓塞虽然罕见,但已有文献记载,其描述为不同部位的血栓形成,包括肺、脑、冠状动脉、肾静脉、门静脉或脾静脉[2]。脾梗死最常见的原因是脾静脉阻塞与药物通过分流的迁移有关。氰基丙烯酸酯内镜硬化治疗中动脉栓塞性脾梗死的报道很少,在临床实践中应引起重视[5,6]。由于超声内镜(EUS)技术的发展,其在氰基丙烯酸酯注射指导下的应用在胃静脉曲张的治疗中备受关注,可以更仔细、准确地评估胃静脉曲张,并实时监测手术过程。与内镜下直接注胶相比,eus引导下的闭塞治疗取得了更有效的闭塞效果,并且出血复发和再干预率更低[8,9]。 此外,EUS可以减少氰基丙烯酸酯用量,减少并发症的风险,并在与线圈联合使用时减少复发性出血[10,11],特别是对于高危异位栓塞和自发性门系统分流的患者[12,13]。在我们的病例中,慢性门静脉和脾动脉血栓栓塞导致肝前门静脉高压、胃静脉曲张和脾缺血。作为脾动脉闭塞的代偿反应,LGA扩张并发展侧支动脉供应脾。这些扩张的动脉在内镜治疗中被误认为是胃静脉曲张,并被错误地注射了氰基丙烯酸酯。结果,氰基丙烯酸酯沿着LGA异常分支流入脾脏,引起脾梗死。据我们所知,氰基丙烯酸酯注射后由异常供应动脉引起脾梗死的报道很少。虽然粘膜静脉曲张血管多起源于粘膜下深部静脉,但当动脉有解剖变异时,尤其是合并血管疾病时,可能难以区分。对于重度胃静脉曲张患者,尤其对于多次内镜栓塞和硬化治疗的患者,可常规应用CTA,在硬化治疗前及时发现异常血管,避免出血和异位栓塞的风险。在术前CTA充分评估腹部血管状况后,也可考虑eus引导下注射氰基丙烯酸酯,以减少并发症的发生,提高高危患者的治疗效果。作者声明无利益冲突。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Splenic Infarction After Sclerotherapy for Gastric Varices due to Anatomical Variation of Left Gastric Artery: A Case Report and Literature Review

Splenic Infarction After Sclerotherapy for Gastric Varices due to Anatomical Variation of Left Gastric Artery: A Case Report and Literature Review

Endoscopic sclerotherapy with cyanoacrylate has been recommended as the first-line therapeutic option for gastric varices with acute bleeding [1]. However, endoscopic injection of cyanoacrylate for treating gastric varices may cause splenic infarction [2], the etiology of which remains unclear. Here we reported a case of a 24-year-old man who presented with splenic infarction after endoscopic sclerotherapy with cyanoacrylate due to splenic arterial occlusion and compensatory dilatation of the left gastric artery (LGA) with collateral branch arteries.

A 24-year-old man was admitted to our hospital due to recurrent gastric variceal bleeding caused by inherited thrombophilia-related cavernous transformation of the portal vein. Inherited thrombophilia was diagnosed 3 years prior to his admission, with extensive arterial thrombosis involving the celiac trunk and its branches as well as venous thrombosis involving the portal vein, superior mesenteric vein, and splenic vein on abdominal computed tomography (CT) scan at diagnosis (Figure 1a). The patient was prescribed warfarin as the long-term anticoagulant therapy, although disease improvement was hardly observed, which was withdrawn 18 months later due to noncompliance of the patient. He was rushed to our Emergency Center due to massive hematemesis and hematochezia 8 months after cessation of treatment. At that admission, esophagogastroduodenoscopy (EGD) showed severe gastroesophageal varices (Figure 1b,c). And abdominal contrast-enhanced CT scan suggested a cavernous transformation of the portal vein (Figure 1a) and abundant collateral vessels. Considering the presence of prehepatic portal hypertension, two sessions of endoscopic band ligation combined with sclerotherapy were performed to treat hemorrhage and prevent rebleeding.

At admission, physical examination and laboratory tests of the patient revealed no remarkable abnormalities. The patient was then hospitalized for sclerotherapy to prevent rebleeding. During the procedure, severe gastric varices were observed (Figure 2a). Spurting hemorrhage occurred immediately after sclerosing agent cyanoacrylate (B. Braun, Melsungen, Germany) was injected (Figure 2b). Although emergency hemostasis was successfully performed by using a titanium clip (Figure 2c), the patient complained of persistent severe pain in the left upper quadrant of the abdomen and left waist accompanied by mild fever (37.4°C) at 30 h after the endoscopic treatment. Peripheral blood tests revealed an elevated white blood cell (WBC) count (15.5 × 109/L; normal range 3.5–9.5 × 109/L) and neutrophil percent (84.1%; normal range 40%–75%). A repeat abdominal contrast-enhanced CT scan revealed a large hypodense area of the spleen (Figure 2d). Splenic infarction due to arterial embolism was then diagnosed.

To investigate the reason why ectopic embolism of the artery occurred in this case, computed tomography angiography (CTA) with three-dimensional reconstruction was performed, showing several abnormally enlarged arteries located at the gastric fundus connecting the LGA and the splenic artery. Intrasplenic occlusion of the abnormal artery that supplies the spleen was observed (Figure 3a), which suggested that sclerosing agents entered the intrasplenic arteries via the enlarged arterial branches of LGA (Figure 3b,c), leading to splenic infarction. The patient was prescribed with oral antibiotics and nonsteroidal anti-inflammatory drugs, and his symptoms gradually improved. The patient was followed up for 2 years, during which splenic infarction was improved, and he did not experience recurrence of variceal bleeding at the time of writing this letter.

Variceal bleeding is a serious complication associated with cirrhotic portal hypertension and non-cirrhotic portal vein thrombosis [1, 3]. Endoscopic sclerotherapy with cyanoacrylate has been regarded as an effective therapeutic option for gastric variceal bleeding [1, 4]. Ectopic embolization after cyanoacrylate injection, although rare, has been documented, which is described as thrombosis at different sites including lungs, cerebral and coronary arteries, renal vein, and portal or splenic veins [2]. Splenic infarction is most frequently caused by splenic vein occlusion related to the migration of the agent through a shunt. Arterial embolization-induced splenic infarction during endoscopic sclerotherapy with cyanoacrylate has rarely been reported, which should be paid attention to in clinical practice [5, 6].

Because of the development in endoscopic ultrasonography (EUS) technology, its utility in the guidance of cyanoacrylate injection has attracted much attention for the management of gastric varices, which can evaluate gastric varices more carefully and accurately and monitor the procedure in real time [7]. Compared with direct endoscopic glue injection, EUS-guided obliteration therapy has achieved more effective obliteration, together with lower rates of recurrent bleeding and reintervention [8, 9]. Furthermore, EUS allows a reduction of cyanoacrylate volume, risk of complications, and recurrent bleeding when combined with the use of coil [10, 11], especially in patients with high-risk ectopic embolism and spontaneous portosystemic shunt [12, 13].

In our case, chronic thromboembolism of the portal vein and splenic artery contributed to prehepatic portal hypertension, gastric varices, and splenic ischemia. As a compensatory response to splenic arterial occlusion, LGA dilated and developed collateral arteries to supply the spleen. These enlarged arteries were misidentified as gastric varices during the endoscopic treatment and were mistakenly injected with cyanoacrylate. As a result, cyanoacrylate flowed along the abnormal branch of LGA to the spleen, causing splenic infarction. To the best of our knowledge, splenic infarction through abnormal supplying arteries after cyanoacrylate injection has been rarely reported. Although mucosal variceal vessels mostly originate from the deep submucosal veins, it may be difficult to distinguish them when there is anatomical variation of arteries, especially in cases complicated with vascular diseases. CTA may be applied routinely in patients with severe gastric varices to timely detect abnormal vessels before sclerotherapy and to avoid the risks of bleeding and ectopic embolism, especially in those who have undergone multiple endoscopic embolization procedures and sclerotherapy. EUS-guide cyanoacrylate injection can also be considered after adequately evaluating the abdominal vascular conditions by preoperative CTA so as to reduce risks of complications and enhance therapeutic effectiveness in high-risk patients.

The authors declare no conflicts of interest.

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来源期刊
Journal of Digestive Diseases
Journal of Digestive Diseases 医学-胃肠肝病学
CiteScore
5.40
自引率
2.90%
发文量
81
审稿时长
6-12 weeks
期刊介绍: The Journal of Digestive Diseases is the official English-language journal of the Chinese Society of Gastroenterology. The journal is published twelve times per year and includes peer-reviewed original papers, review articles and commentaries concerned with research relating to the esophagus, stomach, small intestine, colon, liver, biliary tract and pancreas.
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