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

Abstract

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prescribed warfarin as the long-term anticoagulant therapy, although disease improvement was hardly observed, which was withdrawn 18 months later due to noncompliance of the patient.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.