Splenic arteriovenous fistula causing massive ascites: a case report

A case of splenic arteriovenous fistula leading to portal hypertension and ascites is presented. The recognition of this vascular lesion is important. When portal hypertension is secondary to a splenic arteriovenous fistula, the complications of portal hypertension can be avoided by the resection of the lesion. The diagnosis can be suspected by clinical findings and confirmed by angiographic delineation of the fistula. Surgical resection of splenic arteriovenous fistulae must include the fistula and all dilated venous tributaries to prevent thrombosis and recurrent portal hypertension.     

Melena-associated regional portal hypertension caused by splenic arteriovenous fistula

Regional portal hypertension is a rare cause of upper gastrointestinal bleeding. We reported an extremely rare case in which regional portal hypertension was associated with both the splenic arteriovenous fistula and chronic pancreatitis. In June 2010, our patient, a 41-year-old man, was admitted to a local hospital due to a sudden melena and dizziness without haematemesis and jaundice. The splenic arteriovenous fistula in this patient was successfully occluded through transcatheter arterial embolization. At the 12-mo follow-up, our patient was in good condition.     

Arteriovenous fistula and forward hypertension in the portal circulation

The notorious predilection for rupture of splenic artery aneurysms in women of childbearing age is once more stressed by this case report. Although such ruptures usually result in a catastrophic interabdominal bleeding, in rare instances they lead to the formation of an arteriovenous fistula and consequent portal hypertension. Arterialization of the portal vein results in a progressive development of intrinsic hepatic morphologic changes and hepatoportal sclerosis, which further elevate the pressure in the portal system. This combination of pathophysiologic hemodynamic features closely resembles the original concept of Banti. He postulated that portal hypertension began with pathologic changes within the spleen which were associated with an increased blood flow through this organ. This led to increased flow and pressure in the portal venous system and ultimately cumulated in cirrhosis of the liver. This concept of the pathophysiology of portal hypertension has been universally abandoned, but it could serve as a model of the sequelae of an arteriovenous communication within the portal system.     

Splenic arteriovenous fistula and sudden onset of portal hypertension as complications of a ruptured splenic artery aneurysm： Successful treatment with transcatheter arterial embolization. A case study and review of the literature

Splenic arteriovenous fistula (SAVF) accounts for an unusual but well-documented treatable cause of portal hypertension. A case of a 50-year-old multiparous female who developed suddenly portal hypertension due to SAVF formation is presented. The patient suffered from repeated episodes of haematemesis and melaena during the past twelve days and thus was emergently admitted to hospital for management. Clinical and laboratory investigations established the diagnosis of portal hypertension in the absence of liver parenchymal disease. Endoscopy revealed multiple esophageal bleeding varices. Abdominal computed tomography (CT) and transfemoral celiac arteriography documented the presence of a tortuous and aneurysmatic splenic artery and premature filling of an enlarged splenic vein, findings highly suggestive of an SAVF. The aforementioned vascular abnormality was successfully treated with percutaneous transcatheter embolization. Neither recurrence nor other complications were observed.     

Successful arterial embolization of arteriovenous fistula in the portal circulation.

We successfully performed arterial embolization of an arteriovenous fistula between the left gastric artery and vein. The increased blood flow in the portal vein via the left gastric vein and the arteriovenous fistula induced severe portal hypertension. After obliteration of the left gastric artery, the arteriovenous fistula was not opacified on angiography and the portal hypertension improved.     

Splenic hyperkinetic state and splenic artery aneurysm in portal hypertension.

Forty-eight out of six hundred and thirty patients with portal hypertension undergoing a celiac angiography series were diagnosed as cases of splenic artery aneurysm during the period 1977-1988. The case-control study of patients with portal hypertension with splenic artery aneurysms and those without was designed to characterize the angiological features. The splenic arterial flow was assessed by measuring the radii of the splenic arteries on celiac arteriograms. In the portal hypertensive patients with splenic artery aneurysms, the splenic artery was larger (p < 0.05) and the splenic arterial flow greater (p < 0.05), and these patients were in a more hyperkinetic state, than were those with no splenic artery aneurysm. The study suggests that splenic artery aneurysms in cases of portal hypertension may be the consequence of a hyperkinetic state in the spleen.     

门脉高压症患者脾脏及脾静脉壁NOS分布及其意义研究

目的 探讨一氧化氮（ＮＯ）在门脉高压症内脏血管病理性损伤中可能的作用。方法 采用光镜,电镜及ＮＡＤＰＨ－黄递酶组织化学染色方法观察同压症２脾脏及脾泊病理变化及一氧化氮合酶的分布。结果 与对照组相比 同压症患者脾血窦显著扩张,脾静脉壁增厚,平滑肌增生,血管内皮广泛受损,脾脏及脾静脉壁内ＮＯＳ阳性细胞显著增多,染色增强,结论ＮＯ可能参与门脉高压症内脏高动力循环的发病机制。     

Une cause inhabituelle d’hypertension portale segmentaire: un phéochromocytome gauche

Segmental or sinistral portal hypertension is a rare form of extrahepatic portal hypertension. It results from thrombosis or compression of the splenic vein or the union of superior mesenteric and splenic vein which are usually due to pancreatic disease. The originality of our observation comes from the aetiology of segmental portal hypertension which is a left pheochromocytoma. It is to our knowledge the second case in literature.     

Splanchnic Hemodynamics in Idiopathic Portal Hypertension: Comparison with Chronic Persistent Hepatitis

A comparative study of splanchnic hemodynamics was made in 12 patients with idiopathic portal hypertension and in eight patients with chronic persistent hepatitis, but without portal hypertension, who served as the control. Venous pressures were measured by portal and hepatic vein catheterizations, blood flow by the pulsed Doppler flowmeter, and organ volume by computed tomography. Splenic artery blood flow was 788 +/- 242 ml/min in idiopathic portal hypertension and about four times that in chronic persistent hepatitis (215 +/- 42 ml/min), whereas there was no difference in superior mesenteric artery blood flow between the former and the latter (408 +/- 142 vs. 389 +/- 32 ml/min). Spleen volume in idiopathic portal hypertension was six times that in chronic persistent hepatitis, and splenic artery blood flow showed a significant linear correlation with spleen volume in idiopathic portal hypertension (r = 0.71, p less than 0.02). The sum of splenic artery blood flow and superior mesenteric artery blood flow in idiopathic portal hypertension was 1195 +/- 294 ml/min, twice that in chronic persistent hepatitis (603 +/- 109 ml/min). Portal vascular resistance and intrahepatic portal vascular resistance were three times and four times those in chronic persistent hepatitis, respectively. These results indicate that both increased intrahepatic portal vascular resistance and increased splenic artery blood flow may play roles in the development of portal hypertension in idiopathic portal hypertension.     

胰源性区域性门脉高压症——附14例报告

本文报告了14例胰源性区域性门脉高压症。本病为肝外型门脉高压症中罕见的一种，对未发现肝脏疾病，而有胃底，食管静脉曲张，脾肿大的病人，应考虑本病。门静脉造影可以确立诊断，经皮脾穿刺门静脉造影是确诊本症的三种简单可行的方法。本病可经脾切除治愈。     

Acinar Cell Carcinoma of the Pancreas: A Rare Cause of Left-Sided Portal Hypertension

Isolated splenic vein obstruction with left-sided portal hypertension is a rare clinical condition. Owing to the close relationship of the splenic vein and the pancreas, this rare phenomenon is usually secondary to pancreatic inflammation or neoplasm. Acinar cell carcinoma has long been recognized as a distinctive, rare type of pancreatic carcinoma. A case of isolated splenic vein obstruction with left-sided portal hypertension secondary to acinar cell carcinoma of the pancreas, which we are reporting here, is thought to the first documented in the literature.     

Differences in Portal Hemodynamics in Cirrhosis and Idiopathic Portal Hypertension

A comparative study of portal hemodynamics was made in 79 cirrhotics (24 cirrhotics with a large spleen greater than or equal to 500 cm3 in volume, 55 cirrhotics with a spleen less than 500 cm3 in volume), 22 patients with idiopathic portal hypertension, and 63 healthy adults who served as the control for portal and splenic venous flows. Portal and splenic venous flows were significantly increased in the group order of the cirrhosis without splenomegaly group, the cirrhosis with splenomegaly group, and idiopathic portal hypertension group. Intrahepatic shunt index was significantly greater in the cirrhosis with splenomegaly group than in the cirrhosis without splenomegaly group, and it was negligible in the idiopathic portal hypertension group. Portal vein pressure was significantly elevated in the cirrhosis with splenomegaly group than in the cirrhosis without splenomegaly and idiopathic portal hypertension groups. Postsinusoidal resistances were significantly greater in the two groups of cirrhosis than in the idiopathic portal hypertension group, whereas presinusoidal resistance was significantly greater in the idiopathic portal hypertension group than in the two groups with cirrhosis. It is concluded that these differences are inconsistent with the view that cirrhosis with splenomegaly comes from idiopathic portal hypertension.     

左侧局限性门脉高压并脾梗死1例

本文报道1例左侧局限性门脉高压并脾梗死病例,旨在提高临床医生对左侧局限性门脉高压的认识,以免误诊。     

Animal models for the study of portal hypertension

Animal models allow detailed study of the hemodynamic alterations in portal hypertension syndrome and of the molecular mechanisms involved in the abnormalities in splenic and systemic circulation associated with this syndrome. Models of prehepatic portal hypertension can be used to study alterations in the splenic circulation and the physiopathology of hyperdynamic circulation. Moreover, models of cirrhosis allow the alterations in intrahepatic microcirculation that lead to increased resistance to portal flow to be studied. The present review summarizes currently available animal models of portal hypertension and analyzes their relative utility in investigating the distinct disorders associated with this entity. The criteria for the choice of a particular model, depending on the specific objectives of the study, are also discussed.     

双介入治疗肝硬化门脉高压和脾功能亢进症

目的 探讨经颈内静脉肝内门体分流术(Transjugular intrahepatic portosystemic shunt,TIPS)和部分脾栓塞术(Partial splenic embolization,PSE)联合治疗肝硬化门脉高压及脾功能亢进症的疗效.方法 30例均为肝硬化门脉高压及脾功能亢进症患者,行TIPS术后再行PSE术.用超声检测门、脾静脉内径、门脉主干血流速度、脾脏长径和厚度;血细胞分析仪检测血象.结果 30例患者TIPS术后的门脉压力较术前降低(P＜0.01).门、脾静脉内径较术前缩小(P＜0.01),门脉主干血流速度较术前增快(P＜0.01);术后3～6月的脾脏长径及厚度、白细胞、血小板及血红蛋白较术前均无明显变化(P＞0.05).30例患者PSE术后的门、脾静脉内径、门脉主干血流速度与TIPS术后的比较无明显变化(P＞0,05);而白细胞、血小板及血红蛋白较TIPS术后明显升高(P＜0.01),脾脏长径和厚度较TIPS术后缩小(P＜0.05).结论 联合TIPS和PSE术治疗,能有效降低肝硬化患者的门脉压力,同时又能缓解脾功能亢进.     

Inferior mesenteric arteriovenous fistula associated with portal hypertension and acute ischemic colitis. Successful occlusion by intraarterial embolization with steel coils

The authors report a case of postoperative arteriovenous fistula between the inferior mesenteric vessels. This fistula was revealed by portal hypertension, with bleeding esophageal varices, ascites, and encephalopathy, and by acute ischemic colitis. Histologic examination of the liver was normal. All of the symptoms disappeared after transcatheter embolization of the fistula with stainless steel coils. This case report favors the reality of the so-called "forward" portal hypertension and suggests that inferior mesenteric arteriovenous fistula might be a factor predisposing to nonocclusive ischemic colitis.     

Efficacy of interventional radiology in the management of portal hypertension: A narrative review

Portal hypertension is associated with numerous adverse effects, including the formation of gastroesophageal varices and a portal vein general circulation shunt. Portal hypertension can lead to portal blood flow into the liver and a subsequent reduction in liver function. Clinical interventions can be hampered by a concurrent reduction in circulating platelets associated with increased splenic activity. Pharmaceutical interventions for the treatment of complications associated with portal hypertension have achieved various degrees of success. However, an effective therapeutic strategy for portal hypertension has not yet been established. A literature search was performed using “PubMed.” Database between 1966 and January 2021 using the following keywords: portal hypertension, interventional radiology, balloon-occluded retrograde transvenous obliteration, transjugular retrograde obliteration of gastric varices, percutaneous transhepatic obliteration, partial splenic embolization, and transjugular intrahepatic portosystemic shunting. In this narrative review, we summarize the application of interventional radiology in patients with portal hypertension, including techniques for embolization of collateral veins and portal pressure reduction. These up-to-date interventional radiology techniques can be used to treat portal hypertension. The data that support the findings of this study are available from the corresponding author, upon reasonable request.     

多层螺旋CT全肝灌注成像对不同程度脾功能亢进患者肝脾血流状态的评估

目的应用多层螺旋CT全肝灌注模式,探讨不同程度脾功能亢进患者脾脏体积、肝总动脉、脾动静脉、门静脉内径差异及肝脏血流状态变化情况。方法收集慢性乙型肝炎肝硬化脾功能亢进患者42例,无肝脾疾病患者15例作为对照,所有患者均行多层螺旋CT全肝灌注成像:(1)测量比较不同程度脾功能亢进组与对照组脾脏体积、肝总动脉、脾动静脉、门静脉内径之间的差异;(2)分析比较脾脏体积与各相关血管内径之间的相关性;(3)测量比较基于Couinaud分段肝脏五叶相关灌注参数值:肝动脉灌注量(HAP)、门静脉灌注量(PVP)、总肝灌注量(TLP)和肝动脉灌注指数(HPI)。计量资料采用单因素方差分析,采用Pearson相关分析对脾脏体积与各血管内径进行相关性分析。结果(1)肝硬化脾功能亢进组脾脏体积及脾动脉、脾静脉、门静脉内径均大于对照组,差异有统计学意义(F值分别为37.108、17.484、23.124、13.636,P值均<0.05)。(2)中、重度脾功能亢进组脾脏体积及脾动脉、脾静脉、门静脉内径明显大于轻度脾功能亢进组,差异有统计学意义(F值分别为25.418、13.293、15.136、7.093,P值均<0.05),但中、重度脾功能亢进组间差异无统计学意义(P>0.05)。(3)脾静脉、门静脉、脾动脉内径与脾脏体积呈正相关(r值分别为0.680、0.548、0.726)。(4)脾功能亢进组全肝叶PVP、TLP均低于对照组,差异有统计学意义(P<0.05);不同程度脾功能亢进组HPI均高于对照组,中、重度脾功能亢进组肝右后叶HPI高于轻度脾功能亢进组,差异有统计学意义(F值为3.555、4.570,P值均<0.05);各组间全肝叶HAP差异无统计学意义(P>0.05),但重度脾功能亢进组全肝叶HAP均低于对照组、轻及中度脾功能亢进组。结论不同程度脾功能亢进患者脾动静脉内径均有不同程度的增宽,与脾脏体积增大一致,且中、重度为著;不同程度脾功能亢进患者门静脉灌注量及总肝灌注量均减少,肝动脉灌注量以重度脾功能亢进患者减少显著。     

经脾动脉灌注低分子右旋糖酐在门脉高压症断流术中的应用

目的 探讨门脉高压症断流术中应用低分子右旋糖酐经脾动脉灌注,对预防门静脉系统血栓形成的效果。方法 选取本院2009年1月-2013年10月门脉高压症断流术患者92例,随机分为2组,对照组46例行脾切除及贲门周围血管离断术,实验组46例行门脉高压断流术,且术中应用低分子右旋糖酐脾动脉灌注,对2组病例术后门静脉血栓发生率、术中术后输血量进行统计分析。结果 实验组患者术后门静脉血栓发生率为4.3%（2/46）,浓缩红细胞输血量2 ~ 3 U,对照组患者血栓发生率及浓缩红细胞输血量分别为26.1%（12/46）和4 ~ 6 U,差异有统计学意义（P均< 0.05）。结论 术中经脾动脉低分子右旋糖酐灌注在门脉高压症脾切除术中操作安全可行,能有效降低术后门静脉系统血栓的发生率,且节约血源,减少用血量,值得临床推广应用。