Arterioportal fistula: a rare cause of portal hypertension and abdominal pain.

Esophageal varices are commonly caused by portal hypertension secondary to cirrhosis. We report the case of a 71-year-old woman who presented with esophageal variceal bleeding due to portal hypertension caused by an arteriovenous fistula. The fistula, which was probably brought about by a liver biopsy performed 18 years previously, was complicated by bleeding. Since this event, the patient has reported right upper quadrant pain. Embolization resulted in elimination of the varices as well as abdominal discomfort.     

Percutaneous transarterial embolization of extrahepatic arteroportal fistula

INTRODUCTION Extrahepatic arteroportal fistula is a rare disorderof hepatic vasculature characterized by anomalous communication between arteries and portal vein system most commonly caused by abdominal trauma, and iatrogenic damage induced by procedures …     

Arterioportal Fistula: A Role for Pre-TIPSS Arteriography and Hepatic Venous Pressure Measurements

A 70-yr-old male presented with massive upper gastrointestinal bleeding secondary to esophageal varices. Because the bleeding was not controlled by sclerotherapy or vasopressin and nitroglycerin, the patient was evaluated for a transjugular intrahepatic portosystemic shunt. Preprocedure arteriography was performed because the etiology of the portal hypertension was uncertain. The arteriogram revealed a hepatic artery to portal vein fistula. Hepatic venous pressure measurements documented an elevated hepatic venous pressure gradient, which diminished dramatically upon embolization of the fistula. Rebleeding from the varices was associated with reestablishment of the fistula via collaterals and elevation of the hepatic venous pressure gradient. The case is presented to establish a role for arteriography prior to transjugular intrahepatic portosystemic shunting, especially in patients with unexplained portal hypertension, and to establish the potential value of hepatic venous pressure measurements in the treatment of arterioportal fistulas.     

Hepaticoportal fistula and portal hypertension

Summary A large intrahepatic fistula between the hepatic artery and portal vein was detected at angiography in a patient with portal hypertension and bleeding esophageal varices. Hemodynamic studies demonstrated that increased vascular resistance in the liver rather than increased flow through the fistula was responsible for the portal hypertension and a portocaval shunt was performed. A repeat angiogram two months after the operation showed that the fistula had closed spontaneously.     

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.     

CURATIVE TREATMENT OF BLEEDING ESOPHAGEAL VARICES SECONDARY TO A SPLENIC ARTERIO-VENOUS FISTULA

A 59 year old female, who presented with abdominal pain, diarrhea, and ascites, developed major bleeding from esophageal varices. Celiac angiography demonstrated a splenic arterio-venous fistula with early filling of an enlarged splenic vein and esophageal varices (pre-sinusoidal extra hepatic portal hypertension). The patient underwent splenectomy and resection of the fistula with resultant disappearance of the varices and presenting symptoms.     

门脉高压性小肠病

小肠改变是门脉高压门静脉高压症是一组由门静脉压力持续增高引起的症候群,最常见表现是消化道出血,特别是食管胃静脉曲张破裂出血.随着小肠检查手段的发展,特别是胶囊内镜和双气囊小肠镜,发现门脉高压下小肠发生了病变,被定义为门脉高压性小肠病(PHE),这种改变也是消化道出血的重要原因.消化道出血的患者,胃或食管没有静脉曲张情况...     

孤立性胃静脉曲张110例临床分析

背景：各种疾病引起的门静脉高压常可导致食管胃静脉曲张甚至破裂出血。胃静脉曲张的发生率较食管静脉曲张低，但一旦破裂其出血量大、死亡率高。目前临床上关于孤立性胃静脉曲张（IGV）的研究较少。目的：探讨门静脉高压引起的IGV内镜下形态分型和临床特征。方法：回顾性分析110例IGV患者的临床资料．分析内镜下形态分型与临床特征的关系。结果：110例IGV患者中，内镜下形态分型主要为结节隆起型69例（62．7％）、条索型15例（13．6％）、葡萄串型14例（12．7％）。首发症状以上消化道出血为主（71．8％）。83例（75．5％）IGV的原发病为肝源性疾病。胰源性疾病20例（18．2％）。36例行门静脉CTA检查的患者中，19例（52．8％）示胃．肾分流。内镜下形态分型与IGV的原发病相关（P〈0．0001），而与首发症状无关。结论：IGV内镜下形态分型有助于其病因诊断和治疗方法的选择。     

Development of Gastroesophageal Varices and Risk of Variceal Bleeding in Patients With Cirrhosis

Abstract: We studied the relationships between portal pressure measured using the portal venous pressure gradient, the development of gastroesophageal varices, and the risk of variceal bleeding in 56 patients with cirrhosis. Portal pressure was higher in patients with varices than in those without (P>0.01), and 11 mmHg was the lowest portal pressure measured in the patients with varices. The size of the varices was not associated with the portal pressure. There was no difference in the value of portal pressure measurements for the patients with variceal bleeding and those without and there was no linear-relationship between the degree of portal hypertension and the rate of variceal bleeding. 12 mmHg was the lowest portal pressure measured in the patients with variceal bleeding. The size of the varices was related to the rate of variceal bleeding (P>0.05). We conclude that (a) a portal pressure of 11 mmHg is necessary for the formation of varices, (b) 12 mmHg of portal pressure is necessary for variceal bleeding to occur but the degree of portal hypertension has no predictive value for the risk of variceal bleeding, and (c) the size of the varices does not depend on the degree of portal hypertension but is associated with the risk of variceal bleeding.     

Sclerotherapy of rectal varices

Rectal varices represent a rare condition even in cases of portal hypertension. A case of bleeding ano-rectal varices presenting as the first manifestation of portal hypertension is reported. Treatment by sclerotherapy was successful.     

SUCCESSFUL THERAPY OF BLEEDING DUODENAL VARICES BY TIPS AFTER FAILURE OF SCLEROTHERAPY

Hemorrhage from duodenal varices may be severe and life threatening. We report a patient with portal hypertension and bleeding duodenal varices caused by cirrhosis of the liver. Endoscopic sclerotherapy and intravenous vasopressin failed to control bleeding in this patient. Hemorrhage was subsequently controlled by placement of a transjugular intrahepatic portosystemic shunt. We recommend that in patients with life-threatening hemorrhage from duodenal varices caused by cirrhosis of the liver, transjugular intrahepatic portosystemic shunt be considered in the management.     

Portal hypertension and gastrointestinal bleeding

Variceal bleeding is one of the most serious complications of portal hypertension. The driving force for the development of varices is an increase in portal pressure. As portal hypertension progresses, varices dilate until they finally rupture and bleed. This sequence of events might be prevented by achieving a sufficient decrease in portal pressure or by acting locally at the varices with endoscopic treatments. This article reviews the rationale for the management of portal hypertension and the current recommendations for the prevention and treatment of variceal bleeding.     

Risk factors for haemorrhage from oesophageal varices and acute gastric erosions

Rupture, versus erosion, is the most likely cause of variceal bleeding. The risk of rupture appears to be enhanced in large varices and varices with reddish discoloration. Incompetent perforating veins connecting varices to deeper venous systems may also be important in the pathogenesis of this event. Perhaps one-third of patients with large varices will bleed from them over a period of one to two years. Portal hypertension cannot be used to predict the future risk of bleeding among groups of patients. Nevertheless, it is possible that increases or decreases in portal pressure in individual patients may alter their bleeding risk. We and others have observed portal pressure as low as 10 mmHg in patients with clear-cut, recurrent variceal bleeding. Portal hypertension probably predisposes to gastric mucosal injury by enhancing, by an undefined mechanism, back-diffusion of acid. Consequently, haemorrhagic gastritis is more common in patients with portal hypertension than those without. Whether haemorrhagic gastritis is a more severe lesion in patients with portal hypertension is unclear.     

Posttraumatic intrapancreatic aortosplenic fistula causing portal hypertension

Arterioportal fistulas are uncommon. The case of a patient with massive uncontrollable esophageal variceal bleeding is presented. Reversible portal hypertension was caused by a posttraumatic giant intrapancreatic aortosplenic fistula. Percutaneous closure was unsuccessful, and pancreatectomy was performed to control the bleeding. The case is discussed and the literature on this exceptional cause of portal hypertension is reviewed.     

肝衰竭并发消化道出血的诊断与治疗策略

严重的凝血功能障碍所导致的胃肠道黏膜弥漫性出血以及不同程度的食管胃静脉曲张、门脉高压性胃病以及下消化道异位静脉曲张是肝衰竭并发消化道出血的重要原因,其病情危重,预后极差,病死率高。本文对肝衰竭并发消化道出血与单纯的消化道出血的临床鉴别要点、肝衰竭并发消化道出血的疾病谱以及诊断进行了简要阐述,重点对其治疗的策略及相关进展进行了讨论,同时提出了以药物、内镜下治疗、TIPS 等多种治疗方法为依托的综合治疗策略的概念。     

Gastric variceal bleeding caused by an intrahepatic arterioportal fistula that formed after liver biopsy: a case report and review of the literature

An intrahepatic arterioportal fistula is a rare cause of portal hypertension and variceal bleeding. We report on a patient with an intrahepatic arterioportal fistula following liver biopsy who was successfully treated by hepatectomy after unsuccessful arterial embolization. We also review the literature on symptomatic intrahepatic arterioportal fistulas after liver biopsy. A 48-year-old male with bleeding gastric varices and hepatitis B virus-associated liver cirrhosis was transferred to our hospital; this patient previously underwent percutaneous liver biopsies 3 and 6 years ago. Abdominal examination revealed a bruit over the liver, tenderness in the right upper quadrant, and splenomegaly. Ultrasonographic examination, computed tomography, and angiography confirmed an arterioportal fistula between the right hepatic artery and the right portal vein with portal hypertension. After admission, the patient suffered a large hematemesis and developed shock. He was treated with emergency transarterial embolization using microcoils. Since some collateral vessels bypassed the obstructive coils and still fed the fistulous area, embolization was performed again. Despite the second embolization, the collateral vessels could not be completely controlled. Radical treatment involving resection of his right hepatic lobe was performed. For nearly 6 years postoperatively, this patient has had no further episodes of variceal bleeding.     

Longterm outcome after injection sclerotherapy for oesophageal varices in children with extrahepatic portal hypertension.

A consecutive series of 36 children with bleeding from oesophageal varices secondary to extrahepatic portal hypertension was successfully treated by endoscopic injection sclerotherapy and followed up over a mean period of 8.7 years after variceal obliteration. There were no deaths from portal hypertension or its treatment and morbidity related to oesophageal sclerotherapy was minimal. Endoscopic injection sclerotherapy alone proved safe and effective in controlling variceal bleeding from portal hypertension in over 80% of the children. Recurrent variceal bleeding developed in 10 (31%) patients but half of these were effectively treated by further sclerotherapy. Gastric variceal bleeding unresponsive to sclerotherapy necessitated successful portosystemic shunt surgery in four (13%) patients. Two children required splenectomy for painful splenomegaly. In most children injection sclerotherapy is the best treatment for the primary management of bleeding oesophageal varices, reserving portosystemic shunting or other surgical procedures for those with bleeding from gastrointestinal varices.     

Gallbladder varices

Gallbladder varices are relatively rare ectopic varices in patients with portal hypertension. We present here a case of gallbladder varices accurately diagnosed by color Doppler sonography. A 51-year-old woman was admitted to our unit with recurrent esophageal varices bleeding due to extrahepatic portal vein occlusion after splenectomy. Bleeding was controlled by endoscopic band ligation and esophageal varices were eradicated after the second endoscopic session. Doppler imaging showed the existence of portal cavernoma and gallbladder varices. The close follow-up period after complete eradication of esophageal varices showed no enlargement of varices of the gallbladder or complications related to them. Color Doppler sonography is a valuable noninvasive imaging technique for assessment of portal hemodynamic profile in patients with portal cavernoma as well as useful in detecting gallbladder varices. Preoperative correct diagnosis of gallbladder varices should increase the surgeon's vigilance during biliary tract surgery in patients with portal hypertension in order to avoid hazardous complications.     

Sinistral portal hypertension with bleeding gastric varices as initial manifestation of renal-cell carcinoma

We report a clinic case of renal-cell carcinoma presenting as sinistral portal hypertension; a clinical syndrome consisting of esplenic vein thrombosis manifested as isolated gastric varices with patent portal vein and normal hepatic function. The most frequent cause of this syndrome is pancreatic pathology. Renal-cell carcinoma is characterized by a wide variety of symptoms as initial manifestation. In our case, the patient developed a massive gastrointestinal bleeding secondary to isolated gastric varices caused by splenic vein thrombosis due to extrinsic compression by a hypernephroma that infiltrated the pancreas.     

Gastric Varices: Profile, Classification, and Management

Development of gastric varices is an important manifestation of portal hypertension. In segmental portal hypertension, gastric varices originate from short gastric and gastroepiploic veins. In generalized portal hypertension, intrinsic veins at cardia participate in the formation of gastric varices. Endoscopy and/or splenoportovenography and a high index of suspicion are required for the diagnosis of gastric varices. The incidence of gastric varices in patients with portal hypertension has been variably reported (2-70%), probably due to difficulties in diagnosis. In a small proportion of patients with gastric varices, chronic portal-systemic encephalopathy or significant variceal bleeding develops. Gastric varices can be classified, depending on their anatomical location, into gastroesophageal varices (a continuation of esophageal varices) or "isolated" gastric varices (fundal or ectopic varices). This distinction is necessary for management. Whereas surgery is recommended for bleeding fundal varices, in acute bleeding from gastroesophageal varices, sclerotherapy could be attempted successfully. In more than a quarter of patients, gastric varices disappear after obliteration of esophageal varices. Prophylactic sclerotherapy of gastric varices is not recommended.