Duodenal varices secondary to inferior vena cava obstruction

Summary A case has been reported of duodenal varices secondary to long-standing obstruction of the inferior vena cava. The varices produced nodular defects in the descending duodenum. Opacification of the portal vein by these collaterals was demonstrated on venography. This is a rare cause of duodenal varices never previously reported.     

Diagnosis and management of ectopic varices

Abstract   Ectopic varices are dilated portosystemic venous collateral vessels that may occur anywhere in the gastrointestinal tract. Ectopic varices account for approximately 5% of all hemorrhages from varices. Ectopic varices may occur as a result of portal hypertension from any cause but are more common (particularly duodenal and biliary varices) in patients with extrahepatic portal vein thrombosis. Ectopic varices may also develop following successful endoscopic obliteration of gastroesophageal varices. With the exception of isolated gastric fundal varices, ectopic varices have relatively low risk for bleeding. Diagnosis is often made by endoscopy; however, computed tomography, magnetic resonance imaging and portal venography may be needed in some cases. Endoscopic treatment is successful in many cases and is the safest option provided bleeding is definitively controlled. Surgical options are now reserved for treatment of life-threatening bleeding or for shunt insertion in patients who are not candidates for transjugular intrahepatic portosystemic shunt (TIPS) as a result of portal vein thrombosis. Portal decompression using TIPS, in spite of the risk for encephalopathy, is the treatment of choice for bleeding from ectopic varices that cannot be successfully managed endoscopically.     

Sonographic evaluation of patients with portal hypertension

The availability of real-time sonography has facilitated its use in the assessment of patients suspected of portal hypertension. Dilatation of the portal venous system may occur in portal hypertension, and a portal vein diameter greater than 13 mm is indicative of portal hypertension with a sensitivity of about 50%. Sonographic demonstration of lack of caliber variation of the portal system bas a sensitivity of about 80%. The presence of venous collaterals can be demonstrated in about 90% of patients suitable for sonography. The coronary gastroesophageal varices can be seen in 90% when they are large sized, and in 65% when they are small sized. Other collaterals such as umbilical vein, duodenal varices, and gastrorenal and splenorenal varices can be detected. Sonography is a valuable screening procedure in the evaluation of portal hypertension and provides valuable information regarding the size and morphology of the liver and spleen, caliber and patency of the portal venous system, and the existence and location of the varices.     

Successful balloon-occluded retrograde transvenous obliteration for bleeding duodenal varices using cyanoacrylate

A 76-year-old woman with hepatitis C cirrhosis presented with tarry stools and hematemesis.An endoscopy demonstrated bleeding duodenal varices in the second portion of the duodenum.Contrast-enhanced computed tomography revealed markedly tortuous varices around the wall in the duodenum.Several afferent veins appeared to have developed,and the right ovarian vein draining into the inferior vena cava was detected as an efferent vein.Balloon-occluded retrograde transvenous obliteration (BRTO) of the varices using cyanoacrylate was successfully performed in combination with the temporary occlusion of the portal vein.Although no previous publications have used cyanoacrylate as an embolic agent for BRTO to control bleeding duodenal varices,this strategy can be considered as an alternative procedure to conventional BRTO using ethanolamine oleate when numerous afferent vessels that cannot be embolized are present.     

CLINICAL CHARACTERISTICS AND TREATMENT FOR PATIENTS PRESENTING WITH BLEEDING DUODENAL VARICES

Background and Aim: Bleeding from ectopic varices, including duodenal varices, is uncommon, but it can be difficult to manage. The clinical data of patients diagnosed and treated for duodenal varices were reviewed to investigate the strategy for treatment. Methods: The present study reviewed the clinical data of 10 patients with duodenal varices (mean age, 58.2 ± 15.6 years) at our associated institutes during the period between January 1996 and December 2008. Results: Nine patients had duodenal varices located in the second portion, whereas in one case they were located in the duodenal bulbus. The underlying diseases included liver cirrhosis in eight patients, and extrahepatic portal vein obstruction in two patients. The lesions were identified with bleeding from varices in eight of 10 patients. Initial hemostasis was achieved in all eight patients. However, among four patients treated endoscopically only, two patients died from rebleeding from varices and two died from hepatic failure resulting from variceal bleeding. Additional interventional radiology (IVR) was used in three patients and additional surgery was carried out in one case. One patient who was treated with balloon‐occluded retrograde transvenous obliteration rebled during IVR and died from bleeding. Two patients who underwent double balloon‐occluded embolotherapy and one case who had surgery achieved good clinical outcomes. Conclusions: Although endoscopic treatment is useful for initial hemostasis of hemorrhagic duodenal varices, the patients who underwent additional IVR after endoscopic treatment achieved good outcomes.     

Massive duodenal variceal bleed; complication of extra hepatic portal hypertension: Endoscopic management and literature review

Bleeding from duodenal varices is reported to be a catastrophic and often fatal event. Most of the cases in the literature involve patients with underlying cirrhosis. However, approximately one quarter of duodenal variceal bleeds is caused by extrahepatic portal hypertension and they represent a unique population given their lack of liver dysfunction. The authors present a case where a 61-year-old male with history of remote crush injury presented with bright red blood per rectum and was found to have bleeding from massive duodenal varices. Injection sclerotherapy with ethanolamine was performed and the patient experienced a favorable outcome with near resolution of his varices on endoscopic follow-up. The authors conclude that sclerotherapy is a reasonable first line therapy and review the literature surrounding the treatment of duodenal varices secondary to extrahepatic portal hypertension.     

Usefulness of multi-detector row computed tomography for management of duodenal varices by emergency balloon-occluded retrograde transvenous obliteration

Ectopic varices outside the gastroesophageal region are less common in patients with portal hypertension and liver cirrhosis. Among ectopic varices, bleeding from duodenal varices is often massive and fatal. Several reports have recently described various treatment options for duodenal varices including interventional radiology. It is necessary to thoroughly investigate variceal hemodynamics before conducting interventional radiology. We report a case of bleeding duodenal varices treated successfully with balloon-occluded retrograde transvenous obliteration (B-RTO) after investigating the hemodynamics of the duodenal varices with multi-detector row computed tomography (MDCT). MDCT easily identified the duodenal varices together with the afferent and efferent vessels. Our case suggests the usefulness of MDCT before B-RTO for investigating the hemodynamics and vascular anatomy of the duodenal varices and selection of the most appropriate therapy.     

Portal vein thrombosis following sclerotherapy.

We present the case of a woman with idiopathic portal hypertension who underwent sclerotherapy for bleeding esophageal varices. She had a rebleed 27 months after complete eradication of esophageal varices. Endoscopy showed bleeding gastric varices. Ultrasonography, and later splenoportography, revealed a large thrombus in the right branch of the portal vein causing gross dilation of the portal and splenic vein. A proximal splenorenal shunt was done to decompress the portal system and hence gastric varices. Repeat endoscopy 4 weeks after surgery revealed complete disappearance of the gastric varices, while ultrasonography at 38 weeks showed marked decompression of the portal system with complete disappearance of the thrombus from the right branch of the portal vein. No new thrombus formation was seen.     

Hemorrhagic shock due to rupture of duodenal varices]

A 61-year-old woman was admitted to our hospital for melena and convulsion in shock state. Laboratory data on admission indicated severe anemia and marked liver dysfunction. She improved clinically, after received a large blood transfusion. Angiographic study was performed, and portography revealed duodenal varices supplied via superior mesenteric artery and drained to the left ovarian vein. An endoscopic examination was performed, and large nodular varices were observed in the third portion of the duodenum. The varices were treated by percutaneous transhepatic obliteration of portal systemic collaterals (PTO), and endoscopic injection sclerotherapy (EIS) with n-butyl-2-cyanoacrylate (Histoacryl). After complection of EIS, no further bleeding occurred, and the patient's hemoglobin level was stabilized. No recurrence of the duodenal varices has been detected during the follow-up period of five months after EIS with N-butyl-2-cyanoacrylate.     

Successful Endoscopic Injection Sclerotherapy of a Bleeding Duodenal Varix

Bleeding from duodenal varices is an unusual event. We report the case of a 50-yr-old man with portal hypertension due to alcoholic cirrhosis who presented with upper gastrointestinal bleeding and encephalopathy. Emergent endoscopy revealed an actively bleeding duodenal varix. The bleeding was treated successfully with injection sclerotherapy. Only four cases of injection sclerotherapy of bleeding duodenal varices have been reported previously. We review and compare reported cases of sclerotherapy of duodenal varices and also review the other therapeutic options. Endoscopic injection sclerotherapy of bleeding duodenal varices appears to be a useful first-line therapy.     

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.     

Choledochal varices bleeding: A case report

Choledochal varices are a rare cause of hemobilia associated with chronic portal vein thrombosis. We present a case of chronic portal vein thrombosis complicated with bleeding from choledochal varices. The presentation, clinical manifestations and management are described.     

原发性胆汁性肝硬化患者食管静脉曲张程度与肝功能评价的相关性研究

目的 探讨原发性胆汁性肝硬化食管静脉曲张程度与门脾静脉内径、肝功能Child-Pugh分级,Meld评分间的关系.方法 对2008年9月至2011年5月间选择92例原发性胆汁性肝硬化患者行增强CT,测量门静脉主干及脾门部脾静脉直径,行胃镜了解食管静脉曲张的程度,并对其中44例出现过静脉曲张破裂出血患者采用Child-Pugh分级,Meld评分标准进行肝功能分级.结果 食管静脉曲张程度与门静脉内径（P =0.018）、脾静脉内径（P=O.O02）呈正相关,而Child-Pugh分级（P＞0.05）,Meld评分（P＞0.05）则与食管静脉曲张程度无相关性.结论 根据门、脾静脉内径可预测原发性胆汁性肝硬化的食管静脉曲张程度;而Child-Pugh分级,Meld评分对患者的食管静脉曲张程度及出血风险不能进行有效评估.     

Relationship between encephalopathy and portal vein-vena cava shunt： Value of computed tomography during arterial portography

AIM: TO assess the value of computed tomography during arterial portography (CTAP) in portal vein-vena cava shunt,and analysis of the episode risk in encephalopathy.METHODS: Twenty-nine patients with portal-systemic encephalopathy due to portal hypertension were classified by West Haven method into grade Ⅰ(29 cases), gradeⅡ(16 cases), grade Ⅲ(10 cases), grade Ⅳ( 4 cases). All the patients were scanned by spiraI-CT. Plane scans, artery phase and portal vein phase enhancement scans were performed, and the source images were thinly reconstructed to 1.25 mm. We reconstructed the celiac trunk, portal vein,inferior vena cava and their branches and subjected them to three-dimensional vessel analysis by volume rendering(VR) technique and multiplanar volume reconstruction (MPVR) technique. The blood vessel reconstruction technique was used to evaluate the scope and extent of portal vein-vena cava shunt, portal vein emboli and the fistula of hepatic artery- portal vein. The relationship between the episode risk of portal-systemic encephalopathy and the scope and extent of portal vein-vena cava shunt,portal vein emboli and fistula of hepatic artery- portal vein was studied.RESULTS: The three-dimensional vessel reconstruction technique of spiraI-CT could display celiac trunk, portal vein,inferior vena cava and their branches at any planes and angles and the scope and extent of portal vein-vena cavashunt, portal vein emboli and the fistula of hepatic artery- portal vein. In twenty-nine patients with portal-systemicencephalopathy, grade Ⅰ accounted for 89.7% esophageal varices, 86.2% paragastric varices; grade Ⅱ accounted for 68.75% cirsomphalos, 56.25% paraesophageal varices,62.5% retroperitoneal varices and 81.25% dilated azygos vein; grade Ⅲ accounted for 80% cirsomphalos, 60%paraesophageal varices, 70% retroperitoneal varices, 90% dilated azygos vein, and part of the patients in grades Ⅱand Ⅲ had portal vein emboli and fistula of hepatic arteryportal vein; grade Ⅳ accounted for 75% dilated left renal vein, 50% paragallbladder varices, all the patients had fistula of hepatic artery- portal vein.CONCLUSION: The three-dimensional vessel reconstruction technique of spiraI-CT can clearly display celiac trunk, portal vein, inferior vena cava and their branches at any planes and angles and the scope and extent of portal vein-vena cava shunt. The technique is valuable for evaluating the episode risk in portal-systemic encephalopathy.     

肝硬化食管静脉曲张出血内镜治疗后早期再出血的危险因素分析

目的探讨内镜治疗肝硬化食管静脉曲张破裂出血(EVB)后早期再出血的危险因素。 方法回顾分析2016年8月至2018年8月因肝硬化食管静脉曲张(EV)首次出血就诊于包头医学院二附院并采用内镜下治疗的患者资料,依据术后6周内是否再出血分再出血组和未出血组,对两组患者的一般资料、肝功能、血常规、凝血、门静脉血栓、门静脉异常分流等情况进行单因素分析,探讨内镜治疗EV术后早期再出血的危险因素。 结果(1)入组患者共450例,治疗后6周内出血27例,止血成功率94%;(2)单因素分析AST、GGT、TBIL、ALB、PTA、TG、肝功能、Child-Pugh分级、EV程度、门静脉血栓、门静脉异常分流在出血和未出血组之间的差异具有统计学意义;(3)多因素Logistic回归分析结果显示AST等是影响EV术后再出血的危险因素;ALB、门静脉异常分流是影响EV术后再出血的保护因素(P<0.05)。 结论AST、GGT、PTA、TG、肝功能Child-Pugh分级、EV程度、门静脉血栓是影响EV术再出血的危险因素;ALB、门静脉异常分流是影响EV术后早期再出血的保护因素。     

Laparoscopic splenectomy for variceal bleeding with non-cirrhotic portal vein thrombosis: a case report

A 57-year-old man was referred to our hospital for treatment of refractory gastric bleeding from gastric varices secondary to portal vein thrombosis. The patient's liver function tests and coagulation profile were normal. The venous phase of the superior mesenteric arteriogram, on the other hand, showed superior mesenteric vein-portal vein occlusion with surrounding hepatopetal variceal collaterals. The venous phase of the splenic arteriogram additionally showed splenic vein occlusion and collateral vessels from the gastric and retroperitoneal regions flowing into a portal cavernous transformation. Gastroscopy confirmed that the patient had gastric varices in the cardia. We performed laparoscopic splenectomy to treat refractory gastric bleeding from varices and symptomatic hypersplenism. The postoperative course was uneventful; the patient's gastric varices were less prominent on follow-up gastroscopy and the hematologic profile returned to normal. Extrahepatic portal vein thrombosis is the leading cause of variceal hemorrhage in patients with healthy livers. There is a consensus in the literature that splenectomy alone is of minimal value in preventing variceal bleeding in portal vein thrombosis. Splenectomy is, however, indicated in cases in which the patient has hepatopetal collaterals from the mesenteric vein system and whose hemorrhagic gastric varices are related to splenic vein thrombosis as in our case.     

Fatal spontaneous gallbladder variceal bleeding in a patient with alcoholic cirrhosis

Gallbladder varices are unusual ectopic varices that may develop in patients with portal hypertension, particularly in those with portal vein occlusion. In rare instances, these varices may cause hemobilia, life-threatening bleeding, or even rupture of the gallbladder. We report the first case of a 41-year-old man with alcoholic cirrhosis and patent portal vein who developed massive hemoperitoneum from spontaneous rupture of varices in the gallbladder fossa. The diagnosis of gallbladder varices eluded conventional imaging and was made only at autopsy. Gallbladder variceal hemorrhage is a rare, but potentially catastrophic complication of cirrhosis.     

Duodenal varices

Bleeding from duodenal varices in portal hypertension may not be recognized, resulting in a delay in diagnosis. Early detection is important as duodenal varices are a potential source of massive hemorrhage. We report two cases with recurrent upper gastrointestinal hemorrhage in whom accurate diagnosis was made only after extensive investigation including repeated endoscopic examination.     

Hepatic vascular disease and portal hypertension in polycythemia vera and agnogenic myeloid metaplasia: a clinicopathological study of 145 patients examined at autopsy

The pathogenesis of portal hypertension arising in patients with myeloproliferative disorders has been difficult to understand because liver biopsy findings often show minimal changes. It has been suggested that increased splenic blood flow, hepatic infiltration with hematopoietic cells or sinusoidal fibrosis may be important. We have reviewed the autopsy findings and clinical histories of 97 patients with polycythemia vera and 48 patients with agnogenic myeloid metaplasia collected from three institutions and from the Polycythemia Vera Study Group. Cirrhosis was present in seven patients, one of whom had bleeding varices. Esophageal varices were present clinically in 10 patients without cirrhosis (seven polycythemia and three agnogenic myeloid metaplasia). All of these patients had lesions in small or medium-sized portal veins and four had stenosis of the extrahepatic portal vein with histology compatible with organized thrombi. Nodular regenerative hyperplasia occurred in 14.6% and correlated closely with the presence of portal vein lesions. Thirty patients had greater than 500 ml of ascites, seven of these patients also had varices and six of them had hepatic vein thrombosis. Ascites also correlated with hepatic vein disease confined to small intrahepatic branches. No correlation was seen between hepatic hematopoietic infiltration and signs of portal hypertension. We conclude that esophageal varices are common and are almost always associated with portal vein lesions visible by light microscopy. These portal vein lesions, and the secondary effects of nodular regenerative hyperplasia and portal hypertension, are most likely a result of portal vein thrombosis in patients with myeloproliferative disorders.     

肝硬化患者肝功能失代偿状况与门脉管径的关系

目的:探讨肝硬化患者肝功能失代偿状况、食管静脉曲张程度与门脉主干内径及脾静脉内径的关系。方法:对100例肝硬化失代偿期患者进行肝功能Child-pugh分级,内镜检查判断食管静脉曲张程度,彩色多谱勒B超检测门静脉主干内径及脾静脉内径。结果:肝功能分级越差,门静脉与脾静脉的内径越大(P<0.05),且随着门静脉及脾静脉内径增大,食管静脉曲张程度亦加重(P<0.05)。结论:门静脉及脾静脉内径能间接体现门静脉高压的程度,继而反映肝功能失代偿状况。