Obstruction Of Inferior Vena Cava Research Articles

Prevalence and risk factors of hepatocellular carcinoma in Budd–Chiari syndrome

Budd-Chiari syndrome (BCS) can be incidentally complicated by hepatocellular carcinoma (HCC), thereby decreasing the survival of these patients. Our study aims to systematically review the prevalence and risk factors of HCC in BCS patients. A PubMed search was performed to identify all original articles that reported the prevalence and risk factors of HCC in BCS patients. Primary items were the prevalence and risk factors of HCC in BCS patients. Of 1487 articles identified, 16 were included in our study. The prevalence of HCC in BCS is 2.0-46.2% in 12 Asian studies, 40.0-51.6% in two African studies, 11.3% in one European study, and 11.1% in one American study. Irrespective of hepatitis as the underlying risk factor of HCC, the pooled prevalence of HCC was 17.6% in BCS patients [95% confidence interval (CI): 10.1-26.7%], 26.5% in inferior vena cava obstruction (95% CI: 14.4-40.7%), and 4.2% in hepatic vein obstruction (95% CI: 1.6-7.8%). As patients with HCC and concomitant hepatitis were excluded, the pooled prevalence of HCC was 15.4% in BCS patients (95% CI: 6.8-26.7%). Heterogeneity among studies was statistically significant in these meta-analyses. The risk factors of HCC in BCS included hepatic venous pressure gradient and female sex in two Asian studies, and male sex, factor V Leiden mutation, and inferior vena cava obstruction in one European study. HCC was frequent in BCS. However, there was a huge variation among studies. Routine surveillance for HCC is warranted in BCS patients. The risk factors of HCC in BCS may vary depending on the geographic origin of the studies.

Hepatobiliary and Pancreatic: Budd‐Chiari syndrome with infra‐hepatic obstruction of inferior vena cava

Journal of Gastroenterology and HepatologyVolume 28, Issue 6 p. 905-905 Education and Imaging Hepatobiliary and Pancreatic: Budd-Chiari syndrome with infra-hepatic obstruction of inferior vena cava Xingshun Qi, Xingshun Qi Department of Digestive Interventional Radiology, Xijing Hospital of Digestive Diseases, ChinaSearch for more papers by this authorGuohong Han, Guohong Han Department of Digestive Interventional Radiology, Xijing Hospital of Digestive Diseases, ChinaSearch for more papers by this authorWengang Guo, Wengang Guo Department of Digestive Interventional Radiology, Xijing Hospital of Digestive Diseases, ChinaSearch for more papers by this authorZhanxin Yin, Zhanxin Yin Department of Digestive Interventional Radiology, Xijing Hospital of Digestive Diseases, ChinaSearch for more papers by this authorDaiming Fan, Daiming Fan State Key Laboratory of Cancer Biology and Xijing Hospital of Digestive Diseases, Fourth Military Medical University, Xi'an, ChinaSearch for more papers by this author Xingshun Qi, Xingshun Qi Department of Digestive Interventional Radiology, Xijing Hospital of Digestive Diseases, ChinaSearch for more papers by this authorGuohong Han, Guohong Han Department of Digestive Interventional Radiology, Xijing Hospital of Digestive Diseases, ChinaSearch for more papers by this authorWengang Guo, Wengang Guo Department of Digestive Interventional Radiology, Xijing Hospital of Digestive Diseases, ChinaSearch for more papers by this authorZhanxin Yin, Zhanxin Yin Department of Digestive Interventional Radiology, Xijing Hospital of Digestive Diseases, ChinaSearch for more papers by this authorDaiming Fan, Daiming Fan State Key Laboratory of Cancer Biology and Xijing Hospital of Digestive Diseases, Fourth Military Medical University, Xi'an, ChinaSearch for more papers by this author First published: 22 May 2013 https://doi.org/10.1111/jgh.12228Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. Volume28, Issue6June 2013Pages 905-905 RelatedInformation

Clinical features and etiology of Budd–Chiari syndrome in Chinese patients: A single‐center study

The clinical features and etiology of Budd-Chiari syndrome (BCS) vary from region to region, and there is lack of large sample studies about BCS in China. The aim of the present study was to study the clinical features and etiology of patients with incident BCS in China prospectively. A consecutive case series of patients with incident BCS who were diagnosed in the Affiliated Hospital of Xuzhou Medical College (Jiangsu, China) were enrolled from September 2010 to December 2011. All of the patients had continuous follow-ups to record the symptoms, body features, laboratory and radiology findings, and treatment methods through May 2012. A total of 145 incident cases of BCS were identified. BCS was caused by hepatic venous obstruction in 31% of the patients, inferior vena cava obstruction in 6% of the patients, and 63% suffered from a combination of the two conditions. At least one etiological factor was present in 82% of the patients, with the most common being membranous obstruction (61%). Only 5% of the patients had myeloproliferative neoplasms with a JAK2 V617F mutation, and none of the patients had a factor V Leiden mutation. Eighteen months after a percutaneous transluminal angioplasty was performed, the survival rate and the asymptomatic survival rate were 99% (95% confidence interval, 95-100%) and 93% (95% confidence interval, 89-98%), respectively. The most prevalent etiological factor for BCS in China is membranous obstruction. Moreover, most Chinese patients with chronic BCS are treated with percutaneous transluminal angioplasty and have an excellent clinical outcome.

Long-term Outcomes of Percutaneous Venoplasty and Gianturco Stent Placement to Treat Obstruction of the Inferior Vena Cava Complicating Liver Transplantation

Evaluation of long-term outcomes of venoplasty and Gianturco stents to treat inferior vena cava (IVC) obstruction after liver transplantation. We retrospectively analyzed records from 33 consecutive adult patients referred with the intent to treat suspected IVC obstruction after liver transplantation. Treatment was performed for occlusion or stenosis with a gradient exceeding 3 mmHg. The primary treatment was venoplasty and, if refractory, Gianturco stent placement. Recurrence prompted repeat venoplasty or stent placement. Of the 33 patients, 25 (aged 46.9 ± 12.2 years) required treatment at a mean of 2.3 years (14 days to 20.3 years) after transplantation. For technically successful cases, primary treatment was venoplasty alone (14) or with stent placement (10). Technical success was 96 % (24 of 25) reflecting failure to cross one occlusion. Clinical success was 88 % (22 of 25) reflecting the technical failure and two that died of unrelated complications within 5 weeks. Cumulative primary patencies were 57.1 % at 6 months (n = 21) and 51.4 % at 1 (n = 10), 3 (n = 7), 5 (n = 6), and 7 (n = 5) years. Cumulative primary assisted patency was 95.2 % at 6 months (n = 21) and at 1 (n = 15), 3 (n = 9), 5 (n = 8), and 7 (n = 8) years. The 17 patients stented for refractory (n = 10) or recurrent (n = 7) stenosis had cumulative primary and primary assisted patencies of 86.0 and 100 %, respectively, from 6 months (n = 14) to 7 years (n = 3). No major complications occurred; one fractured stent was observed after 11.6 years. For IVC obstruction following liver transplantation, excellent long-term outcomes can be achieved by venoplasty and Gianturco stent placement.

English

Budd-Chiari syndrome is the clinical picture caused by occlusion of the hepatic veins. It presents with the abdominal pain, ascites and hepatomegaly. The syndrome can be fulminant, acute, chronic, or asymptomatic. One such middle aged female patient came to the clinic with history of chronic jaundice, ascites, and hyper pigmentation of both legs. After complete physical examination and investigations, the reports revealed membranous web causing obstruction of inferior vena cava resulting in venous stasis of the Lower limbs and in turn the hepatic veins has resulted in esophageal varices with early liver cell necrosis and

Outcomes of Thrombolysis With and Without Predilation of the Inferior Vena Cava (IVC) in Patients With Budd–Chiari Syndrome With Old IVC Thrombosis

To compare the efficacy of thrombolysis with and without predilation of the inferior vena cava (IVC) for Budd-Chiari syndrome (BCS) with old IVC thrombosis. We divided 40 patients with BCS with old IVC thrombosis into 2 groups, group A (n = 21), thrombolysis after dilation of the obstructed IVC and group B (n = 19), thrombolysis without predilation of the obstructed IVC. Thrombolysis was performed via urokinase administration through the dorsal vein of the foot. Color Doppler ultrasonography at 30 days showed complete resolution of the thrombus in 21 (100%) group A patients and 6 group B patients (31.6%; P < .001). Thrombolysis was achieved using a lower dose of urokinase and within a shorter time frame in group A than in group B (P < .001). Thrombolysis after dilation was superior to thrombolysis alone and was safe and efficacious in patients with BCS with old IVC thrombosis.

A caval homograft for Budd-Chiari syndrome due to inferior vena cava obstruction

Transjugular intrahepatic portosystemic shunt (TIPS) is the standard treatment of Budd-Chiari syndrome (BCS) non responsive to medical therapy. However, patients with inferior vena cava (IVC) obstruction proximal to the atrium do not benefit from TIPS and a surgical approach is mandatory. We report the case of BCS due to intrapericardial IVC obstruction. We describe a novel surgical approach using a fresh caval homograft. An attempt to balloon dilatation of the IVC obstruction was complicated by right atrial disruption with tamponade and ventricular fibrillation. Lately, the patient successfully underwent a reconstruction of the cavo-atrial continuity by the interposition of a fresh caval homograft, a novel surgical approach never described before for BCS. Further follow-up revealed progressive reduction and resolution of ascites, and overall clinical improvement. IVC obstruction near to the atrium can be surgically approached with a new technique consisting in inferior vena cava resection and replacement with a caval homograft.

An Idiopathic Membranous IVC Obstruction: Presenting as a Variant of the BCS

An Inferior Venacaval (IVC) lumen obstruction, whether it is partial or complete, is not a common phenomenon and it may be caused by the thrombosis or compression which may result from neoplastic or non neoplastic masses. There are cases which are idiopathic and which are typically referred to as membranous obstructions of the IVC. Here, we are presenting a 40 years old male with multiple tortuous veins over the abdomen, with non healing ulcers in the leg for 12 years, without ascites, who underwent a successful percutaneous transluminal balloon dilatation of the IVC membrane which was located above the hepatic veins, which resulted in a successful palliation of his symptoms.

Interrupted Inferior Vena Cava Combined with Partial Anomalous Pulmonary Venous Return Drainage to the IVC in a 67‐Year‐Old Adult

A 67-year-old woman presented with lower body edema and was found to have a suprarenal inferior vena cava (IVC) obstruction without hepatic vein obstruction and partial anomalous pulmonary venous return (PAPVR) draining the right pulmonary veins to the IVC below the obstructed IVC on CT angiography. The patient underwent retrohepatic cavoatrial bypass with a polytetrafluoroethylene (PTFE) 16-mm ringed graft via a posterolateral thoracotomy and retroperitoneal approach.

Percutaneous Removal of a Bard Simon Nitinol Permanent Inferior Vena Cava Filter

Inferior vena cava (IVC) filters are used to treat thromboembolic disease when there is a contraindication to anticoagulation or failure of therapeutic anticoagulation therapy. Although there are retrievable IVC filters available, permanent IVC filters remain the most commonly placed IVC filters worldwide. Permanent IVC filters have been associated with long-term complications such as IVC thrombosis and obstruction, migration, and erosion into surrounding structures. Such complications may require removal of permanent IVC filters, which has been previously described with open surgery involving venotomy of the IVC. We report a case of a Bard Simon Nitinol permanent IVC filter that was removed by using percutaneous endovascular techniques.

Living donor liver transplantation for Budd–Chiari syndrome with hepatic inferior vena cava obstruction after open pericardial procedures

Living donor liver transplantation (LDLT) for Budd-Chiari syndrome (BCS) presents a unique challenge as it does not involve replacement of the hepatic inferior vena cava (IVC). We report a case of successful LDLT in a patient with BCS associated with occlusion of the hepatic veins as well as the IVC. A 34-year-old woman with a history of two open pericardial procedures had decompensated liver failure and portal hypertension. Venography showed complete obstruction of the hepatic IVC and well-developed collateral vessels. We performed LDLT via sternotomy and laparotomy, with an end-to-end anastomosis between the left hepatic vein of the donor and the patient's suprahepatic vena cava in the pericardium. The patient recovered uneventfully and has been doing well for 5years. LDLT without caval replacement for BCS in a patient with hepatic IVC obstruction is feasible if the patient has good functional collaterals before liver transplantation.

Multiple Choice Questions

1.Regarding drug induced liver injury (DILI) the following are TRUE EXCEPT:1.Most common cause of drug induced acute liver failure in India is paracetamol.2.Most common cause of drug induced liver injury in India is antitubercular drugs.3.Degree of liver enzyme elevation correlates with severity of liver disease.4.Clinical jaundice is a predictor of mortality.5.Cholestatic pattern of DILI can be prolonged even on stopping the offending drug.2.Regarding surgery in patients with liver disease the following are TRUE:1.Child-Turcotte-Pugh (CTP) and model for end-stage liver disease (MELD) scores can reliably predict operative mortality in chronic liver disease.2.Acute viral hepatitis is not a contraindication for surgery.3.Laparoscopic cholecystectomy can be safely performed in compensated cirrhotics.4.Umbilical hernias have low risk of complications in cirrhotics and elective repair should not be attempted.5.Preferred anaesthetic agents include sevoflurane, desflurane and isoflurane.3.Regarding peri-operative monitoring after liver transplantation the following are TRUE:1.Cardiovascular events are the most common cause of readmission to intensive care and non-graft related deaths after liver transplantation.2.Conventional tests of coagulation like prothrombin time, activated partial thromboplastin time, platelet count and plasma fibrinogen levels are sufficient measure of coagulation intra-operatively.3.Hyperglycemia is an ominous sign of poor graft function.4.Serum potassium levels are independent predictors of death after liver transplantation.5.Commonest acid-base disorder in the immediate post-operative period is metabolic acidosis.4.Regarding tuberculosis (TB) in chronic liver disease the following are TRUE EXCEPT:1.Cirrhotic patients have a higher chance of developing extra-pulmonary tuberculosis than those without cirrhosis.2.Adenosine deaminase for diagnosis of TB in cirrhosis with ascites has high sensitivity.3.Tuberculin skin testing is sensitive for the diagnosis of TB in cirrhotic patients.4.Likelihood of anti-tubercular drug induced hepatotoxicity is higher in pre-existing liver disease patients.5.Isoniazid induced hepatotoxicity is more common in slow acetylators.5.Regarding hepatotoxicity of anti-tubercular therapy (ATT) the following are TRUE:1.Rechallenge with isoniazid is contraindicated if patient has history of isoniazid induced hepatotoxicity.2.Isoniazid induced transaminitis is self limited and asymptomatic in majority of patients.3.Isolated conjugated hyperbilirubinemia is seen with rifampicin.4.Pyrazinamide mainly causes idiosyncratic hepatotoxicity.5.Inactive carriers of hepatitis B do not have increased risk of ATT induced hepatotoxicity.6.Regarding Budd-Chiari syndrome (BCS) the following are TRUE EXCEPT:1.Most common cause of BCS in India is membranous obstruction of inferior vena cava.2.Ascites with high protein and high serum ascitic albumin gradient is suggestive of BCS.3.Initial imaging modality of choice to diagnose BCS is magnetic resonance venogram.4.Failure to visualize the hepatic veins on Doppler is diagnostic of BCS.5.Direct intrahepatic portosystemic shunt can be done even if all hepatic vein ostia are blocked.7.Regarding the role of gut microbiota in hepatic encephalopathy (HE) the following are TRUE:1.Markers of systemic inflammation are better correlated with HE than the severity of liver disease.2.Pathogen associated molecular patterns (PAMPs) are microbial components that initiate inflammatory cascade.3.Gut microbiota of patients with cirrhosis and normal controls is similar.4.Lactulose exerts its actions in HE predominantly by altering the composition of gut microbiota.5.Stool microbiota is an accurate estimate of intestinal microbiota.8.Regarding primary sclerosing cholangitis (PSC) the following are TRUE:1.Majority of patients with PSC have isolated extrahepatic disease.2.Magnetic resonance cholangiography is the diagnostic modality of choice.3.Dominant stricture is a stenosis with a diameter of <1.5 mm in the hepatic duct or of <1 mm in the common bile duct.4.Inflammatory bowel disease is usually diagnosed after diagnosis of PSC.5.Cholecystectomy is recommended in a patient with PSC with a gallbladder mass lesion, irrespective of its size.9.Regarding primary biliary cirrhosis (PBC) the following are TRUE EXCEPT:1.Antimitochondrial antibodies (AMA) are highly sensitive and specific for the diagnosis of PBC.2.AMA negative cases of PBC have less aggressive disease and better prognosis.3.Ursodeoxycholic acid improves symptoms but does not alter natural course of PBC.4.Modafinil may improve fatigue in patients with PBC.5.Sjogren's syndrome occurs more frequently in PBC than matched controls.10.Regarding overlap syndromes the following are TRUE:1.Overlap of autoimmune hepatitis (AIH) and PBC is the most common variant.2.Overlap of PSC and PBC is common.3.Autoimmune sclerosing cholangitis refers to features of PSC in children with AIH.4.The components of the overlap syndrome may develop sequentially with one appearing years after the first.5.UDCA does not have a beneficial role in overlap syndromes.

Secondary Budd–Chiari syndrome complicating calcified right atrial thrombosis related to ventriculoatrial shunt

A 33-year-old female patient underwent diagnostic gynecologic laparoscopy for assessment of a cystic ovarian mass and moderate amounts of ascites. Operative exploration, unexpectedly, uncovered a coarsely multinodular liver surface suspicious of cirrhosis, and surgery was terminated by resection of the left adnexa. Histopathology of the surgical specimen and ascitic fluid analysis yielded no indication of underlying malignancy, and the patient was referred for hepatology work-up. Liver function tests were unremarkable; however, ultrasound revealed an inhomogeneous, nodular liver parenchyma with portal vein dilation and reduced portal venous flow suggestive of portal hypertension. Furthermore, the hepatic veins appeared compressed and duplex sonography failed to trace an unequivocal hepatic venous Doppler flow signal. Upper gastrointestinal endoscopy identified small esophageal varices. Comprehensive serological work-up was negative with respect to viral, metabolic, hereditary, or autoimmune liver disease. Given the insufficient visualization of hepatic veins on ultrasound, the patient underwent magnetic resonance imaging (MRI) indicating inhomogeneous hepatomegaly with regenerative nodules. Furthermore, hepatic vein and, in part, inferior vena cava (IVC) obstruction by a calcified mass extending up towards the right heart was detected. To better characterize the cardiac mass, transthoracic and transesophageal echocardiogram as well as cardiac MRI were performed. Echocardiography depicted a tumor-like right atrial (RA) structure spreading alongside the tricuspid valve (Fig. 1a, Supplemental Videos 1–2). Continuous-wave Doppler across the structure and along the right ventricular inflow tract demonstrated a pressure gradient of 8 mmHg, comparable to a relevant tricuspid stenosis. Likewise, cardiac MRI and CT reinforced the suspicion of a large calcified thrombus arising from the basal RA with appositional growth into the IVC and the hepatic veins (Fig. 1b–d, Supplemental Video 3). No signs of pulmonary embolism were found. Given the clinical diagnosis of subacute Budd–Chiari syndrome (BCS), a comprehensive laboratory assessment for potential prothrombotic conditions including JAK2 V617F testing remained without pathological finding [1]. However, a thorough review of medical history revealed that the Electronic supplementary material The online version of this article (doi:10.1007/s00392-012-0510-9) contains supplementary material, which is available to authorized users.

Thrombectomy and cavocavostomy for inferior vena cava thrombosis and torsion after piggyback liver transplantation

Inferior vena cava (IVC) complications after orthotopic liver transplantation continue to be rare but serious concerns.1,2 Although numerous surgical and percutaneous techniques have been suggested for the management of different IVC complications, there is no consensus about a standard method of treatment. Here we describe a unique case in which a liver allograft caused kinking of the recipient's IVC and subsequent thrombosis after piggyback liver transplantation. Our case involves a 48-year-old male with end-stage liver disease secondary to hepatitis C. He underwent piggyback liver transplantation in which the suprahepatic allograft IVC was anastomosed with 3 recipient hepatic veins. On postoperative day 3, the patient developed significant hemodynamic instability and was re-explored through the same bilateral subcostal incision. An intraoperative Doppler examination revealed patent hepatic veins with pulsatile flow but also a nearly occlusive thrombus in the recipient's IVC extending from the suprarenal IVC to the retrohepatic IVC inferior to the piggyback anastomosis. The absence of an outflow obstruction was confirmed by the lack of a pressure gradient across the piggyback anastomosis, which was demonstrated by the direct measurement of the pressures of the recipient's suprahepatic IVC and the donor's IVC. Graft rotation and IVC kinking inferior to the piggyback anastomosis were also observed to be causing IVC stenosis. The decision was made to perform a thrombectomy through a venotomy on the suprarenal IVC with Fogarty balloons. Once an adequate caval flow was obtained, vascular clamps were applied inferior to the piggyback anastomosis and slightly superior to the renal veins. The lower aspect of the donor's IVC was untied and anastomosed to the opening on the recipient's IVC (the site of the thrombectomy) in an end-to-side fashion (Fig. 1). By anchoring the donor's IVC in 2 separate locations, we were able to relieve the kinking of the IVC. End-to-side cavocavostomy. Reprinted with permission from Transplantation Proceedings.3 Copyright 2001, Elsevier Science, Inc. Three days after the re-exploration, a Doppler ultrasound examination revealed normal directional flow and patency of the hepatic vasculature. A retrievable Gunther Tulip IVC filter was inserted to prevent any further risk of a pulmonary embolism. The patient's remaining postoperative course was unremarkable. The laboratory values on April 2011 were as follows: total bilirubin, 1.4 mg/dL; aspartate aminotransferase, 41 U/L; alanine aminotransferase, 32 U/L; and creatinine, 1.5 mg/dL. Recent abdominal magnetic resonance imaging demonstrated the patency of the cavocavostomy (Fig. 2). Magnetic resonance imaging (May 2011) demonstrating the patency of the cavocavostomy (black arrows). It is well known that graft rotation is an infrequent but serious complication after orthotopic liver transplantation because of its potential association with IVC obstructions. Our patient developed graft rotation and subsequent IVC kinking because of a size discrepancy between the graft and the recipient's right upper quadrant cavity. In addition, we believe that the construction of a significant portion of the piggyback anastomosis in the anterior wall of the IVC (where a substantial separation existed between the right hepatic vein and the confluence of the middle and left hepatic veins) may have further contributed to the graft rotation, which led to the IVC kinking and the subsequent caval flow obstruction and thrombosis. Although cavocaval anastomoses after piggyback liver transplantation have been reported, they have been used primarily to address IVC outflow obstructions.3, 4 We addressed graft rotation and kinking of the recipient's IVC by anchoring the donor's IVC in 2 separate locations. By using both IVC thrombectomy and an additional cavocaval anastomosis, we were able to successfully provide stability to the graft and re-establish adequate blood flow through the piggyback anastomosis. Our patient was still alive and doing well more than 3 years after liver transplantation. The utilization of IVC thrombectomy and infrahepatic cavocavostomy provided excellent management of graft rotation, IVC kinking, and retrohepatic/infrahepatic IVC thrombosis. In our view, this should be considered another option for the treatment of patients with similar complications after orthotopic liver transplantation. Aaron M. Williams B.A.*, Jonathan C. Hundley M.D.*, Michael F. Daily M.D.*, Malay B. Shah M.D.*, James T. Lee M.D.*, Roberto Gedaly M.D.*, * Division of Transplantation Department of Surgery College of Medicine University of Kentucky Lexington, KY.

Replacement of the Vena Cava with Aortic Graft for Living Donor Liver Transplantation in Budd-Chiari Syndrome Associated with Hydatid Cyst Surgery: A Case Report

A 12-year-old girl, operated because of a hydatid cyst of the liver, with Budd-Chiari syndrome was evaluated for postoperative development of ascites and paraumbilical varicose veins. A vena caval stent was placed for the relief of inferior vena caval obstruction. The patient was admitted because of progressive deterioration in ascites and liver functions. Imaging techniques showed degeneration adjacent to the right hepatic vein in liver segments 7 to 8, a partially calcified 5-cm hydatid cyst, and a thrombosis in the inferior vena cava was that addressed with a 10-cm metal stent. A living donor segments 2 to 3 liver transplantation was obtained from the patient's mother. After completion of the donor operation without complications, the vena caval stent was removed following the recipient hepatectomy. Suprarenal flow continued after resection of the fibrotic vena cava and placement of a cadaveric cryopreserved aortic graft for the vena cava, anastomosed between the suprarenal and subdiaphragmatic segments of the vena cava. An end-to-side anastomosis was performed between the left hepatic vein of the donor liver and the aortic graft. There was no complication and the patient was discharged on postoperative day 19. Follow-up Doppler ultrasonography showed the aortic vena caval graft to be open, along with the hepatic/portal vein and hepatic artery. This case demonstrated that operations for liver hydatid cyst surgeries can iatrogenically induce Budd-Chiari syndrome; a cryopreserved aortic graft can be an alternative to ensure the continuity of the vena cava in living donor liver transplantation.

May Extraspinal Lumbar Compression Mimic Lumbar Pain and Sciatica? A Presentation of Unusual Cases

IntroductionCompression of sciatic nerve may often cause symptoms of lumbar radiculopathy. In 90% of patients with sciatica, spinal causes may be found. On the other hand, extraspinal compression of the sciatic nerve is very rare, found only in 10%. Most frequently, the lesion is in the pelvis due to tumors and bony compression. Clinical features are very similar to the usual causes of sciatica. Precise diagnosis is difficult to establish with standard diagnostic procedures due to absence of specific tests. We present cases of extraspinal sciatic nerve compression. Materials and MethodsAt our department, patients with concomitant intra- and extraspinal sciatic nerve compression were treated. All had typical sciatica that was unresponsive to conservative treatment in the beginning, as well as to standard surgical spinal decompression. ResultsExtraspinal origin was found as a cause for the pain: in one case, the tumor in presacral region behind the bladder with destruction of sacrum and compression of sacral plexus; in the second, femoral vein thrombosis, which resulted in massive pulmonary embolism; in the third, abscess of the Douglas pouch, involving the sacral plexus; in the fourth, abscess of psoas muscle and in the fifth, paravertebral muscle abscess. ConclusionClinically, extraspinal compressive pain may hardly be distinguished from intraspinal radicular pain. In contemporary double compressions particularly, the diagnosis is aggravated. The candidates are patients with no improvement after appropriate intraspinal surgery as a result of initial sciatic pain. Early diagnosis of extraspinal compression leads to effective treatment and additional extended diagnostic workup is therefore important.I confirm having declared any potential conflict of interest for all authors listed on this abstractYesDisclosure of InterestNone declaredKleiner JB, Donaldson WF, Curd JG, et al. Extraspinal causes of lumbosacral radiculopathy. Journal of Bone and Joint Surgery 1991;73:817–821Paksoy Y, Gormus N. Epidural venous plexus enlargements presenting with radiculopathy and back pain in patients with inferior vena cava obstruction or occlusion. Spine 2004;29:2419–2424Servant CT. An unusual cause of sciatica: a case report. Spine 1998;23:2134–2136Doniec J, Gaździk T, Folta K, et al. Extraspinal sciatica. Chir Narzadow Ruchu Ortop Pol 1988; 53(5):359–361Arct W. Extraspinal symptomatic sciatica. Chir Narzadow Ruchu Ortop Pol 1980;45:71–75

May Extraspinal Lumbar Compression Mimic Lumbar Pain and Sciatica? A Presentation of Unusual Cases

Introduction Compression of sciatic nerve may often cause symptoms of lumbar radiculopathy. In 90% of patients with sciatica, spinal causes may be found. On the other hand, extraspinal compression of the sciatic nerve is very rare, found only in 10%. Most frequently, the lesion is in the pelvis due to tumors and bony compression. Clinical features are very similar to the usual causes of sciatica. Precise diagnosis is difficult to establish with standard diagnostic procedures due to absence of specific tests. We present cases of extraspinal sciatic nerve compression. Materials and Methods At our department, patients with concomitant intra- and extraspinal sciatic nerve compression were treated. All had typical sciatica that was unresponsive to conservative treatment in the beginning, as well as to standard surgical spinal decompression. Results Extraspinal origin was found as a cause for the pain: in one case, the tumor in presacral region behind the bladder with destruction of sacrum and compression of sacral plexus; in the second, femoral vein thrombosis, which resulted in massive pulmonary embolism; in the third, abscess of the Douglas pouch, involving the sacral plexus; in the fourth, abscess of psoas muscle and in the fifth, paravertebral muscle abscess. Conclusion Clinically, extraspinal compressive pain may hardly be distinguished from intraspinal radicular pain. In contemporary double compressions particularly, the diagnosis is aggravated. The candidates are patients with no improvement after appropriate intraspinal surgery as a result of initial sciatic pain. Early diagnosis of extraspinal compression leads to effective treatment and additional extended diagnostic workup is therefore important. I confirm having declared any potential conflict of interest for all authors listed on this abstract Yes Disclosure of Interest None declared Kleiner JB, Donaldson WF, Curd JG, et al. Extraspinal causes of lumbosacral radiculopathy. Journal of Bone and Joint Surgery 1991;73:817–821 Paksoy Y, Gormus N. Epidural venous plexus enlargements presenting with radiculopathy and back pain in patients with inferior vena cava obstruction or occlusion. Spine 2004;29:2419–2424 Servant CT. An unusual cause of sciatica: a case report. Spine 1998;23:2134–2136 Doniec J, Gaździk T, Folta K, et al. Extraspinal sciatica. Chir Narzadow Ruchu Ortop Pol 1988; 53(5):359–361 Arct W. Extraspinal symptomatic sciatica. Chir Narzadow Ruchu Ortop Pol 1980;45:71–75

Bland thrombus association with tumour thrombus in renal cell carcinoma: analysis of surgical significance and role of inferior vena caval interruption

What's known on the subject? and What does the study add? The surgical implications of renal cell carcinoma with coexisting bland and tumour thrombi of the inferior vena cava is not well described. In this study we review our experience managing these tumours. On multivariate analysis, we found that the presence of bland thrombus was associated with an increased need for surgical interruption of the inferior vena cava. • To study the role of interruption of the inferior vena cava (IVC) in patients with renal cell carcinoma (RCC) and associated bland and tumour thrombi. • We reviewed 129 consecutive patients with the preoperative diagnosis of RCC with tumour thrombus who underwent radical nephrectomy and tumour thrombectomy in one academic institution between May 1997 and February 2011. • Percentages of patients with levels I, II, III and IV tumour thrombus were 29%, 13%, 48% and 9%, respectively. • The perioperative mortality rate was 2.3%. There were 29 (22%) perioperative complications recorded. • In all, 19 patients underwent surgical interruption of the IVC by ligation or segmental resection, including one level II, 14 level III and four level IV thrombi. • A total of 15 patients (12%) had bland thrombus associated with the tumour thrombus; four of these underwent intraoperative IVC filter placement and eight underwent surgical IVC interruption. • Advanced level of tumour thrombus was the only significant factor predicting association of bland thrombus (odds ratio [OR]= 2.09, 95% confidence interval [CI]: 1.082-4.037, P= 0.028). • On multivariate analysis, level of thrombus (OR = 3.1, 95% CI: 1.30-7.74, P= 0.011) and association of bland thrombus (OR = 9.07, 95% CI: 2.42-34.01, P= 0.001) were significant factors for IVC interruption. • Surgical interruption of the IVC is a feasible option in selected patients with chronic IVC obstruction. Association of bland thrombus with tumour thrombus should alert the surgical team to the potential for a challenging surgery. • Precise preoperative imaging to assess the degree of venous obstruction and to help with differentiation between bland and tumour thrombus is key to achieving a surgical outcome with minimal morbidity.

Analysis of surgical treatment results in 120 cases of Budd-Chiari syndrome

To evaluate the results of the surgical treatment of patients with Budd-Chiari syndrome (BCS). The clinic data of 120 BCS patients who underwent various consecutive surgical treatments from July 2001 to October 2010 was analyzed. There were 82 male and 38 female patients, aging from 11 to 72 years with a mean age of (41 ± 13) years. All patients experienced various examinations to identify the pathological type of BCS. There were 5 cases of small hepatic veins type, 28 cases of large hepatic veins (LHV) type, 31 cases of inferior vena cava (IVC) type and 56 cases of combined obstruction of LHV and IVC. Totally, 25 patients experienced interventional treatment, include percutaneous transluminal angioplasty and/or stenting for stenosis of hepatic vein and/or IVC, 77 patients experienced open-thorax operation for BCS radical resection under protection of right atrium by-pass with extracorporeal circulation. Totally 97 cases were followed up from 1 to 120 months after various surgical treatment methods. Perioperative mortality was 6.2% (6/97). Follow-up period mortality was 8.2% (8/97). The restenosis of IVC and/or hepatic vein happened in 3 cases out of 25 cases in intervention treatment group in contrast with 15 cases out of 77 cases in radical resection group. The 5-year patency and survival rate of IVC/hepatic vein were 64.5% and 83.3%. The surgical treatment of BCS need to get accurate diagnosis and pathological classification firstly, then, to choose appropriate therapeutic strategies based on individual pathological classification. The BCS radical resection can be an alternative method in some particular pathological classifications and the cases who failed in interventional treatment.

Application of obstruction of Glission pedicle combined with partial occlusion obstruction of inferior vena cava in regional liver resection

This study aims to investigate the clinical effect of Glission pedicle obstruction combined with partial obstruction of inferior vena cava in regional liver resection. A total of eight liver cancer patients were retrospectively analyzed. They underwent regional liver resection using a combined method of Glission pedicle obstruction and partial obstruction of inferior vena cava. Among these cases, three received right liver resection, two received left liver resection and others received right posterior lobe resection. Operation time and blood loss were measured. After operation, aspartate transaminase (AST), alkaline phosphate (ALP), albumin, ascites and enterocinesia recovery time were calculated, respectively. Preoperative evaluation of these cases showed that they shared the features of indocyanine green (ICG)-15 min retention rate of 40%. The operation time ranged from 60 to 90 min, and the average blood loss was 100 to 200 ml. There were no significant differences in AST and ALP before and after operation. The postoperative albumin decreased by about 10 g. Ascites occurred in all cases after operation, but after infusion of albumin,diuretics disappeared, and enterocinesia was restored two days later. Glission pedicle obstruction combined with partial obstruction of the inferior vena cava can notably shorten the operation time of regional liver resection and reduce the blood loss. Key words: Glission pedicle, partial obstruction of the inferior vena cava, regional liver resection.