Spontaneous Splenorenal Shunt Research Articles

Recurrent Portal Vein Thrombosis In Liver Transplantation With Renoportal Anastomosis Caused by Spontaneous Reno-Caval Shunts: A Case Report

Orthotopic liver transplantation (OLT) in patients with cirrhosis complicated by portal hypertension, portosystemic shunts, and chronic portal vein thrombosis (PVT) has long been challenging. Spontaneous spleno-renal shunts (SRS) allow new surgical techniques to restore portal vein patency and hepatopetal flow. Renoportal anastomosis (RPA) has emerged as an accepted method for transplanting these patients, with good long-term patient and graft survival. Orthotopic liver transplantation with RPA is known to be complicated by recurrent PVT, with few details discussed in the literature. We present a case of a 56-year-old woman with decompensated cirrhosis who underwent deceased donor whole graft OLT using RPA with iliac vein conduit. The postoperative course was complicated by occlusive thrombosis in the portal vein and iliac vein conduit. Venography revealed enlarged left gonadal and lumbar vein varices acting as reno-caval shunts with hepatofugal flow. Embolization of the varices re-established durable venous patency that was confirmed on post-transplant day 68 with no other hemodynamic complications. This showcases an interesting mechanism by which recurrent PVT may occur in patients undergoing OLT with RPA. Because durable portal vein patency can be achieved with Interventional Radiology embolization of reno-caval varices, assessing these communications is an important preoperative consideration for planned OLT with RPA.

Hemodynamic alterations with large spontaneous splenorenal shunt ligation during adult deceased donor liver transplantation.

A large spontaneous splenorenal shunt (SRS) will greatly impact portal inflow to the graft during liver transplantation (LT). Direct ligation of a large SRS is an uncommon surgical procedure and the hemodynamic consequences of this procedure are unknown. In this retrospective study, we described our technique for direct ligation of a large SRS and the consequent hemodynamic changes during LT. 3-Dimensional computed tomography and Doppler ultrasonography were used to evaluate SRS and portal vein blood flow volume (PFV). A total of 22 recipients had large SRS including 13 with PFV <85 ml/min/100 g (ligation group) and 9 with PFV ≥85 ml/min/100 g (no ligation group). The diameter of SRS was significantly larger in the ligation group than in the non-ligation group (22.92 ± 4.18 vs. 16.24 ± 3.60 mm; p = 0.0009). In all ligation patients, the SRS was easily identified and isolated, it was located just below the distal pancreas and beside the inferior mesenteric vein. PV flow increased significantly from 68.74 ± 8.77 to 116.80 ± 16.50 ml/min/100 g (p < 0.0001) after ligation; this was followed by a reduction in peak systolic velocity of the hepatic artery from 58.17 ± 14.87 to 46.67 ± 13.28 cm/s (p = 0.0013). Direct ligation of large SRS was an effective and safe surgical procedure to overcome the problem of portal hypoperfusion during LT.

Interventional Radiology Management of Adult Liver Transplant Complications.

Liver transplant remains the definitive therapy for patients with end-stage liver disease. Outcomes have continued to improve, in part owing to interventions used to treat posttransplant complications involving the hepatic arteries, portal vein, hepatic veins or inferior vena cava (IVC), and biliary system. Significant hepatic artery stenosis can be treated with angioplasty or stent placement to prevent thrombosis and biliary ischemic complications. Hepatic arterioportal fistula and hepatic artery pseudoaneurysm are rare complications that can often be treated with endovascular means. Treatment of hepatic artery thrombosis can have mixed results. Portal vein stenosis can be treated with venoplasty or more commonly stent placement. The rarer portal vein thrombosis can also be treated with endovascular techniques. Hepatic venous outflow stenosis of the hepatic veins or IVC is amenable to venoplasty or stent placement. Complications of the bile ducts are the most encountered complication after liver transplant. When not amenable to endoscopic intervention, biliary stricture, bile leak, and ischemic cholangiopathy can be treated with percutaneous transhepatic cholangiography with biliary drainage and other interventions. New techniques have further improved care for these patients. Transsplenic portal vein recanalization has improved transplant candidacy for patients with chronic portal vein thrombosis. Spontaneous splenorenal shunt and splenic artery steal syndrome (nonocclusive hepatic artery hypoperfusion syndrome) remain complicated topics, and the role of endovascular embolization is developing. When patients have recurrence of cirrhosis after transplant, most commonly due to viral hepatitis, transjugular intrahepatic portosystemic shunt (TIPS) may be required to treat symptoms of portal hypertension. Online supplemental material is available for this article. ©RSNA, 2022.

Computed Tomography Images of Spontaneous Portosystemic Shunt in Liver Cirrhosis.

Spontaneous portosystemic shunt (SPSS) refers to collateral vessels that communicate between the portal vein system and systemic circulation. SPSS mainly includes esophageal varices, gastric varices, left gastric vein, recanalized paraumbilical vein, abdominal wall varices, and spontaneous splenorenal shunt. SPSS contributes to the development of hepatic encephalopathy caused by portal vein inflow bypassing and carries a higher risk of death in liver cirrhosis. Abdominal contrast-enhanced computed tomography is a major imaging approach to establish a diagnosis of SPSS and evaluate its location and feature. This review primarily describes the main contrast-enhanced CT features of SPSS in liver cirrhosis.

Splenic vein embolization as a feasible treatment for patients with hepatic encephalopathy related to large spontaneous splenorenal shunts

Introduction and objectivesAlthough splenic vein embolization (SVE) has been performed for the management of patients with hepatic encephalopathy (HE) related to large spontaneous splenorenal shunts (SSRS) in recent years, its role remains poorly defined. In this study, we aimed to explore the safety and efficacy of SVE for HE patients with large SSRS. Materials and methodsData from cirrhotic patients who were confirmed to have recurrent or persistent HE related to large SSRS and underwent SVE from January 2017 to April 2021 were retrospectively collected and analyzed at our center. The primary endpoints were the change of HE severity at 1 week after embolization and the recurrence of HE during the follow-up period. The secondary endpoints were procedure-related complications and changes in laboratory indicators and hepatic function (Child-Pugh score/grade and model for end-stage liver disease score). ResultsOf the eight cirrhotic patients included in the study, six were diagnosed with recurrent HE, and the others were diagnosed with persistent HE. Embolization success was achieved for all patients (100%), and no immediate procedure-related complications, de novo occurrence, or aggravation of symptoms related to portal hypertension were observed during the long-term follow-up. HE status was assessed at 1 week after embolization. The results demonstrated that the symptoms were mitigated in three patients and resolved completely in five patients. During the follow-up period, all patients were free of HE within 1 month after embolization, but one patient experienced the recurrence of HE within 6 months and another one experienced the recurrence of HE within 1 year. Compared with the preoperative parameters, the Child-Pugh score and grade were significantly improved at 1 week and 1 month after embolization (all P<0.05), and the serum ammonia level was significantly lower at 1 month after embolization (P<0.05). ConclusionsSVE could be considered as a feasible treatment for patients with HE related to large SSRS, but further validation is required.

Impact of spontaneous splenorenal shunt on liver volume and long-term survival of liver cirrhosis.

Spontaneous splenorenal shunt (SSRS) is one of the manifestations of portal hypertension in liver cirrhosis. However, the impact of SSRS on long-term survival of cirrhotic patients remains unclear. We hypothesize that SSRS may worsen liver dysfunction and deteriorate prognosis in liver cirrhosis by decreasing hepatic perfusion. Patients with liver cirrhosis who were admitted to our department between December 2014 and August 2019 and underwent contrast-enhanced computed tomography or magnetic resonance imaging scans were prospectively collected. The maximum diameters of SSRS and portal vein system vessels were retrospectively measured. Liver-to-abdominal area ratio, Child-Pugh, and model for end-stage liver disease scores were calculated. Overall, 122 cirrhotic patients were included. The prevalence of SSRS was 30.3% (37/122). Median diameter of SSRS was 13.5mm. Patients with SSRS had significantly thinner diameters of right portal vein (9mm vs 11.2mm, P=0.001) and main portal vein (15.3mm vs 16.8mm, P=0.017) than those without SSRS. Patients with SSRS had significantly lower liver-to-abdominal area ratio score (25.39 vs 31.58, P<0.001) and higher Child-Pugh (7 vs 6, P=0.046) and model for end-stage liver disease (12.17 vs 9.79, P<0.006) scores than those without SSRS. Patients with SSRS had a significantly lower cumulative survival rate than those without SSRS (P=0.014). Cox regression analysis also showed that SSRS was a risk factor of death of cirrhotic patients (hazard ratio=4.161, 95% confidence interval=1.215-14.255, P=0.023). Spontaneous splenorenal shunt may narrow portal vein diameter and shrink liver volume, thereby worsening liver function and increasing mortality in liver cirrhosis.

S2392 Diagnosis and Management of Spontaneous Splenorenal Shunts

INTRODUCTION: Splenorenal shunts are a rare complication of liver diseases including liver cirrhosis. Diseases of the liver can cause portal hypertension leading to a backflow of blood in the portal circulation and potential formation of a shunt between the splenic and left renal vein. This shunt can cause blood to bypass the liver, leading to less liver perfusion and worsening liver disease. This can cause hepatic encephalopathy due to a buildup of liver toxins adversely affecting the brain. We describe the outcomes of two different patients who developed splenorenal shunts. CASE DESCRIPTION/METHODS: Patient 1 was a 71 year old female who initially presented with periodic bouts of abrupt hepatic encephalopathy. She had been previously diagnosed with cryptogenic cirrhosis and portal hypertension. Head CT showed no brain abnormalities, but abdominal CT revealed a splenorenal shunt. She underwent shunt embolization which resulted in improved cognition and mentation. One year later she again presented to the ER with altered mental status. A CT scan showed a new splenorenal shunt. During embolization, she aspirated with subsequent pneumonia, renal failure, encephalopathy, and hypotension. The patient was moved into hospice care, and she expired three days later. Patient 2 was a 54 year old male with a history of living donor liver transplant for cryptogenic cirrhosis with incidental liver cancer seen on explant. His course was complicated by multiple bouts of acute cellular rejection and encephalopathy. He presented two years after transplant with altered mental state. Head CT and MRI showed no abnormalities, but abdominal CT showed the presence of a splenorenal shunt. He underwent embolization of the shunt without complications. At his follow up visits he has shown marked cognitive improvement and is without confusion since the procedure. He has not had any recurrence of confusion or the splenorenal shunt. DISCUSSION: Splenorenal shunts present added complications for individuals suffering from liver disease. In these cases, the patients developed hepatic encephalopathy as a result of their shunts, and in both cases the doctors initially believed the problem to be with their brains before detailed abdominal imaging. Embolization of the shunts lead to recovery from the hepatic encephalopathy. While the procedure to repair the shunts is effective it is not without risks. Close attention to abdominal imaging in liver patients presenting with encephalopathy is key to proper diagnosis and subsequent management.

A Single-Center Experience in Portal Flow Augmentation in Liver Transplantation With Prior Large Spontaneous Splenorenal Shunt

Large portosystemic shunts may cause portal steal syndrome in liver transplantation (LT). Because of the possible devastating consequences of the syndrome, the authors recommend perioperative management of these large shunts. Fourteen adult recipients who underwent portal flow augmentation, including left renal vein ligation (LRVL), renoportal anastomosis (RPA), shunt ligation (SL), and splenic vein ligation (SVL) for large spontaneous splenorenal shunt (SSRS), are included in this study, and the results were analyzed. A total of 13 patients had a large SSRS, and in 1 patient, the large shunt was placed between the superior mesenteric vein and the right renal vein. LDLT was performed in 13 patients. LRVL (n = 5), SVL (n = 6), RPA (n = 2), SL (n = 1) were performed to the patients as graft inflow augmentation. The graft-recipient weight ratios (GRWR) were less than 0.8% in 5 patients (35.7%): 2 had LRVL, and 3 had SVL. Small-for-size syndrome (SFSS) occurred only in these 2 patients with LRVL (GRWR ≤0.8%) and, splenic artery ligation was performed for graft inflow modulation. No mortality or serious complications were reported during follow-up. We consider that in patients with large SSRS and small-for-size grafts, SVL can be performed safely and with satisfactory outcomes.

Ligation Of The Left Renal Vein In Liver Transplant Recipients Diagnosed With A Spontaneous Splenorenal Shunt – Case Report

IntroductionFor patients diagnosed with hepatic cirrhosis and portal hypertension, qualified for liver transplantation, the presence of portosystemic collateral circulation constitutes a typical phenomenon. One of its types is the spontaneous splenorenal shunt. Large or multiple ones may cause the steal syndrome and graft hypoperfusion. An attempt to remove such shunts directly is technically difficult and fraught with complications. An easier and safer method would involve ligating the left renal vein. The aim of this paper is to present a case where proper perfusion of a transplanted liver is ensured by the left renal vein ligation, performed in a recipient with a splenorenal shunt, and to review the scientific reports devoted to portosystemic shunts in liver transplant recipients. Case reportA 63-year-old female with alcoholic liver disease was qualified for liver transplantation. The CT-angiography showed numerous splenorenal shunts with diameter up to 13 mm. During the anhepatic phase of the liver transplantation a very weak effusion from the portal vein was observed, which improved significantly following clamping of the left renal vein. Thus renal vein orifice was ligated in order to achieve the correct graft reperfusion. Postoperative Doppler ultrasound showed a correct portal blood flow. The early liver and renal function was good. Finally, in the 7th month, the patient underwent a re-transplantation due to biliary necrosis caused by late hepatic artery thrombosis. ConclusionLigation of the left renal vein efficiently prevents the steal syndrome in the liver transplant recipients with splenorenal shunt and ensures good graft perfusion.

Advances in research of spontaneous splenorenal shunt in patients with liver cirrhosis

Advances in research of spontaneous splenorenal shunt in patients with liver cirrhosis

062 Alcohol associated toxic myelopathy with normal hepatic function

IntroductionAlcohol related neurological dysfunction affects the central and peripheral nervous system. We present a rare consequence of excessive alcohol consumption. A 42-year-old female consuming 2 bottles of wine daily for the preceding 5 years presented with 12 months of progressive gait disturbance. Examination revealed a spastic paraparesis with prominent dorsal column signs. Extensive work up found no alternate cause for her presentation. The final diagnosis was direct alcohol mediated toxic myelopathy. We reviewed the current literature on this rare condition.MethodsWe searched PubMED/OVID databases with the terms ‘alcohol AND myelopathy’.ResultsThere is a paucity of research on this clinical entity. Sage et al.1 described 5 well-nourished alcoholics presenting with a progressive myelopathy. As with our patient, routine laboratory tests, including nutritional screen, were normal. CT Myelogram revealed no structural cause. CSF was normal. In contrast, a myelopathic syndrome can occur in alcoholic hepatic failure, attributed to portosystemic shunting of blood, with resultant hyper-ammonaemia and demyelination of corticospinal tracts.2–4ConclusionAlcohol associated toxic myelopathy is a rare entity, distinct from hepatic myelopathy. It is thought to result from direct toxic effects of ethanol on corticospinal and large myelinated sensory tracts. The sensory involvement is unique for this entity, which distinguishes it from hepatic myelopathy, where corticospinal involvement predominates. It is prudent to look for other potentially treatable secondary causes of myelopathy. Abstinence from alcohol results in modest improvement in symptoms. Minimal literature exists on this clinical entity and further research is required.ReferencesSage JI, et al. Alcoholic myelopathy without substantial liver disease. A syndrome of progressive dorsal and lateral column dysfunction. Arch Neurol. 1984 Sep;41(9):999–1001.Premkumar M, et al. Hepatic Myelopathy in a Patient with Decompensated Alcoholic Cirrhosis and Portal Colopathy. Volume 2012, Article ID 735906, 4 pages.Koo JE, et al. Hepatic myelopathy as a presenting neurological complication in patients with cirrhosis and spontaneous splenorenal shunt. Korean J Hepatol. 2008 Mar;14(1):89–96.Kori P, et al. Hepatic myelopathy: an unusual neurological complication of chronic liver disease presenting as quadriparesis. BMJ Case Rep. 2013; 2013: bcr2013009078.

Adjuvant Transjugular Variceal Occlusion at Creation of a Transjugular Intrahepatic Portosystemic Shunt (TIPS): Efficacy and Risks of Bucrylate Embolization

The retrospective study evaluated 104 of 237 cirrhotic patients with TIPS for variceal bleeding who received adjuvant bucrylate embolization. For TIPS creation, bare stents were used in 35 patients (33.7%) and covered stents in 69 patients (66.3%) patients. Isolated gastric varices were seen in 10 patients (9.6%). Six patients (5.8%) rebled during a median follow-up time of 26months (1-57months). Rebleeding occurred in 14% (5/35) of patients with a bare stent but only in 1.4% (1/69) of patients with a covered stent. The 1- and 2-year rebleeding rates of all patients were 0.9 and 2.9% and of patients receiving a bare stent were 2.9 and 8.6%, respectively. Bucrylate migration was seen in 13 patients (12.5%). In 9 of these patients (8.7%), asymptomatic lung embolization occurred. This was rare in patients with esophageal varices (3.1%) but frequent (60%) in patients with isolated gastric varices and a spontaneous splenorenal shunt. Our results suggest that adjuvant embolization using bucrylate is effective and delays variceal rebleeding. The general use of covered stents, however, alleviates the utility of adjuvant bucrylate embolization which may be restricted to patients with a high risk of rebleeding indicated by large varices, active, acute or recent variceal bleeding and advanced cirrhosis. Bucrylate should not be used in isolated gastric varices because it bears a high risk of migration into the lungs.

Left Renal Vein Ligation for Spontaneous Splenorenal Shunts During Deceased-Donor Orthotopic Liver Transplant Is Safe and Can Mitigate Complications from Portal Steal: A Case Series

Large spontaneous splenorenal shunts can result in portal vein steal syndrome and is a risk factor for portal vein thrombosis after orthotopic liver transplant. Disconnection of these shunts by left renal vein ligation has been suggested as a potential technique for improving portal venous flow and mitigating risk of portal vein thrombus, thus improving graft perfusion. We present a series of 6 patients who underwent left renal vein ligation for spontaneous splenorenal shunts and their outcomes. This retrospective analysis included all orthotopic liver transplant recipients who underwent left renal vein ligation for spontaneous splenorenal shunts between 2016 and 2017. Portal venous flow, patency, and renal function were assessed postoperatively. Liver Doppler ultrasonography scans were obtained 1, 3, and 5 days postligation, and serum creatinine was evaluated at 1 and 2 weeks and 1, 3, 6, and 12 months postligation. Over the 1-year study period, 92 orthotopic liver transplants were performed. In 6 patients who underwent left renal vein ligation, spontaneous splenorenal shunts were identified preoperatively. One patient received a retransplant complicated by portal vein thrombus and underwent thrombectomy with left renal vein ligation. Concurrent left renal vein ligation and liver transplant were performed in 5 patients, 2 with known portal vein thrombus at the time of transplant requiring thrombectomy. All patients had subjective intraoperative improvements in portal venous flow after ligation. Zero patients developed postoperative portal vein thrombus. No patients developed clinically significant renal dysfunction at 1-year follow-up. Left renal vein ligation is technically feasible, has minimal and transient effects on renal function, and can improve portal venous flow, thus mitigating the risk for portal vein thrombus, graft hypoperfusion, and possible dysfunction.

Impact of portal vein resection with splenic vein reconstruction after pancreatoduodenectomy on sinistral portal hypertension: Who needs reconstruction?

Resection of the porto-mesenterico-splenic confluence is at times necessary during pancreatoduodenectomy with portal vein resection for pancreatic cancer. Although splenic vein ligation can cause sinistral portal hypertension, the incidence of clinically relevant sinistral portal hypertension remains unknown, and the roles of the preservation of potential collateral veins and splenic vein reconstruction are controversial. Patients with pancreatic cancer who underwent pancreatoduodenectomy with porto-mesenterico-splenic confluence resection were assessed for incidence of development of varices by computed tomography at 6 months after pancreatoduodenectomy. We evaluated the risk factors for sinistral portal hypertension and the impact of splenic vein reconstruction on sinistral portal hypertension. Of the 118 patients who underwent pancreatoduodenectomy with porto-mesenterico-splenic confluence resection, 31 (26%) underwent splenic vein reconstruction, 44 patients (37%) developed gastroesophageal varices, and 5 (11%) experienced varix rupture. Sacrifice of all 3 potential collateral veins (what we refer to as the critical veins: left gastric vein, middle colic vein, and superior right colic vein arcade) and absence of any spontaneous splenorenal shunt had a substantial impact on formation of varices. The risk of variceal formation could be stratified based on the number of preserved critical veins, and patent splenic vein reconstruction was associated with a decreased incidence of varices (60% versus 100%, P = .018) among the patients without preservation of the critical veins. In contrast, patients with multiple intact critical veins developed no varices, regardless of splenic vein reconstruction. Sinistral portal hypertension is not uncommon after pancreatoduodenectomy with porto-mesenterico-splenic confluence resection, and the number of preserved critical veins helps to predict the risk of sinistral portal hypertension. Thus, the indication for splenic vein reconstruction should be tailored according to individual risk factors.

Liver transplantation in patients with spontaneous spleno-renal shunt

Aim: Our aim was to describe the outcomes of liver transplantation (LT) in patients with spontaneous spleno-renal shunt (SSRS) and a defined protocol of mínimum portal flow. Methods: Recipients with SSRS before LT between January 2005 and January 2017 were included in a retrospective study. Our policy was to achieve a final portal flow >80 mL/min/100 gr of liver weight or >1000 mL/min. The primary endpoint was patient survival. Results: Sixty patients comprised the study group. Portal thrombendvenectomy was performed in 15. Portal reconstruction was porto-portal in 56 cases, including 9 cases with left renal vein (LRV) ligation. Reno-portal reconstruction was performed in 4 cases. Median portal flow in those patients with LRV ligation increased from 850 mL/min (266-1419) to 1732 mL/min (1063-3240) after ligation. This was comparable to the patients with porto-portal reconstruction and no need for LRV ligation (1782 mL/min (672-3780)). Moreover, median portal flow/100 gr of liver weight increased from 56 mL (34-79) to 111 mL (61-183) after LRV ligation, also comparable to the patients who did not need LRV ligation (118 mL (69-295)). Mean (SD) portal flow after reno-portal reconstruction was 1372 ± 798 mL/min. Early primary dysfunction was observed in 12 patients (20%). Only 1 patient suffered a primary non-function.1- and 5-year patient survival was 93.3% and 91%. Conclusión: A high patient survival was observed after LT in recipients with pretransplant SSRS when a final portal flow >80 mL/min/100 gr of liver weight or >1000 mL/min was achieved.

Influence of spontaneous splenorenal shunts on clinical outcomes in decompensated cirrhosis and after liver transplantation.

Cirrhosis and portal hypertension can lead to the formation of a spontaneous splenorenal shunt (SSRS) that may divert portal blood flow to the systemic circulation and reduce hepatic perfusion. Our aims were to evaluate SSRSs as an independent prognostic marker for mortality in patients with decompensated cirrhosis and the influence of SSRSs on liver transplantation (LT) outcomes. We retrospectively analyzed adult patients with decompensated cirrhosis undergoing LT evaluation from January 2001 to February 2016 at a large U.S. center. All patients underwent liver cross‐sectional imaging within 6 months of evaluation, and images were reviewed by two radiologists. Clinical variables were obtained by electronic health record review. The cohort was followed until death or receipt of LT, and the subset receiving LT was followed for death after LT or graft failure. Survival data were analyzed using multivariable competing risk and Cox proportional‐hazards regression models. An SSRS was identified in 173 (23%) of 741 included patients. Patients with an SSRS more often had portal vein thrombosis and less often had ascites (P < 0.01). An SSRS was independently associated with a nonsignificant trend for reduced mortality (adjusted subhazard ratio, 0.81; Gray's test P = 0.08) but had no association with receipt of LT (adjusted subhazard ratio, 1.02; Gray's test P = 0.99). Post‐LT outcomes did not differ according to SSRS for either death (hazard ratio, 0.85; log‐rank P = 0.71) or graft failure (hazard ratio, 0.71; log‐rank P = 0.43). Conclusion: Presence of an SSRS does not predict mortality in patients with decompensated cirrhosis or in LT recipients. (Hepatology Communications 2018;2:437‐444)

Value of balloon closure combined with endoscopic therapy for gastric varices with portasystemic shunt

Objective To evaluate the clinical effect of balloon closure combined with endoscopic therapy on spontaneous gastrorenal shunt(SGRS) and spontaneous splenorenal shunt(SSRS). Methods The data of 33 patients of gastric varices with SGRS or SSRS diagnosed in the Chinese PLA General Hospital between January 2009 and February 2016 were collected. All patients were treated with the balloon retrograde distributary channel blocking technique and endoscopic histoacryl injection. Patients′ clinical data, complications and effect of endoscopic therapy were retrospectively analyzed. Results In the 33 patients of gastric varices, gastrorenal shunt was found in 28(84.8%) cases and splenorenal shunt was found in 5(15.2%) cases. After the balloon blocking technique, 24 cases (72.7%) were occluded successfully. Four cases failed in occlusion of SSRS due to tortuosity. There were no postoperative ectopic embolism, infection, hepatic encephalopathy, liver function deterioration, and other complication. Early latex varices were found in 21 cases after three months follow-up. Conclusion The balloon blocking technique combined with tissue adhesive injection could safely and effectively avoid the risk of ectopic embolism and plays an important role in the treatment of gastric varices in merger portasystemic shunt. Key words: Endoscopes; Esophageal and gastric varices; Balloon embolization; Portasystemic shunt

Lessons Learned from Inappropriate Ligation of the Left Renal Vein for a Large Splenorenal Shunt in Living Donor Liver Transplantation

During living donor liver transplantation, a large spontaneous splenorenal shunt (SRS) should be addressed to obtain adequate portal inflow. Various procedures such as direct ligation of the SRS, splenectomy, left renal vein ligation (LRVL), and renoportal anastomosis can be applied to treat a large SRS according to the hemodynamics of the portal flow and anatomic conditions. Of these surgical procedures, LRVL is a simple and effective solution for treatment of a large SRS. However, to perform a LRVL, rigorous evaluation of the recipient`s anatomic and hemodynamic variations is mandatory. In the present case, we ligated the left renal vein to treat a large SRS, which resulted in an unexpected thrombosis of the left renal vein and remaining portal vein stenosis in the SRS. Therefore, we revised our decisions regarding whether the LRVL was properly applied.

Tips and pitfalls in direct ligation of large spontaneous splenorenal shunt during liver transplantation.

Patients with large spontaneous splenorenal shunts (SRSs) prove challenging during liver transplantation (LT), regardless of organizing portal vein (PV) thrombosis. Here, we detail the clinical outcomes of 26 patients who underwent direct ligation of large SRSs during LT. Direct ligation of large SRS was applied in poor portal flow during LT. We performed temporary test clamping of the SRS before direct ligation and applied PV pressure monitoring in patients who showed signs of portal hypertension, such as bowel edema. We retrospectively reviewed and evaluated their clinical outcomes. Among 843 patients who underwent LT between 2010 and 2015, 26 (3.1%) underwent direct ligation of SRS without any intraoperative event. Mean preoperative Model for End-Stage Liver Disease score was 16.7 ± 9.0. The main PV diameter on preoperative computed tomography was 8.3 ± 3.4 mm (range, 3.0-14.0 mm). SRS was easily identified at just below the distal pancreas and beside the inferior mesenteric vein in all patients. Accompanying PV thrombectomy was done in 42.3% of patients. Among 26 patients, massive and prolonged ascites was evident in 15.4% (n = 4) postoperatively. They were all living donor LT recipients with a small PV diameter (4.0-6.7 mm). Except for 1 patient who underwent splenic artery embolization, ascites was tolerable and well controlled by conservative management. There was a 7.7% rate of major complications related to direct ligation, including reoperation due to combined ligation of SRS along with a left renal vein at the confluence. Except for 1 hospital mortality due to sepsis, 25 patients (96.2%) are alive with no evidence of further PV complications. In conclusion, direct ligation of large SRS during LT is a safe and feasible method to overcome the effects of a large SRS. Liver Transplantation 23 899-906 2017 AASLD.

Prevalence and Clinical Characteristics of Spontaneous Splenorenal Shunt in Liver Cirrhosis: A Retrospective Observational Study Based on Contrast-Enhanced Computed Tomography (CT) and Magnetic Resonance Imaging (MRI) Scans.

BackgroundThis is a retrospective observational study evaluating the prevalence and clinical characteristics of spontaneous splenorenal shunt in liver cirrhosis.Material/MethodsWe included a total of 105 cirrhotic patients who were admitted to our hospital between June 2012 and December 2013 and underwent contrast-enhanced CT and/or MRI scans at admissions. Spontaneous splenorenal shunt was identified. Clinical and laboratory data were compared between cirrhotic patients with and without spontaneous splenorenal shunt.ResultsThe prevalence of spontaneous splenorenal shunt was 10.5% (11/105). The prevalence of hepatic encephalopathy was higher in patients with spontaneous splenorenal shunt than in those without spontaneous splenorenal shunt (18.2% vs. 4.3%, p=0.062), but the difference between them was not statistically significant. The prevalence of acute upper-gastrointestinal bleeding was lower in patients with spontaneous splenorenal shunt than in those without spontaneous splenorenal shunt (0% vs. 18.1%, p=0.205), but the difference between them was not statistically significant. Patients with spontaneous splenorenal shunt had significantly higher Child-Pugh scores (9.50±1.65 vs. 7.43±2.02, p=0.002) and MELD scores (11.26±7.29 vs. 5.67±6.83, p=0.017) than those without spontaneous splenorenal shunt. In-hospital mortality was similar between them (0% vs. 4.3%, p=1.000).ConclusionsSpontaneous splenorenal shunt might be associated with worse liver function in liver cirrhosis, but not with in-hospital mortality.