Fatty liver caused by portal vein thrombosis after living donor liver transplantation: a case report

Portal vein thrombosis (PVT) is a rare complication that occurs after liver transplantation: however, it cannot be ignored as a cause of graft loss and death. We herein report a pediatric case of PVT that caused a fatty change in the graft after living donor liver transplantation. The portal vein was successfully reconstructed using the left great saphenous vein of the same donor. Moreover, the fatty liver recovered after the operation. Our case suggests that the finding of fatty liver is an important marker of PVT and immediate portal reconstruction is performed.     

Simultaneous hepatic artery and portal vein thrombosis after living donor liver transplantation

Simultaneous hepatic artery and portal vein thrombosis rarely occurs after liver transplantation. The etiology is unknown. Of 213 patients (72 children and 141 adults) that underwent living donor liver transplantation (LDLT) from January 1996 to March 2003, 4 (2%) developed simultaneous thrombosis at 3 hours to 7 days (median, 4 days) after the operation. Emergent thrombectomy was performed in three patients; the remaining patient was registered in the Japan organ transplant network. All of the patients died due to hepatic failure (range, 18 hours to 6 days after the diagnosis; median, 2 days). Portal vein, hepatic artery, and hepatic vein velocity in the liver graft were measured every 12 hours by Doppler ultrasonography for 2 weeks after liver transplantation. These parameters were stable until just before the simultaneous thrombosis. These findings indicate that protocol Doppler ultrasonography can diagnose, but not predict, this fatal complication.     

Acute portal vein thrombosis secondary to donor/recipient portal vein diameter mismatch after orthotopic liver transplantation: a case report

The incidence of portal vein thrombosis in end-stage liver disease is estimated as varying between 5% and 21%, whereas in candidates undergoing liver transplantation, this is 3-13%. Portal vein thrombosis occurring after liver transplantation can be managed surgically by thrombectomy, retransplantation, splenorenal shunt, or Wall-stent placement, or nonsurgically by angioplasty, local high-dose infusion of thrombolytic agents, combination of portal thrombolysis, or embolization of a pre-existing spontaneous splenorenal shunt. We report a case of portal vein thrombosis after liver transplantation diagnosed on postoperative day 1 in a 57-year-old patient who received a liver from an 8-year-old donor. The patient was successfully treated surgically with portal vein thrombectomy and systemic anticoagulation. Portal vein thrombosis, in this case, was considered to be secondary to size discrepancy between the donor and the recipient portal veins. Routine use of daily Doppler ultrasound was the key factor in early diagnosis.     

术前门静脉血栓对活体肝移植预后的影响

目的 探讨术前门静脉血栓对活体肝移植的影响.方法 回顾性分析天津市第一中心医院2007至2011年完成的99例成人间活体肝移植患者,根据术前是否有门静脉血栓分为2组,血栓组26例,无血栓组73例.比较2组的术前危险因素及门静脉血栓对活体肝移植手术和术后患者预后的影响.结果 26例门静脉血栓患者Ⅰ级血栓23例,Ⅱ级血栓3例.肝移植术前的脾切除是发生门静脉血栓的独立危险因素(x2 =10.211,P=0.001).术前门静脉血栓会延长手术的无肝期(Z=-2.430,P=0.015),但2组患者术后并发症发生率(x2=0.326,P=0.568)及死亡率均无统计学差异,而且对患者的1年生存率和3年生存率均无影响(x2=0.505,P =0.477).结论 对于活体肝移植合并Ⅰ级或Ⅱ级门静脉血栓的患者,通过合理的术中处理及术后预防,门静脉血栓不会影响患者的预后.但门静脉血栓增加了一定的手术难度,需要详尽的术前评估和仔细的术中操作.     

Salvage procedure for unexpected portal vein thrombosis in living donor liver transplantation

Portal vein thrombosis (PVT) is considered a relative contraindication to living donor liver transplantation (LDLTx) due to technical difficulty and ethical considerations. So far, there have been a few reported cases of LDLTx with PVT, most of which were treated by thrombectomy with or without a venous conduit. We report a case of LDLTx in an unexpected recipient with grade 4 diffuse PVT, which was successfully managed using a variceal left gastric vein and a deceased donor iliac vein conduit to create a "de novo portal vein" for splanchnic inflow to the right lobe. The patient experienced an uneventful postoperative course with normal blood flow in the de novo portal vein at 1-year follow up. This report demonstrated that a variceal collateral vein can be used as appropriate alternative inflow for the right lobe in LDLTx cases in which an unexpected PVT is encountered.     

Risk factors for intraoperative portal vein thrombosis in pediatric living donor liver transplantation

Pathologic changes of the recipient native portal venous system may cause thrombosis of the portal vein, especially in pediatric living donor liver transplantation (LDLT). This study assessed the utility of Doppler ultrasound (US) for the detection of intraoperative portal vein occlusion and identification of predisposing risk factors in the recipients. Seventy-three pediatric recipients who underwent LDLT at Chang Gung Memorial Hospital, Taiwan, from 1994 to 2002 were included. Preoperative and intraoperative Doppler US evaluation of the portal vein was performed. Age, body weight, native liver disease, type of graft, graft recipient weight ratio (GRWR), type of portal anastomosis, portal velocity, portal venous size and presence of portosystemic shunt were analyzed for statistical significance of predisposing risk factors. Eight episodes of intraoperative portal vein thrombosis, with typical findings of absent Doppler flow in portal vein and prominent hepatic artery with a resistant index lower than 0.5 (p < 0.001), were detected during transplantation, which was then corrected by thrombectomy and re-anastomosis. Children age < or =1 yr (p = 0.025), weight < or =10 kg (p = 0.024), low portal flow < or =7 cm/s (p = 0.021), portal venous size < or =4 mm (p = 0.001), and GRWR >3 (p < 0.017) were all risk factors for intraoperative portal vein thrombosis. Doppler US is essential in the preoperative evaluation, early detection and monitoring of outcome of the portal vein in liver transplant.     

Isolated dissection of the superior mesenteric artery after living donor liver transplantation: a case report

Isolated dissection of the superior mesenteric artery (SMA) not associated with aortic dissection is rare, particularly after living donor liver transplantation (LDLT). We experienced a case of isolated dissection of the SMA after LDLT performed in a 56-year-old man diagnosed with hepatitis B virus-related cirrhosis and hepatocellular carcinoma within the Milan criteria. He had no past history of hypertension or diabetes mellitus. At 6 days after LDLT, the patient underwent an emergency portal vein thrombectomy with ligation of a huge left gastric vein shunt. Thereafter anticoagulant and antiplatelet therapy were initiated. At 12 days after LDLT, a contrast-enhanced computer assisted tomography (CT) scan revealed the presence of a thrombus in a false lumen and a thin flap enlarged in the SMA. Because he presented neither abdominal pain nor biochemical data suggesting mesenteric ischemia, he was treated with antihypertensive agents in addition to anticoagulant and antiplatelet therapy. The thrombus in the false lumen was reduced and the intimal flap in the SMA disappeared according to the results of a CT scan 4 months after LDLT. He has remained free of symptoms for 4 years. The strategy to treat isolated SMA dissection is not well established. Urgent surgery is indicated for acute symptomatic forms with a suspicion of mesenteric ischemia; conservative treatment is indicated for patients with minimal, resolving, or no pain, but requires close follow-up.     

门静脉-下腔静脉吻合术预防活体肝移植术后小肝综合征3例报道

目的探讨门静脉-下腔静脉吻合术用于预防活体肝移植术后小肝综合征(small-for-size liver syndrome,SFSS)的效果。方法 3例活体肝移植均采用不含肝中静脉的右半肝作为移植物。术中发现实测移植物(肝)重量/受体的体质量(体重)的比值(graft to recipient weight ratio,GRWR)为0.58%、0.77%及0.71%,均<0.8%,符合小移植物的诊断。处理:首先吻合肝静脉流出道,其次吻合门静脉,将受体门静脉右支与移植肝门静脉右支端端吻合,将受体门静脉左支与下腔静脉行端侧吻合达到门腔分流的作用,之后按顺序吻合动脉和胆道。术中均未行脾静脉结扎或脾切除等处理。术后定期随访。结果 3例患者术后均未发生SFSS并顺利出院,出院时间分别为术后25d、34d及56d。移植肝功能逐步好转,术后1d门静脉流速理想。移植肝增长良好。门静脉-下腔静脉短路通畅时间:除1例通畅持续仅104d,其余2例持续通畅。结论 LDLT术中进行门静脉-下腔静脉吻合术可以及时有效预防小移植物背景下的SFSS,受体门静脉左支与下腔静脉行端侧吻合的分流技术安全可靠。     

Ligation of left renal vein for large spontaneous splenorenal shunt to prevent portal flow steal in adult living donor liver transplantation

Persistance of a large spontaneous splenorenal shunt (SRS) may result in graft failure in adult living donor liver transplantation (LDLT) because it reduces the effective portal perfusion to the partial liver graft by diversion of hepatotrophic portal flow into this hepatofugal pathway. We performed a prospective study to evaluate the efficacy of ligation of left renal vein (LRV) to prevent portal flow steal and the safety of this procedure to the renal function in adult LDLT patients with SRS. Between October 2001 and January 2005, 44 cirrhotic patients with large SRS underwent LDLT with ligation of LRV. Each patient received pre- and postoperative computed tomography and Doppler USG to assess the changes of collaterals and portal flow, as well as serial renal and liver function tests. Portal flow after ligation of LRV was statistically and significantly increased when compared with pre-operative value (P = 0.001). Whereas four patients (9.1%) demonstrated sustained, elevated serum creatinine levels after operation, the renal function tests returned to normal in 40 patients. All patients recovered with satisfactory regeneration of the partial liver graft and there was no procedure-related permanent renal dysfunction. In conclusion, ligation of LRV to prevent a 'portal steal phenomenon' seems to be a safe and effective graft salvage procedure for large spontaneous SRS (>10-mm diameter) in adult LDLT.     

Clinical analysis of living donor liver transplantation in patients with portal vein thrombosis

Kim S‐J, Kim D‐G, Park J‐H, Moon I‐S, Lee M‐D, Kim J‐I, Yoon Y‐C, Yoo Y‐K. Clinical analysis of living donor liver transplantation in patients with portal vein thrombosis.
Clin Transplant 2011: 25: 111–118. © 2010 John Wiley & Sons A/S. Abstract: The aim of this study was to improve outcomes in living donor liver transplantation (LDLT) patients with portal vein thrombosis (PVT). Of 246 adult patients who underwent LDLT with a right lobe graft between January 2000 and May 2007, PVT was diagnosed in 50 patients (20.3%), who were further subdivided into partial (n = 39, 78%) and complete (n = 11, 22%) types. Patients with PVT, especially complete PVT, showed high incidences of variceal bleeding (p = 0.021), operative RBC transfusion (p < 0.046) and a post‐transplantation complications related to bleeding (p = 0.058). We also classified PVT according to its location and the presence of collaterals: type I (n = 41, 82%): PVT localized above the confluence of the splenic and superior mesenteric veins (SMV); type II (n = 7, 14%): PVT extending below the confluence with a patent distal SMV; type III (n = 2, 4%): complete portal vein and SMV thrombosis except for a coronary vein. LDLT could be safely undertaken in patients with PVT without increased mortality. In our type II and III PVT, when thrombectomy fails, jump grafting using a cryopreserved vessel may serve as a reliable alternative method to restore portal flow.     

Right posterior portal vein stenosis developed after living donor liver transplantation using a modified right lobe graft with a type 2 portal vein: a case report

Portal vein complications after liver transplantation (LT) can lead to graft liver failure. In this living donor liver transplantation case a stenosis developed in the right posterior branch of the portal vein of the graft liver from a living donor with type 2 portal vein variation. A 61-year-old woman diagnosed with hepatocellular carcinoma due to hepatitis B received a liver graft revealing a single lumen divided by a septum. The portal vein was anastomosed to the recipient portal vein without venoplasty. Postoperative Doppler sonogram revealed poor flow in the right posterior portal vein with compensatory arterial hyperperfusion. The postoperative computed tomography (CT) scan revealed narrowing of the proximal part of the right posterior portal vein with periportal tracking. Without intervention, the liver enzyme and bilirubin levels decreased to normal and the follow-up CT scan showed decreased periportal tracking. The patient was discharged without major complications. We believe that the posterior portal vein stenosis resulted from the direct anastomosis of the portal vein without a further venoplasty. Although there was no major complication due to the posterior portal vein stenosis in our patient, we suggest a venoplasty to prevent portal vein stenosis when using right lobe grafts with a type 2 portal vein, even if a single lumen is present and there is a margin for a direct anastomosis.     

Outcome of modified portal vein anastomosis for recipients with portal vein thrombosis or stenosis before living donor liver transplantation

Background

Portal vein thrombosis (PVT) or stenosis (PVS) often requires challenging techniques for reconstruction in living donor liver transplantation (LDLT).

Materials and Methods

A total of 57 LDLTs were performed between October 1996 and December 2010. There were 16 cases (28%) with PVT/PVS that underwent modified portal vein anastomosis (m-PVa). The m-PVa techniques were classified into 3 groups: patch graft (Type-1), interposition graft (Type-2), and using huge shunt vessels (Type-3). The reconstruction patterns were evaluated with regard to age, graft vessels, PV flow, and complication rate.

Results

The m-PVas were Type-1 in 10 cases, Type-2 in 3 cases, and Type-3 in 3 cases. The vessel graft in Type-1 was the inferior mesenteric vein (IMV) in 8 and the jugular vein in 2 cases, whereas the vessel graft in Type-2 was IMV in 2 and the saphenous vein in 1 case; in Type-3, the vessel grafts were renoportal, gonadal-portal, and coronary-portal anastomoses, respectively. The postoperative PV flow was sufficient in all types and slightly higher in Type-3. The postoperative complications occurred in 20% of the patients who underwent Type-1, in 33% who underwent Type-2, and in 0% who underwent Type-3.

Conclusion

The m-PVa was effective to overcome the surgical difficulty during transplantation. Pretransplant planning for the selection of the type of reconstruction is important for recipients with PVT/PVS.     

Left lobe living related liver transplantation in the absence of an extrahepatic left portal vein

Absence of a normal left extrahepatic portal vein is considered to be a contraindication to left lobe living-related liver transplantation. This report is of a successful case of living- related liver transplantation using a left lobe procured in a patient presenting with an absent horizontal segment of the left extrahepatic vein.     

Distal inferior mesenteric veins to renal vein shunt for treatment of bleeding anorectal varices: case report and review of literature

Isolated intractable bleeding from anorectal varices is a rare complication of portal hypertension. We report a case of a patient with cirrhosis and hepatofugal flow who had severe lower gastrointestinal bleeding from anorectal varices. This is the first case report of construction of a distal inferior mesenteric vein shunt to left renal vein as a selective shunt for treatment of bleeding anorectal varices in a patient with hepatofugal flow. The patient is a 39-year-old white man with a medical history significant for alcohol abuse who was seen with bright red blood per rectum requiring 10 units of packed red blood cells over the course of a year. The work-up revealed anorectal varices with no other colonic lesions. The patient underwent construction of a distal inferior mesenteric vein to left renal vein shunt.     

肝移植术后迟发性门静脉血栓形成12例

目的 总结肝移植术后迟发性门静脉血栓形成的治疗方法,并分析其预后.方法 单中心3100例次尸体全肝移植中发生迟发性门静脉血栓形成12例,发生时间平均为移植术后29.8个月.12例中,2例合并严重胆道并发症(肝内胆道狭窄),2例表现为移植肝功能衰竭,1例影像学检查可见肝门部肿物致门静脉受压,均接受再次肝移植;2例表现为急性上消化道出血,分别行经胃镜下套扎、注射硬化剂治疗;余5例无任何临床表现,口服抗凝或抗血小板药物治疗.结果 12例中,除1例失访外,其他患者至随访结束时存活8例,包括2例行再次肝移植者.存活者肝功能检查结果均正常.结论 肝移植术后发生迟发性门静脉血栓形成,应根据患者的临床表现不同采用不同的治疗方法.

Abstract：

Objective To summary therapeutic method for delayed portal vein thrombosis after liver transplantation. Methods In 3100 cases undergoing cadaveric whole liver transplantation in a single center, there were 12 cases of delayed portal vein thrombosis after liver transplantation.Average occurring time was 29. 8 months after liver transplantation. Among these 12 patients, 2 cases were complicated with severe biliary complication (intrahepatic stricture) , 2 cases presented with liver failure of transplanted liver, and one case had portal vein compression by hepatic hilum tumor under the image examination, who received liver re-transplantation; two patients presented upper gastrointestinal bleeding, and they experienced endoscopic ligation and sclerotherapy respectively; the rest five patients without any clinical presentation were subjected to anticoagulation and antiplatelet therapy. Results Among 12 cases, 8 patients survived by the time of follow-up, including two patients undergoing re-transplantation; one patient lost follow-up. The liver function tests of the patients who survived were all normal. Conclusion The individualized therapeutic methods should be adopted for the patients with delayed portal vein thrombosis after liver transplantation.