Hematologic aspects of liver transplantation for Budd-Chiari syndrome with special reference to myeloproliferative disorders

BACKGROUND: Patients who undergo orthotopic liver transplantation (OLT) for Budd-Chiari syndrome (BCS) traditionally have been anticoagulated with warfarin postoperatively. Because a significant proportion of BCS patients are found to have an underlying myeloproliferative disorder (MPD), antiplatelet therapy may be a more rational treatment strategy for this subgroup. METHODS: All patients who underwent OLT for the diagnosis of BCS at our institution through March 2000 were included in this analysis. Posttransplant therapy consisted of hydroxyurea and aspirin for those with MPDs. Standard anticoagulation or no antithrombotic treatment was given to BCS patients with other causes. Major posttransplantation complications (thrombosis and bleeding) and mortality were determined. RESULTS: Seventeen patients underwent OLT for BCS at our institution. The mean follow-up was 68.4 months. Two of seventeen patients died; one patient died of recurrent thrombosis (124 months after OLT) and the other patient died of acute hepatitis B (7 months after OLT). Twelve patients (71%) had evidence of a MPD. Two of the MPD patients were treated with warfarin before the initiation of hydroxyurea and aspirin therapy. The remaining 10 MPD patients were placed on only hydroxyurea and aspirin after OLT. Anagrelide was used in place of hydroxyurea in two patients because of cytopenias caused by the latter agent. The mean follow-up of this group of 10 patients was 59.9 months. Only one patient experienced recurrent thrombosis, which occurred more than 10 years after the original transplant. There were no major bleeding complications and posttransplant liver biopsies were well tolerated. CONCLUSIONS: Antiplatelet therapy that consists of hydroxyurea and aspirin is a safe and effective alternative to anticoagulation to prevent recurrent thrombosis in MPD patients with BCS after liver transplantation. For patients with a hypercoagulable state corrected by OLT, antithrombotic therapy probably is not required. For those patients with conditions not corrected by OLT or with idiopathic BCS, anticoagulation or other therapy to control the hypercoagulable state should be given.     

Liver transplantation for Budd-Chiari syndrome

BACKGROUND: Budd-Chiari syndrome (BCS) is a clinical condition characterized by hepatic venous outflow obstruction secondary to an underlying systemic predisposition to thrombosis. METHODS: We reviewed our experience of 19 adult patients who underwent orthotopic liver transplantation for BCS from April 1988 to May 1999 to assess their long-term outcome and specific complications related to this procedure. RESULTS: Of these patients, 13 presented with chronic and 6 with acute liver failure. At presentation predisposing factors included polycythemia rubra vera in five, an undefined myeloproliferative disorder in four, essential thrombocythemia in two, presence of lupus anticoagulant in one, antiphospholipid antibody positivity in one, post-gestational in one, oral contraceptive pill in one, and idiopathic in four. Five patients had undergone previous porto-systemic shunt. Of the 19 patients, 16 are alive at a median follow-up of 89 months (range 1-119) with 2 patients developing disease recurrence at 4 months and 7 years posttransplant, respectively. Four patients have been retransplanted: one for progressive graft dysfunction due to nodular regenerative hyperplasia secondary to azathioprine toxicity, two for hepatic artery thrombosis (one soon after and the other 47 months posttransplant), and one for recurrent BCS. Three patients have died: one from an intra-abdominal bleed secondary to acute hemorrhagic pancreatitis 8 years posttransplant, another from acute myeloid leukemia at 6 years posttransplant, and the third patient from graft failure secondary to severe rejection 1 month posttransplant. CONCLUSION: Liver transplantation for BCS provides good long-term survival with acceptable morbidity. Long-term survival may be prejudiced by progression of the underlying hematological disorders.     

Reassessing the role of medical therapy in the management of hepatic vein thrombosis

Hepatic venous outflow obstruction caused by hepatic vein thrombosis (HVT) is a manifestation of a hypercoagulable state, most commonly a myeloproliferative disorder (MPD). In the past, HVT was thought to have a poor prognosis unless treated surgically with portosystemic shunt or orthotopic liver transplantation (OLT). The aim of this study was to assess whether early diagnosis of the underlying hematologic disorder and institution of appropriate medical therapy have altered outcome. We reviewed the charts of 22 patients with HVT evaluated at our center from January 1986 to January 1995. The median age was 32 years (range, 14 to 59 years). Underlying etiologies were MPD, 13 (polycythemia vera, 8; essential thrombocythemia, 4; undefined, 1); dysfibrinogenemia, 1; anticardiolipin antibody, 1; oral contraceptive use, 3; and idiopathic, 4. All patients had ascites, hepatomegaly, and/or abdominal pain. Two underwent mesocaval shunting, and 1 had a peritoneal-venous shunt. Seven patients, including 1 with a mesocaval shunt, underwent OLT. The median duration of symptoms before transplantation was 6 months (range, 1.5 to 11 months). Six transplant patients are alive on long-term anticoagulation therapy at a mean post-OLT follow-up of 42 months (range, 2 to 77 months), without recurrence. Of 13 patients treated medically, 10 (77%) are alive at a median follow-up of 40 months (range, 17 months to 14 years 8 months), 1 has died, and 2 have been lost to follow-up. In a majority of patients, symptoms improve with prompt treatment of the underlying hematologic disorder, with a favorable long-term prognosis. Patients with decompensated liver disease can successfully undergo OLT with a low risk of recurrence on long-term oral anticoagulation. (Liver Transpl Surg 1997 Jul;3(4):423-9)     

A 27-year experience with surgical treatment of Budd-Chiari syndrome

OBJECTIVE: To determine the effects of surgical portal decompression in Budd-Chiari syndrome (BCS) on survival, quality of life, shunt patency, liver function, portal hemodynamics, and hepatic morphology during periods ranging from 3.5 to 27 years. SUMMARY BACKGROUND DATA: Experiments in the authors' laboratory showed that surgical portal decompression reversed the deleterious effects of BCS on the liver. This study was aimed at determining whether similar benefit could be obtained in patients with BCS. METHODS: From 1972 to 1999, the authors conducted prospective studies of the treatment of 60 patients with BCS who were divided into three groups: the first had occlusion confined to the hepatic veins treated by direct side-to-side portacaval shunt (SSPCS); the second had occlusion involving the inferior vena cava (IVC) treated by a portal decompressive procedure that bypassed the obstructed IVC; and the third group, who had advanced cirrhosis and hepatic decompensation and were referred too late for treatment by portal decompression, required orthotopic liver transplantation. RESULTS: In the 32 patients with BCS resulting from hepatic vein occlusion alone, SSPCS had a surgical death rate of 3%, and 94% of the patients were alive 3.5 to 27 years after surgery. All 31 survivors remained free of ascites and almost all had normal liver function. No patient with a patent shunt had encephalopathy. The SSPCS remained patent in all but one patient. Liver biopsies showed no evidence of congestion or necrosis, and 48% of the biopsies were diagnosed as normal. Mesoatrial shunt was performed in eight patients with BCS caused by IVC thrombosis. All patients survived surgery, but five subsequently developed thrombosis of the synthetic graft and died. Because of the poor results, mesoatrial shunt was abandoned. Instead, a high-flow combination shunt was introduced, consisting of SSPCS combined with a cavoatrial shunt (CAS) through a Gore-Tex graft. There were no surgical or long-term deaths among 10 patients who underwent combined SSPCS and CAS, and the shunts functioned effectively during 4 to 16 years of follow-up. Ten patients with advanced cirrhosis were referred too late to benefit from surgical portal decompression, and they were approved and listed for orthotopic liver transplantation. Three patients died of liver failure while awaiting a transplant, and four patients died after the transplant. The 1- and 5-year survival rates were 40% and 30%, respectively. CONCLUSIONS: SSPCS in BCS with hepatic vein occlusion alone results in reversal of liver damage, correction of hemodynamic disturbances, prolonged survival, and good quality of life when performed early in the course of BCS. Similarly good results are obtained with combined SSPCS and CAS in patients with BCS resulting from IVC occlusion. In contrast, mesoatrial shunt has been discontinued in the authors' program because of an unacceptable incidence of graft thrombosis and death. In patients with advanced cirrhosis from long-standing, untreated BCS, orthotopic liver transplantation is the only hope of relief and results in the salvage of some patients. The key to long survival in BCS is prompt diagnosis and treatment by portal decompression.     

Caroli's disease and orthotopic liver transplantation.

Caroli's disease is a rare congenital hepatic disease, characterized by segmental dilatation of the biliary tree. Patients who have recurrent bouts of biliary infection, particularly those with complications related to portal hypertension, may require orthotopic liver transplantation (OLT). Few case reports have described the outcome of OLT in patients with Caroli's disease and to date there is no large series reported in the literature. We retrospectively analyzed the outcome of OLT in patients with Caroli's disease who underwent OLT between 1982 and 2002 at Starzl Transplantation Institute, University of Pittsburgh. Patients were identified and data was collected by computerized search of the electronic database system. All patients had confirmation of diagnosis by histopathology of explanted liver. A total of 33 patients with Caroli's disease were listed for liver transplantation, 3 of whom were excluded, as they were not transplanted. A total of 90% had signs of hepatic decompensation at the time of OLT. Median posttransplantation follow-up was 7.7 yr. Short-term graft and patient survival at 1 month was 83% and 86%, whereas overall long-term graft survival rates at 1, 5, and 10 yr were 73%, 62%, and 53%, respectively, and patient survival rates were 76%, 65%, and 56%, respectively. Long-term outcome in patients who survived the first year after transplantation was significantly better. Their survival rate at 5 and 10 yr was 90% and 78%. On univariable analysis, recipient age, donor male gender, coexistent congenital hepatic fibrosis, and re-OLT were associated with poor patient survival. Eight patients were retransplanted, 3 of whom had primary nonfunction. A total of 13 patients died; the most common cause of death being sepsis and cardiovascular complications. Patients who died of sepsis had cholangitis pre-OLT. In conclusion, OLT is a form of curative and life-saving therapy in patients with Caroli's disease, especially in those with decompensated liver disease. Overall survival is better with liver transplantation and is comparable with the survival of recipients who undergo OLT for other etiologies of chronic liver disease. Survival was poor in patients with congenital hepatic fibrosis (Caroli's syndrome) and in those who had cholangitis at the time OLT.     

Eighteen years of liver transplantation experience in patients with advanced Budd-Chiari syndrome.

The long-term results of liver transplantation for Budd-Chiari syndrome (BCS) and timely indication for the procedure are still under debate. Innovations in interventional therapy and better understanding of underlying diseases have improved therapy strategies. The aim of this study was the analysis of patient and disease characteristics, outcome, and specific complications. Between September 1988 and December 2006 we performed 42 orthotopic liver transplantations (OLTs) in 39 patients with BCS. A total of 29 (74%) women and 10 men (26%) had a median age of 35 years; the median follow-up period was 96 months. Etiologically, 27 patients had a preoperative diagnosis of hematologic disease, including myeloproliferative disorders (MPD), followed by factor V Leiden mutation and antiphospholipid syndrome. The actuarial 5-year and 10-year survival rates were 89.4% and 83.5%, respectively, compared to 80.7% and 71.4%, respectively, for other indications (n = 1742). Retransplantation was necessary in 3 patients (7.1%) with portal vein thrombosis or recurrent BCS. Although the number of bleeding events was similar, incidence of vascular complications was significantly higher in patients with BCS. Thrombosis of the portal vein was observed in 4.8% versus 0.8% of the patients, whereas liver veins were affected in 7.1% versus 0.2%. Our data shows that severe acute or chronic forms of BCS with liver failure can be successfully treated by OLT. Despite higher rates of vascular complications, patient and graft survival are similar or even better compared to other indication groups. In conclusion, patients with reversible hepatic damage should be treated by combined strategies, including medical therapy and surgical or interventional shunting.     

Results of portal systemic shunts in Budd-Chiari syndrome.

Nine patients with Budd-Chiari syndrome (BCS) were treated by a portal systemic shunt. One had thrombosis of the superior mesenteric vein (SMV) and another had complete obstruction of the retrohepatic inferior vena cava (IVC). All other patients had a marked stenosis of the retrohepatic IVC with caval pressure ranging from 12 to 24 mmHg (mean: 17 mmHg). Seven patients had an interposition mesocaval shunt using an autologous jugular vein. The patient with a thrombosed SMV had a portoatrial shunt. The patient with an obstructed IVC had a cavoatrial shunt after an erroneous portacaval shunt had failed to relieve ascites. There were no operative deaths and no major postoperative complications. One patient died 19 months after operation of acute leukemia complicating polycythemia rubra vera. All other patients were alive and well 8 months to 6 years after operation. None of them had encephalopathy. These results suggest several comments: Portal systemic shunts are a good treatment for BCS and have a low operative risk. The mesocaval shunt is an efficient procedure, even when there is stenosis of the IVC with high caval pressure; shunts to the right atrium should be performed only in the case of complete obstruction or inaccessibility of the IVC. The long-term prognosis is excellent, except in patients with potential malignancies. Therefore, portal systemic shunts should be indicated early in patients with symptomatic BCS.     

布-加综合征下腔静脉阻塞合并血栓形成的治疗

目的 探讨下腔静脉阻塞并血栓形成的布-加综合征的治疗方法.方法 回顾分析近6年间收治的75例下腔静脉阻塞并血栓形成的布一加综合征患者的临床资料.其中行根治性隔膜切除、血栓取出22例,腔-腔(房)人工血管架桥41例,放射介入+内支架放置12例.结果 73例手术成功,手术死亡2例,手术后下腔静脉压力明显下降.临床症状及体征消失或缓解.随访6个月至6年,复发4例;其中人造血管堵塞2例,再发下腔静脉狭窄2例.结论 对下腔静脉阻塞合并血栓形成的布一加综合征患者,根据阻塞节段及血栓长度选择相应手术方式,大多可以取得满意效果.     

Histological recurrent hepatitis C after liver transplantation: Outcome and role of retransplantation.

Impact of hepatitis C virus (HCV) recurrence on long-term outcome after orthotopic liver transplantation (OLT) is highly variable, and the role of retransplantation is still debated. From 1996 to 2003, 131 OLT with histologically proven HCV recurrence and 6 months of follow-up were retrospectively reviewed. One and 5-yr overall survivals were 90.7 and 81.3%, respectively. The mean time of HCV recurrence was 10.1 +/- 6.2 months in patients whose donor's age was less than 70 yr old, and 6.6 +/- 4.7 in patients whose donor's age was more than 70 (P < 0.01). The mean time between OLT and HCV recurrence was 10.7 +/- 8.2 months among patients still alive, and 5 +/- 4.2 among the 20 who died (P = 0.02). In 16 (12.2%) patients, retransplantation was required for severe HCV recurrence; 5 are still alive and 11 (68.7%) died. The mean survival time was 16.2 +/- 6 months if re-OLT was performed within 12 months from first OLT, and it was 45.9 +/- 10 months if re-OLT was performed later (P < 0.01). In conclusion, donors older than 70 yr are at high risk of early HCV recurrence; expectancy of life is significantly reduced in case of histologically proven recurrence within 6 months. Outcome is quite dismal in patients with early HCV recurrence requiring retransplantation within 1 yr of first OLT.     

肝移植术后门静脉系统血栓形成的诊治

目的 总结肝移植术后门静脉系统血栓形成的临床特点及诊疗体会.方法 回顾2003年1月至2007年2月期间402例接受肝移植患者的临床资料,对其中9例肝移植术后门静脉系统血栓形成的原因、预后及诊治方案进行回顾性分析.结果 9例患者均接受全身抗凝、祛聚治疗,其中1例行经皮腔内血管成形术并血管内支架置入术、1例行经皮门静脉置管溶栓并再次肝移植、1例行外科手术取栓治疗.有6例患者分别于术后9、30、34、40、48、62d死于多器官功能衰竭,3例长期存活.结论 门静脉病变、血流状态改变、高凝状态及手术操作不当是造成术后门静脉血栓形成的主要原因,对高危患者进行预防性治疗,对已形成的病变早期诊断,积极的综合性干预是提高预后的关键.     

Successful Liver Transplantation in a Patient With Budd-Chiari Syndrome Caused by Homozygous Factor V Leiden

Budd-Chiari syndrome (BCS) is a rare form of portal hypertension characterized by hepatic venous outflow obstruction. Although hematologic disorders are the most common cause of this syndrome, to date, 30% of the cases have been classified as idiopathic. Resistance to activated protein C caused by factor V Leiden is the most common cause of thrombophilia; its role in the pathogenesis of BCS is now becoming apparent. We report successful liver transplantation in a patient with BCS caused by homozygous factor V Leiden. The patient was administered standard heparin anticoagulation until activated protein C resistance was normalized by the liver allograft. Liver transplantation corrected the thrombophilic state. The patient has excellent graft function, is not on anticoagulation therapy, and has had no recurrent venous thrombosis at 5 months posttransplantation. Activated protein C resistance caused by the factor V Leiden mutation may be responsible for idiopathic cases of BCS. To avoid unnecessary long-term anticoagulation after liver transplantation, factor V Leiden should be considered as a pathogenic factor in BCS. In addition, because of the high prevalence of factor V Leiden in the world population, cadaveric organ donors with a history of venous thrombosis should be screened for activated protein C resistance lest thrombophilia be transmitted to the recipient. (Liver Transpl 2000;6:654-656.)     

重症下肢深静脉血栓形成治疗的临床研究

目的 探讨综合应用下腔静脉滤器置入、手术取栓、同时处理Cockett综合征、术后抗凝及溶栓等方法 治疗重症下肢深静脉血栓(股青肿)的疗效.方法 回顾近10余年9例重症下肢深静脉血栓患者的临床资料.9例中8例行下腔静脉滤器置入、手术取栓、术后抗凝及溶栓,8例中有7例为左下肢深静脉血栓患者.均发现合并不同程度的Cockett综合征,其中2例同时处理Cockett综合征;9例中1例(左下肢深静脉血栓患者)行下肢静脉溶栓术.结果 所有患者均无肺栓塞发生,经手术的8例患者除1例(左下肢深静脉血栓患者)术后出现湿性坏疽,被迫截肢外,其余7例均取得较为满意的疗效,挽救了患肢.1例行下肢静脉溶栓的患者死亡.1个月后复查彩超,没有同时处理Cockett综合征的5例中有2例左下肢血栓患者复发血栓,但均未再次发展为股青肿.7例随访1.5～10年,均未发生严重并发症.结论 综合应用下腔静脉滤器置人、手术取栓、同时处理Cockett综合征、术后抗凝及溶栓等方法 是治疗重症下肢深静脉血栓(股青肿)的有效方法 ,Cockett综合征是左下肢DVT取栓术后复发的重要原因.     

Treatment of Budd-Chiari syndrome due to inferior vena cava occlusion by combined portal and vena caval decompression.

This study concerns Budd-Chiari syndrome (BCS) caused by occlusion of the subdiaphragmatic inferior vena cava (IVC). It describes the experimental and clinical evaluation of the treatment of this disorder by one-stage combined portal and vena caval decompression with a direct side-to-side portacaval shunt (PCS) and a caval-atrial shunt (CAS) graft. BCS was produced in rats by gradual occlusion of the suprahepatic IVC with an ameroid constrictor. When ascites and portal hypertension were established, 12 control rats survived a sham thoracolaparotomy, 16 rats survived a mesoatrial shunt, and 16 rats survived combined PCS and CAS graft. All control rats re-formed ascites and died within 2 months. Nine of 16 rats with mesoatrial shunt developed graft thrombosis, re-formed ascites, and died within 2 months. In contrast, only 2 of 16 rats that underwent combined PCS and CAS developed graft thrombosis, re-formed ascites, and died. Liver biopsies showed reversal of severe pathologic changes in rats with patent grafts. Clinical evaluation of combined PCS and CAS using a 20-mm ring-reinforced Gore-Tex graft has been undertaken in five patients with BCS and ascites, hepatosplenomegaly, intense hepatic congestion on biopsy, and angiography showing occlusion of both the IVC and hepatic veins. All five patients are alive and well 6 months to 7.5 years postoperatively with patent grafts, no ascites or need for diuretics, no encephalopathy, normal liver function, and reversal of liver pathology. It is concluded that combined PCS and CAS create a high-flow shunt that decompresses both the portal system and IVC, has a low incidence of graft thrombosis, has been consistently effective in relieving BCS caused by IVC occlusion, and appears to be superior to mesoatrial shunt.     

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

BackgroundOrthotopic 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.Case ReportWe 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.DiscussionThis 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.     

Budd-Chiari syndrome in the course of Behcet's disease: clinical and laboratory analysis of four cases

ObjectivesBudd–Chiari syndrome (BCS) is an uncommon manifestation of Behcet's disease (BD) characterized by hepatic venous outflow obstruction either within the liver or in the inferior vena cava (IVC). Clinical and laboratory findings, as well as treatment options and prognosis of four BD patients with BCS, were analyzed retrospectively.MethodsFour male patients with BCS due to BD, ranging in age from 22 to 46 (median 24 years), were included in the present study. The presence of BCS was confirmed by Doppler ultrasonography and computed tomography and/or venography. Levels of protein C, protein S, antithrombin III, anticardiolipin antibodies and lupus anticoagulants were evaluated in all patients during the acute stage of BCS and both 6 months and 1 year after. Activated protein C resistance and prothrombin gene mutation were also determined in three patients.ResultsTwo of the four patients with BCS had already been diagnosed with BD, while the other two were diagnosed with concurrent BD and BCS upon their admission to our clinic. All patients had deep venous thrombosis and superficial migratory thrombophlebitis prior to development of BCS. Case 1 died due to hepatic failure 1 month after his admission. The overall health state of the other three patients has remained good thanks to anticoagulation and immunosuppressive treatments. Three of these patients had one or more than one factor predisposing to thrombosis.ConclusionsThe number of occluded hepatic veins and right hepatic vein involvement, as well as inferior vena cava thrombosis, can be deemed as a major determinant of prognosis. Although the presence of a thrombophilic condition may not be a factor for the clinical prognosis of BCS on its own, it may still necessitate a long-term anticoagulation for prevention of further thrombotic events.     

Proximal deep vein thrombosis after hip replacement for oncologic indications

BACKGROUND: Patients with cancer who undergo surgery about the hip are at increased risk for the development of deep vein thrombosis. We implemented a program of chemical and mechanical prophylaxis to prevent this problem. This study was performed to assess the effectiveness of that program. METHODS: Eighty-seven consecutive patients with an active malignant tumor who underwent hip replacement surgery at our institution over a two-year period were included in the study. All patients were treated with intermittent pneumatic compression devices. Seventy-eight patients received anticoagulants, and nine did not. Postoperative surveillance for proximal deep vein thrombosis was routinely performed on all patients with duplex Doppler ultrasonography. RESULTS: Four patients had proximal deep vein thrombosis, and one patient, who did not receive anticoagulation, had a nonfatal pulmonary embolism. The use of prophylactic low-molecular-weight heparin (dalteparin) was associated with a 4% rate of proximal deep vein thrombosis (three of seventy-eight patients). Proximal deep vein thrombosis developed in three of eight patients with pelvic disease, one of nineteen patients with femoral disease, and zero of sixty patients with hip disease (p < 0.00001). The prevalence of proximal deep vein thrombosis was significantly higher (p < 0.02) following replacements in patients with sarcoma (three of twenty-one) than it was after replacements in patients with carcinoma (zero of fifty-seven) or hematologic malignant disease (one of nine). On multivariate analysis, only the location of the disease (the pelvis, femur, or hip) was found to be independently significant for an association with deep vein thrombosis. A wound complication developed in four of twenty-one patients with sarcoma and no patient with carcinoma or hematologic malignant disease (p < 0.001). The pathologic type was the only factor studied that was independently significant for an association with wound complications on multivariate analysis. CONCLUSIONS: The rate of proximal deep vein thrombosis in patients who had undergone hip replacement for oncologic indications was low when the use of an intermittent pneumatic compression device was supplemented with prophylaxis with low-molecular-weight heparin.     

Thromboembolic complications in patients with advanced cancer: Anticoagulation versus greenfield filter placement

Thirty patients with Stage III/IV cancer and thromboembolic complications between 1987–89 were reviewed. Twelve patients had a deep venous thrombosis proximal to the calf diagnosed by duplex scanning or contrast venography, 15 patients had a pulmonary embolism diagnosed by a high-probability pulmonary ventilation/perfusion scan or arteriogram, and three patients had both deep vein thrombosis and pulmonary embolism. Patients were treated primarily with anticoagulation (Group A =20 patients) or a Greenfield filter (Group B=10 patients). Seventy-five percent (15/20) of the Group A patients developed 19 bleeding or thrombosis-related complications: major bleeding (7), recurrent deep venous thrombosis/pulmonary embolism (4), inability to attain consistent therapeutic anticoagulation levels (3), heparininduced thrombocytopenia (3), or progression of deep vein thrombosis (2). A Greenfield filter was eventually placed in 10 (50%) of the Group A patients without complications. Thirty percent (3/10) of the Group B patients developed progression of deep vein thrombosis that required anticoagulation. One other Group B patient died due to a guidewire-induced arrhythmia. Although patients with advanced cancers and venous thromboembolic disease have a high complication rate with either treatment, initial treatment with a Greenfield filter appears more definitive. Anticoagulation should be reserved for patients with progressive, symptomatic deep vein thromboses after placement of a filter.Presented at the Fifteenth Annual Meeting of the Peripheral Vascular Surgery Society, June 2, 1990, Los Angeles, California.Supported by a grant from the John F. Connelly Foundation.     

Liver Transplantation for Hepatitis C: Recurrence and Disease Progression in 300 Patients

The time progression of allograft damage in patients with recurrent hepatitis C after orthotopic liver transplantation (OLT) is not precisely determined. The aim of this analysis is to study the progression of disease recurrence and its impact on patient and graft survival. Data for 300 patients who underwent OLT for hepatitis C were analyzed regarding the incidence of histological recurrence, risk factors, immunosuppressive regimen, rejection episodes, and survival. For patients with histological recurrence, the timing and risks for disease progression were analyzed. Data for 30 patients who underwent retransplantation were studied. Histological recurrence occurred in 40.3% of patients, 27.2% of whom progressed to bridging fibrosis or cirrhosis. Eighty-seven percent of the patients experienced recurrence of disease within 24 months of OLT. Patients with histological recurrence within 6 months of OLT had an increased risk for progression to cirrhosis compared with patients with recurrence later than 6 months (risk ratio, 2.3). Recurrence within 1 year was associated with decreased patient and graft survival rates at 1 and 5 years (65.1% and 56.4% versus 80.6% and 78.4%; P = .004 andP = .0008, respectively). Patients with histological recurrence had a greater incidence of acute cellular rejection, as well as multiple episodes of rejection, steroid-resistant rejections, and greater cumulative doses of corticosteroids. Histological recurrence after OLT for hepatitis C is common and usually occurs within 2 years of OLT. Early recurrence negatively affects patient and graft survival. Host factors impacting on recurrence need further study. A relation between the hepatitis C virus, allograft rejection, and immunosuppression exists and needs investigation. (Liver Transpl 2000;6:553-561.)     

联合腔肠房人工血管转流术治疗布加综合征14例体会

目的：探讨联合腔肠房人工血管转流术在中青年患者因下腔静脉血栓形成致下腔静脉和肝静脉回流障碍型布加综合征的应用。方法：本组14例，平均年龄28．6岁，均为肝段或长段下腔静脉血栓形成致肝静脉出口阻塞，其中12例下腔静脉完全阻塞，2例为肝段下腔静脉严重狭窄，采用3种腔肠房人工血管转流术，分别应用11例，1例和2例。结果：围手术期无死亡，随访时间4－52个月，平均24个月。方法：（1）术后2例人工血管因栓形成，1例最后改行腹膜腔颈内静脉腹水转流术；另1例并发上消化道出血，肝昏迷死亡。随访期死亡率为7％，总人工血管通畅率为86％，而腔房人工血管的通畅率为93％，本组患者门静脉压力下降范围为5－26cmH2O，平均下降15．5cmH2O，无其他严重并发症。结论：对于下腔静脉长段血栓致下腔静脉和肝脉回流障碍的中青年患者，联合腔肠房人工血管转流术不失为一种能同时缓解门脉和下腔静脉高压的手术方法，其远期通畅率尚有待于进一步评价。     

Post-liver transplant acute renal failure: factors predicting development of end-stage renal disease

BACKGROUND: Acute renal failure (ARF) occurs in 5-50% of patients undergoing orthotopic liver transplantation (OLT). The aim of this study was to determine factors that might predict the development of end stage renal disease (ESRD) in patients who had ARF after OLT. METHODS: We studied all OLT recipients between 9/1/1988 through 12/31/2000. RESULTS: A total of 1602 patients underwent OLT during the study period. About 350 patients (22%) developed ARF requiring dialysis post-operatively. One hundred and twenty-three (39.8%) died within a year after OLT. Median follow up was 5.8 yr (range 1-12 yr). Forty-three patients (23%) developed ESRD over median of 3.79 yr (range 1-8 yr). Multivariate logistic regression analysis revealed creatinine levels > 1.7 mg/dL at 1 yr (p < 0.001), cyclosporine as immunosuppression (p = 0.026), and the presence of diabetes pre-OLT (p < 0.001) to be associated with the development of ESRD. The development of ESRD did not decrease patient survival (p = 0.111). ESRD patients who received subsequent kidney transplantation had significantly improved survival rates (p = 0.005). CONCLUSIONS: Serum creatinine levels at 1 yr, cyclosporine as immunosuppression, and the presence of diabetes pre-OLT are independent predictive factors for the development of ESRD. ESRD patients who received kidney transplantation had higher 10-yr survival rates when compared with patients maintained on dialysis.