肝移植术后肝动脉血栓形成的预防

目的 探讨肝移植术后肝动脉血栓形成(hepatic artery thrombosis,HAT)的预防.方法 2004年1月至2007年12月我院器官移植科共实施596例成人尸肝移植,自2005年开始采取综合措施预防HAT形成,包括术中重建变异肝动脉,受体肝动脉条件不好的患者采取供体肝动脉与受体腹主动脉搭桥,动脉吻合全部采用显微缝合技术,术后常规监测移植肝血流,对肝动脉峰值流速低于40 cm/s的患者行抗凝治疗.比较2004年实施的181例肝移植患者(A组)与2005-2007年实施的415例肝移植患者(B组)HAT发生情况.结果 A组共有8例患者出现HAT,发生的中位时间为术后11 d(3～41 d),3例表现为急性肝功能恶化,3例表现为胆漏,1例表现为肝脓肿,1例无明显临床症状.B组共有6例患者出现HAT,发生时间为术后8 d(1～21 d),3例表现为急性肝功能恶化,1例表现为胆漏,2例无明显临床症状.B组患者HAT发生率明显低于A组(1.44%vs4.42%,X~2=4.86,P=0.027).A组3例行再次肝移植,共死亡5例,B组3例行肝动脉重建联合肝动脉局部溶栓治疗,2例患者康复出院,1例患者因严重感染、肾功能衰竭死亡.3例患者接受再次肝移植.结论 肝动脉血栓形成是肝移植术后的严重并发症,术中采用显微缝合方式,注意重建变异肝动脉,术后严密监测,及时抗凝治疗可以有效预防肝动脉血栓形成.     

肝移植术后肝动脉血栓形成的溶栓治疗3例报道

目的 探讨肝移植术后肝动脉血栓形成的溶栓治疗价值。方法对50例同种异体肝移植病例，术后以彩色多普勒超声(CDI)定期监测肝动脉血流，怀疑肝动脉血栓形成(HAT)行动脉造影，确诊3例，即刻行介入溶栓治疗，经导管分别在20分钟内予尿激酶12．5万单位、30分钟内予尿激酶25万单位和肝素50mg，及4小时内注入尿激酶60万单位。结果3例溶栓治疗后，肝动脉均再通。1例因二次血栓形成再次溶栓成功。但均发生不同程度的腹腔内出血，1例保守治疗痊愈，1例经开腹手术止血后痊愈，另1例死于多器官功能衰竭。结论对怀疑HAT病例，应尽早行动脉造影。改进后的溶栓疗法有可能成为治疗HAT的可选择方法。     

肝移植后肝动脉血栓形成的危险因素及防治措施

目的探讨肝移植后肝动脉血栓形成的好发因素及其防治措施。方法收集国内、外近年来关于肝移植后肝动脉血栓形成的好发因素及防治方面的文献并作一综述。结果肝移植后肝动脉血栓形成的好发因素有第五因子莱顿、受体的代谢性肝脏疾病和受体的性别、肝移植中Roux-en-Y法胆管重建术的应用、病毒感染等方面;防治措施主要有早期诊断、检测激活蛋白C抵抗性与预防性应用抗凝剂、改进肝动脉重建的方法、高压氧疗法、经导管持续溶栓治疗、再次肝移植等方面。结论肝移植后肝动脉血栓形成的好发因素及其防治措施的研究对改善肝移植患者的预后有指导作用。     

肝移植后无症状性肝动脉血栓形成一例

目的 探讨导致移植肝动脉阻塞后无症状的可能原因。方法 通过肝功能监测、彩色多普勒超声、肝动脉造影、肝组织活检以及胆道造影等手段追踪观察肝动脉血栓形成的临床经过，综合分析导致“无症状”的各种可能因素。结果 肝移植术后第4d肝动脉吻合出现血栓形成，至20d肝动脉接近完全阻塞；肝组织学检查见肝内胆汁淤积、肝细胞水样变性、小胆管上皮细胞萎缩以及汇管区纤维化等病理学改变。肝功能检查提示除γ0谷氨本主酶和碱笥磷酸酶升高之外，肝功能恢复顺利。术后71d血管造影显示肝动脉完全阻塞，但有侧枝循环建立和门静脉代偿性扩张。术后患者始终未出现肝动脉阻塞所特有的临床症状。结论 侧枝循环的建立和门静脉的代偿，使移植肝得以存活；术后2周之内经常进行彩色多普勒超声检查对肝动脉血栓形成的早期诊断有帮助。     

原位肝移植术中肝动脉变异及术后肝动脉血栓形成的处理

目的探讨肝移植术中肝动脉变异及术后肝动脉血栓形成的处理。方法统计2000年8月至2002年12月期间进行肝移植术的67例次供、受者肝动脉的变异情况；分析肝动脉的重建方式，探讨肝动脉变异与手术后肝动脉血栓形成的关系、肝动脉血栓形成的危险因素及肝动脉血栓形成后的处理。结果67例次供者肝脏和65例受者肝脏共出现肝动脉变异12例次，发生频率最高的为右肝动脉起源于肠系膜上动脉(5例)及左肝动脉起源于胃左动脉(3例)。肝动脉的重建方式如下：供者及受者肝总动脉与胃十二指肠动脉分叉处成型后吻合58例；腹主动脉与肝动脉搭桥2例；利用变异的肝动脉分支吻合7例。手术后发生肝动脉血栓形成3例，均经腹股沟处股动脉插管行肝动脉溶栓治疗，此3例患者中死亡1例。结论避免变异的肝动脉损伤、选择适当的肝动脉吻合方式可以保证移植肝脏的动脉血供。肝动脉血栓形成与肝动脉变异无关。作为肝动脉血栓形成后的保守治疗方法，肝动脉内溶栓治疗有可能避免2次移植。     

成人肝移植术后早期肝动脉血栓形成的诊断与治疗

目的 探讨成人肝移植术后肝动脉血栓形成(hepatic artery thrombosis,HAT)的诊断与治疗,及其对患者预后的影响.方法 2007年6月至2010年10月我中心共实施成人尸体肝脏移植387例.术后采用床边彩色多普勒超声监测移植肝血流.疑有肝动脉血栓形成时,采用超声造影或肝动脉造影明确诊断,根据病情采用介入溶栓治疗、手术再血管化治疗及再次肝移植等治疗.结果 387例中术后共有10例患者发生HAT,发生率2.6％.发生HAT的中位时间为肝移植术后7(范围2～18)d.2例采用介入溶栓治疗,其中1例伴肝动脉狭窄放置支架,均痊愈;3例再次手术行肝动脉重建联合肝动脉局部溶栓治疗,其中1例术后再次出现HAT,死亡;2例行再次肝移植,痊愈;3例出现肝内脓肿,严重感染,肝功能恶化死亡.死亡率为40％(4/10).结论 肝移植术后常规彩色多普勒超声监测肝动脉血流是早期发现HAT的关键,超声造影及肝动脉造影可明确诊断;及时采用介入溶栓、手术再血管化及再次肝移植等治疗虽然可减少患者死亡,但预防HAT发生更为重要.     

活体肝移植术后肝动脉血栓形成的危险因素

肝动脉血栓形成(HAT)是活体肝移植术后的严重并发症之一,为研究与HAT相关的危险因素,作者收集了1990.6~2004.11的222例活体肝移植病例进行分析。全组病例的术后平均随访时间为1777天,其中成人113例,儿童109例。当彩色多普勒超声及三维螺旋CT或肝血管造影发现肝动脉血流完全断流后即确珍为肝动脉血栓形成。作者将以下因素作为相关危险因素列入研究:供体的性别、年龄、体重,受体的性别、年龄、体重、原发肝病种类、术前PT、动脉重建方式,受体与供体的体重比例,二次肝移植。结果:所有病例术中血管重建完成后即开放血流,其中12例(5·4%)发生…     

原位肝移植术后肝动脉血栓形成的诊断和治疗

目的探讨原位肝移植术后肝动脉血栓形成的诊断与治疗。方法回顾性分析我科1996年10月至2004年3月施行的98例次原位肝移植术．其中8例原发性肝癌患者术前有多次TACE史。结果本组病例仅术前有多次TACE史的患者发生肝动脉血栓5例,均经选择性血管造影证实。3例、1例和1例受者分别接受介入溶栓、再血管化手术和再次肝移植。与肝动脉栓塞有关的死亡率为60％(3／5)。结论术前多次TAcE史是移植术后发生肝动脉血栓的高危因素。彩色多普勒超声是监测血管并发症的首选方法。再血管化手术或再次肝移植是治疗肝动脉血栓的有效方案。     

原位肝移植肝动脉血栓形成的预防和治疗

目的 总结原位肝移植肝动脉重建及其并发症的防治经验，以提高肝移植疗效和受体存活率。方法 分析9年间实施的85例原位肝移植患者的临床资料。肝动脉重建采用供者腹腔动脉干Carrell’s袖片或肝总动脉-脾动脉汇合部与受者肝左-右动脉部吻合16例(18．82％)，与受者胃十二指肠-肝固有动脉汇合部吻合61例(71．76％)，采用髂动脉-腹主动脉搭桥8例(9．42％)。术后根据凝血酶原时间(PT)，使用普通肝素或低分子肝素预防性抗凝。术中、术后应用多普勒超声监测肝动脉血供。结果 1例术中发生肝动脉血栓形成(HAT)，立即行血栓切除，重新吻合动脉，现已随访13个月，肝动脉保持通畅。其余84例随访2～54个月，未见HAT发生。全组HAT发生率为1．2％。结论 正确选择肝动脉重建吻合的部位和术后有效的抗凝治疗可以减少HAT的发生；多普勒超声监测能早期发现HAT，挽救移植物，避免再移植。     

导管接触性溶栓治疗在肝移植术后早期肝动脉血栓形成中的应用

目的探讨肝移植术后早期肝动脉血栓形成(EHAT)的导管接触性溶栓(CDT)治疗的有效性和安全性。方法 2009年1月～2019年11月接受CDT治疗的肝移植术后EHAT病人23例。结果本组均接受CDT治疗,放置CDT导管手术操作平均时间(78±24)分钟,溶栓治疗平均时间(87.4±22.8)小时,尿激酶平均用量(344.5±62.3)万U,经CDT治疗,19例肝动脉内血栓完全溶解,CDT治疗有效率为82.6%(19/23)。溶栓过程中,腹腔轻微出血(100 ml)2例,无其他相关并发症发生。平均随访时间(60.4±3.7)个月,19例肝动脉血栓完全溶解病人术后1年、2年、5年肝动脉通畅率分别为94.7%(18/19)、89.5%(17/19)、79%(15/19)。结论 CDT是一种安全、有效、微创的治疗方式,在肝移植术后EHAT病人的治疗及预后过程中发挥了重要作用。     

Hepatic artery thrombosis in pediatric liver transplantation

PURPOSE: Children have been reported to be at greater risk for hepatic artery thrombosis when compared to adults due to small arterial size, nonuse of intraoperative microscope, and postoperative hypercoagulable state. METHODS: We evaluated arterial anastomosis type, intraoperative field magnification, and hepatic artery complications and how they were managed. All patients underwent ultrasound, anticoagulation consisted of 41 mg aspirin once a day, and 35 patients received alprostadil (PGE) for the first 7 days after transplantation. No patients were administered intravenous heparin following liver transplantation. RESULTS: Of the 74 livers transplanted, 36 grafts (48.6%) were whole organ transplants and 38 grafts (51.4%) were partial livers. We observed HAT in 1 of 74 (1.35%) transplants in our pediatric liver transplant population. The only patient with HAT was a young girl with a history of biliary atresia. The occurrence of a hepatic artery thrombosis on day 7 was caused by the migration of an intimal plaque dissection within the artery graft. She was emergently taken back into the operating room for graft revision. This individual currently has a survival time of 426 days following her last transplant. CONCLUSIONS: Hepatic artery thrombosis may be minimized in pediatric liver transplantation without the use of microsurgery. Anticoagulation utilizing ASA and alprostadil is sufficient to avoid HAT. Accurate use of ultrasound is crucial to avoid this complication. Graft and patient salvage is possible with expedient surgical treatment; microsurgery, anticoagulant therapy, site of arterial inflow, and recipient size and weight.     

Hepatic artery thrombosis in pediatric liver transplantation

The incidence of hepatic artery thrombosis was analyzed in a series of 59 consecutive liver transplants performed in 52 children less than 15 years of age at the University of Louvain Medical School, Brussels, from March 1984 to March 1987. This incidence was 17% for the whole series; it was increased in small recipients less than 3 years of age and less than 15 kg (23%) in weight, as well as when the liver was harvested from a small donor less than 15 kg in weight (38%). It was also increased when the donor liver was supplied by more than one artery. This incidence was markedly reduced by arterial revascularization from the aorta, either directly or by interposition of an iliac segment; the reduced-size livers had a much lower incidence of arterial thrombosis (5%) than the whole livers (23%). In the present series, we did not find any argument to support the view that poorly controlled rejection could be implicated in the pathogenesis of arterial thrombosis.     

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目的 探讨原位肝移植术后肝动脉血栓形成的诊治经验。方法 总结３４例原位肝移植术后的临床资料,结合文献,分析肝移植术后肝动脉血栓形成的诊断和不同治疗方法的结果。结果 本组肝动脉血栓形成发生率为８．８％（３／３４）,３例均经彩超检查诊断,例１术后第５７天死于上消化道出血,经尸检证实,例２和例３经肝动脉造影证实后给予动脉内溶栓,球囊扩成形及放置血管内支架等介入治疗,病人分别在术后第１８,６５天死于感染和     

Hepatic artery thrombosis and liver malignancy in pediatric liver transplantation

BackgroundHepatic artery thrombosis (HAT) remains a significant cause of graft failure and mortality after pediatric liver transplantation. Conditions not associated with hepatic failure, such as liver tumors, may be more prone to thrombotic problems after transplant. We hypothesized that liver transplant for hepatic malignancies may be associated with increased rates of HAT in the posttransplant period.MethodsWe conducted a retrospective review of pediatric patients (age, 0-21 years) who underwent primary liver transplantation at a free-standing children's hospital from 1990 to 2009. We reviewed cause of underlying liver disease, age, sex, weight, occurrence of HAT, use of antiplatelets and anticoagulants perioperatively, as well as reintervention, retransplant, and death.ResultsA total of 129 children underwent 146 liver transplants, and 15 (12%) patients developed HAT. Nine liver transplants were performed for hepatic malignancy, and 4 (44%) of these patients developed HAT (relative risk, 4.85; 95% confidence interval, 1.9-12.2; P = .0015). All 4 children with hepatic malignancy and HAT required reintervention, including 3 retransplants (75%). One of these patients died.ConclusionsHepatic artery thrombosis occurs approximately 5 times more often and appears to be more morbid in children with hepatic malignancy after transplantation. Prospective evaluation of prophylactic anticoagulation regimens in the setting of hepatic malignancy requiring transplantation is warranted.     

Hepatic artery reconstruction for hepatic artery thrombosis after orthotopic liver transplantation

We evaluated the efficacy of reconstruction of the hepatic artery for intraoperative or postoperative thrombosis in orthotopic liver transplantation. Of 37 grafts with artery thrombosis, 13 (35.1%, 6 intraoperative and 7 postoperative) underwent reconstruction of the hepatic artery. The arterial flow was reestablished and maintained in 5 (38.5%) of the 13. Recurrent thrombosis in the other 8 grafts developed 2 to 24 days (mean, 13.8 days) after transplantation. Reconstruction was successful in 50% (4/8) of the adults, compared with only 20% (1/5) of the children. Satisfactory results were obtained when a definitive cause of thrombosis could be identified. We conclude that early recognition and correction of the cause of hepatic artery thrombosis during or after orthotopic liver transplantation, especially in adults, is often a graft-saving and lifesaving procedure worthy of consideration.     

Endovascular treatment of hepatic artery thrombosis following liver transplantation

Hepatic artery thrombosis (HAT) is the most frequent vascular complication following orthotopic liver transplantation. Urgent retransplantation has been considered as the mainstay therapy. Surgical revascularization is an effective alternative in asymptomatic patients. Endovascular therapies including intra‐arterial thrombolysis, percutaneous transluminal angioplasty (PTA), and stent placement have shown encouraging results in recent years; however, their use remains controversial because of potential risk of hemorrhage. Until June 2009, 69 cases were published in 16 reports describing therapeutic potential of endovascular modalities. Interventions were performed as early as within 4 h to as late as 120 days in patients ranging from 4 months to 64 years of age. Majority of published reports suggested the use of urokinase. Thrombolysis was successful in 47 out of 69 (68%) patients. Bleeding was the most common complication including fatal intra‐abdominal hemorrhage in three patients. Twenty‐nine out of 47 (62%) patients underwent further intervention in the form of PTA, stenting, or both. The follow‐up patency ranged from 1 month to 26 months. In conclusion, whenever possible, efforts should be made to rescue the liver grafts through urgent revascularization (surgical and/or endovascular) depending on patient’s condition and interventional expertise at the transplant center; reserving the option of retransplantation for failure, complications, and cases with severe clinical symptoms or allograft dysfunction.