肝移植术中超声检查对肝动脉并发症的应用价值

目的　探讨肝移植术中超声 (IOUS)对肝动脉并发症的应用价值。方法　对 2 6例肝移植受者施行IOUS检查 ,以峰值速度 (HAV) >4 0cm/s和阻力指数 (RI) >0 5为正常肝动脉的标准。结果　共施行 2 7例次IOUS检查 ,其中检查阳性 (HAV <4 0cm/s或RI <0 5 ) 7例次 ,经 0 5 %普鲁卡因浸泡 ,解除血管痉挛或再次吻合后 ,仍未能达到上述标准的 3例中术后出现HAT和HAS各 1例 ,其余病人术后均未出现肝动脉并发症。IOUS对动脉并发症诊断的敏感度、特异度、阳性预测价值和阴性预测价值分别为 10 0 % (2 / 2 )、96 % (2 4 / 2 5 )、6 6 7% (2 / 3)和 10 0 % (2 4 / 2 4 )。结论　IOUS对肝动脉并发症较高的诊断价值 ,吻合后肝动脉RI应大于 0 5 ,HAV应大于 4 0cm/s ,对于RI <0 5 ,HAV<4 0cm/s的病例在排除动脉扭曲成角和解除血管痉挛后仍不能达到上述标准者应重新吻合肝动脉。     

原位肝移植术后胆道并发症的预防与诊治

目的　探讨肝移植术后胆道并发症的预防、诊断和治疗。　方法　对 1993年 4月～2 0 0 1年 11月我科实施的 12 3例肝移植患者临床资料进行回顾性分析。　结果　 12 3例肝移植患者中11例通过胆道造影确诊为肝移植术后胆道并发症 ,9例治愈 ,1例好转 ,死亡 1例。胆道并发症发生率为 8 9% ( 11/ 12 3) ,与胆道并发症相关的死亡率为 0 8% ( 1/ 12 3) ,与T管相关的胆道并发症发生率为4 2 % ( 5 / 119) ,与肝动脉供血相关的胆道并发症发生率为 1 6 % ( 2 / 12 3)。热缺血时间 >3min、冷缺血时间 >8h组胆道并发症发生率明显升高 (P <0 0 5 )。　结论　保存性损伤和缺血性损伤是肝移植术后胆道并发症的重要原因。修肝时应维护肝外胆管的血供和警惕变异胆管的存在。改进T管置管方法可显著降低与T管相关的胆道并发症发生率。术后早期胆道造影有助于及时诊断胆道并发症。介入技术是胆道并发症的主要治疗手段。     

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目的 探讨肝移植术后血管并发症的诊断与治疗。方法 回顾性分析1993年4月至2002年8月施行的180例次原位肝移植的临床资料。结果 发生血管并发症19例(10．6％)，18例经选择性血管道影证实，1例经尸体检查证实。彩色多普勒超声(CDI)的诊断敏感度和特异度分别为94．7％和92.5％。术中超声检查(I0US)对动脉并发症诊断的敏感度和特异度分别为100％和96.0％。11例、3例、3例和1例受者分别接受介入、再血管化、保守治疗和再次肝移植。与血管并发症有关的病死率为3.9％(7／180)。结论 CDI是监测血管并发症的首选方法，选择性血管造影是早期诊断血管并发症必不可少的手段。应根据血管并发症类型、诊断时间、全身情况、有无其他并发症、肝功能损害程度等来决定血管并发症的治疗方案。非肝动脉的血管并发症首选介入方法治疗，肝动脉血栓形成或狭窄则应选择再血管化或再次肝移植，部分病人可尝试保守治疗。     

婴幼儿活体肝移植后的血流动力学变化及血管并发症

目的 探讨婴幼儿活体肝移植术后的血流动力学变化及血管并发症的发生情况.方法 应用彩色多普勒超声观测34例婴幼儿活体肝移植术后2个月内门静脉、肝动脉、肝左静脉最大流速及肝动脉阻力指数变化情况,并观察术后血管并发症的发生情况及其预后.结果 34例受者中,术后超声显示血管通畅者29例(85.3%,29/34),发生血管并发症5例(14.7%,5/34).29例血管通畅的患儿,术后第1天时门静脉最大流速(vmax)为(53.97±21.44)cm/s,肝动脉收缩期最大流速(PSV)为(52.88±17.87)cm/s,阻力指数(RI)为0.73±0.09,肝左静脉最大流速为(40.53±25.07)cm/s.与术后第1天比较,术后1周时门静脉vmax、肝动脉PSV、肝左静脉vmax及肝动脉RI的差异均无统计学意义(P＞0.05);术后2周时门静脉vmax为(44.26±17.43)cm/s,明显低于术后第1天(P＜0.05);术后2个月时门静脉vmax为(40.31±26.29)cm/s,肝动脉PSV为(41.50±8.67)cm/s,均明显低于术后第1天(P＜0.01,P＜0.05).5例血管并发症均发生在术后7 d内,其中肝动脉血栓形成3例(2例行取栓术,1例行溶栓治疗),门静脉血栓形成2例(1例行取栓术,1例行溶栓治疗),5例中3例死亡.结论 婴幼儿活体肝移植术后门静脉vmax和肝动脉PSV呈下降趋势;血管并发症发生时间早,发生率较高,活体肝移植术后7 d内至少应每天进行1次超声检查.     

彩色多普勒超声对肝移植术后11例血管并发症的诊断

目的评价彩色多普勒超声对肝移植术后血管并发症的诊断意义。方法回顾性分析和总结11例肝移植术后血管并发症的彩色多普勒超声检查资料,检测指标包括肝动脉及左右分支的峰值速度、阻力指数、加速度及加速时间,门静脉平均流速。结果5例经手术或造影证实为动脉并发症(血栓形成2例,肝动脉狭窄2例,肝动脉痉挛1例),彩色多普勒超声表现有肝动脉狭窄处的高速高阻血流并伴有湍流,而狭窄远端肝内动脉峰值速度<40cm/s,阻力指数<0.5,加速时间>0.08s,加速度<300cm/s2,2例肝动脉血栓形成肝门部无动脉血流信号;6例为门静脉并发症(3例门静脉狭窄,3例门静脉血栓形成)。结论彩色多普勒超声对肝移植术后血管并发症的诊断具有重要的指导意义。     

彩色多普勒超声在肝移植术后发生肝动脉狭窄及其围介入治疗中监测价值

目的探讨彩色多普勒超声在肝移植术后发生肝动脉狭窄及其围介入治疗中的监测作用。方法回顾性分析71例原位肝移植病人的超声检查资料,其中发生肝动脉狭窄并进行介入治疗的5例,并与同期血管造影对照。结果发生肝动脉狭窄病人彩色多普勒血流显像(CDFI)可见肝动脉纤细迂曲,多呈间断性星点闪烁状;近狭窄处肝动脉血流峰速(S1)升高(163．62±14．66)cm／s,远端动脉血流峰速(S2)降低(19．10±3．91)cm／s;阻力指数(RI)降低(0．38±0．07);收缩期血流加速时间(SAT)延长(98．00±9．41)ms;行经皮血管成形术,当狭窄部分、全部解除时,肝动脉各段血流峰速均相应不同程度向正常恢复,S1为(73．68±8．81)cm／s;S2为(37．18±4．80)cm／s,而阻力指数仍长时间维持降低(0．42±0．06),SAT长时间维持延长(98．20±6．80)ms。结论彩色多普勒超声在肝移植术后发生肝动脉狭窄及其围介入治疗中具有较高监测价值。     

原位肝移植术后动脉并发症的诊断与治疗

目的 探讨肝移植术后动脉并发症的早期诊断与治疗方法。方法 回顾性分析本院180例次原位肝移植术后动脉并发症的监测、诊断与处理。结果 动脉并发症发生率为5．0％(9／180)，其中肝动脉血栓形成(HAT)5例，肝动脉狭窄(HAS)3例，腹腔动脉狭窄1例。8例动脉造影证实，1例尸检证实。彩色多普勒超声(CDI)的诊断敏感度和特异度分别为88．9％和95．9％；术中超声(IOUS)的敏感度、特异度，阳性预测值和阴性预测值分别为100％，96．0％，66．7％和100％。3例患者接受介入治疗、3例接受再血管化手术、2例分别接受再次肝移植和非手术治疗。3例治愈，6例死亡。结论CD1是监测动脉并发症的首选方法；IOUS有助于术中的早期诊断。HAS和HAT治疗应首选再血管化或再次肝移植；介入溶栓的疗效不佳；个别患者可尝试非手术治疗。     

原位肝移植术后胆道并发症治疗经验

目的总结原位肝移植术后胆道并发症的治疗经验。方法1999年2月至2004年2月,我中心采用胆总管-胆总管端端吻合术施行原位肝移植236例,96例采用置“T”管引流的胆管间断吻合;39例采用未置“T”管的胆管间断吻合技术;101例采用未置“T”管、前壁间断后壁连续的胆管吻合。结果全组术后32例(13·3%)发生胆道并发症,其中胆管狭窄24例(10·0%),胆漏6例(2·5%),胆管结石2例(0·8%)。3组胆道并发症发生率分别为17·7%、15·4%和7·9%,其中肝门部/肝内胆管狭窄发生率分别为8·3%,2·6%和1·0%。第3组胆道并发症发生率和胆管狭窄发生率显著降低(P<0·05)。20例胆管狭窄患者接受放射和/或内镜介入治疗,其中单纯吻合口狭窄治愈率90%,肝门部/肝内胆管狭窄治愈率60%。结论弃用“T”管的胆管前壁间断后壁连续的吻合方式能显著减少胆道并发症;非缺血相关性胆管吻合口狭窄和单纯肝门部胆管狭窄应首选介入治疗。     

肝移植血流动力学参数的变化及其临床意义

目的利用彩色多普勒超声检测移植肝血流动力学的参数,探讨参数变化的临床意义。方法利用彩色多普勒超声检测65例肝移植患者不同时期的肝动脉、肝静脉及门静脉的峰值血流速度(PS)、时间平均血流速度(TAV)、阻力指数(RI)及肝动脉血流灌注指数(DPI)。结果术后15d内,移植肝正常者门静脉TAV及肝动脉RI均明显高于对照组(P<0.05);肝动脉PS及DPI均明显低于对照组(P<0.05)。肝动脉血栓形成时,肝动脉PS明显降低,门静脉TAV明显增高,呈锯齿波。发生排斥反应时,门静脉TAV降低,肝动脉PS降低、RI增高,肝静脉三相波消失,呈锯齿波。结论利用彩色多普勒超声监测移植肝的血流动力学参数变化,可为移植肝的血管并发症及排斥反应的诊断提供辅助依据,且安全、无创。     

经内镜逆行胆管造影在肝移植术后胆管并发症中的应用价值

目的探讨经内镜逆行胆管造影在肝移植术后胆管并发症中的应用价值。方法回顾分析本中心2003年10月至2006年3月经内镜逆行胆管造影诊断及治疗的71例肝移植术后胆管并发症的资料。71例胆管并发症包括52例胆管狭窄、6例胆漏和13例胆管结石。结果经内镜逆行胆管造影诊断胆管狭窄、胆漏和胆管结石的成功率分别为98．1％（51／52）、100％和100％（13／13）。经内镜逆行胆管造影介入治疗胆管吻合口狭窄、肝外型、肝门型、肝内型和弥漫型胆管狭窄的治愈率分别均为66．7％、66．7％、0、0和0,治疗胆漏的治愈率为66,7％,治疗胆总管结石和肝内胆管结石的治愈率分别为77．8％和0。结论经内镜逆行胆管造影是肝移植术后胆管并发症的有效诊断方法。不同类型的胆管并发症经内镜逆行胆管造影介入治疗的疗效不同。经内镜逆行胆管造影介入治疗仅能治愈部分胆管并发症（如胆管吻合口狭窄、肝外型胆管狭窄、轻中度胆漏及胆总管结石）。     

Biliary Atresia: histopathologic observations and reflections upon its natural history

Operative liver biopsies and specimens of the extrahepatic ducts and porta hepatis have been studied in 12 cases of biliary atresia. In all cases, the liver showed giant cell transformation and inflammation with mononuclear cells and neutrophils. Most had other features of neonatal hepatitis, including necrosis of hepatocytes. In the intrahepatic bile ducts of all cases but one, the hepatic ducts and glands at the porta hepatis, and in the extrahepatic ducts where epithelium remained, there was degeneration of the epithelium and intramural inflammation. In the ducts at the porta hepatis and in 6 of 8 extrahepatic ducts where epithelium remained, there was extensive mural fibrosis compromising the diameter of the duct lumens. Three cases showed the inflammatory changes distal to sites of closure of the extrahepatic ducts. These findings demonstrate that in biliary atresia, hepatitis, intrahepatic cholangitis, and sclerosing cholangitis of the extrahepatic ducts all interact to produce acquired obstruction to bile flow.     

New clues for the developing human biliary system at the porta hepatis

The human biliary system is formed from the hepatic diverticulum, a structure which develops from the embryonic foregut in the fourth week of gestation. The cephalic portion of the hepatic diverticulum lies within the septum transversum, and gives rise to entodermal cells which become the primitive hepatocytes. The caudal part of the hepatic diverticulum is molded by mesenchyme to form the gallbladder, cystic duct, and extrahepatic bile duct. The gallbladder is initially tubular in shape, and undergoes morphological changes to become saccular during the 11th week of gestation. The extrahepatic bile duct elongates and widens as gestation progresses, and intramural mucus glands develop. There is no solid stage during the development of the extrahepatic bile duct. The extrahepatic bile duct is a well-defined tubular structure by the 6th week of gestation, whereas the intrahepatic biliary system during this period of gestation is represented by the primitive ductal plate. The ductal plate undergoes structural changes from the 11th week of gestation, beginning at the porta hepatis and progressing through gestation to the periphery of the liver. This remodeling process shapes the ductal plate from a flat sheath of biliary epithelium surrounding the portal vein branches into a network of interconnecting tubular structures. Mesenchyme plays an important role in ductal plate remodeling. The intrahepatic biliary system is in luminal continuity with the extrahepatic bile duct throughout gestation at the porta hepatis. The major bile ducts at the porta hepatis are fully formed by the 16th week of gestation. Received: September 30, 2000 / Accepted: January 10, 2001     

Correlation between graft arterial anatomy and biliary complications after liver transplantation

Knowledge of the arterial vascular anatomy of the liver is important for orthotopic liver transplantation (OLT) because the lack of an adequate arterial blood supply results in biliary and parenchymal complications or graft loss. A number of reports have shown a relationship between aberrations of graft arteries and an increased incidence of early or late complications. Recent studies suggest no differences unless multiple anastomoses are required. The aim of this study was to report the incidence of aberrant hepatic arterial anatomy and its impact on vascular and biliary complications. We retrospectively reviewed data of 90 OLT performed on 82 patients, including 4 who underwent retransplantation from March 2003 to March 2006. The means recipient age was 52.47 years and 49 were men. The main caval vein reconstruction technique was piggyback (n = 55; 61.2%). The biliary reconstruction was performed by an end-to-end choledocho-choledocho anastomosis in 83 cases (92.3%) with choledocho-jejunal anastomosis (Roux-in-Y) in 7 cases (7.7%). Aberrant arterial anatomy was noted in 20 liver grafts (22.2%), namely, accessory right hepatic artery (n = 6; 6.6%), accessory left (n = 10; 11%), both accessory right and left (n = 3; 3.3%), and hepatic common artery from mesenteric artery (n = 1; 1.1%). Among the transplantations of grafts with aberrant arterial anatomy, 2 cases (10%) developed hepatic artery thrombosis (HAT) and 4 (20%) biliary complications. The rate of HAT and biliary complications among grafts with normal arterial anatomy was 3 and 8 cases (4.2% and 11.42%), respectively. Despite a greater number of complications among OLT with aberrant arterial anatomy, the Fisher test showed no significant relationship between HAT or biliary complications and aberrant arterial anatomy.     

深低温对肝脏Glisson管道三级分支以上区域的冷冻效应

目的了解深低温对肝脏Ghsson管道三级分支以上区域的冷冻效应。方法30只小猪，随机分为4组．用平底冷冻头分别对A组动物第一肝门部、B组动物左肝外叶的Ghsson管道、C组动物左肝外叶Ghsson管道的主要分支区域进行3分钟的直接深低温冷冻（冷冻时阻断肝门）；对照组：仅阻断肝门3分钟。术后观察动物血清肝功能的改变，患肝的病理变化，并用彩超了解受冻管道的情况。结果A组动物肝门部的胆管系统在冷冻后出现严重损伤．表现为进行性、不可逆的胆管坏死、狭窄、胆瘘、化脓性胆管炎等并发症，肝门部较大坏死物质也会对门静脉造成压迫；在B、C组，冷冻可造成受冻部位肝实质、胆管及门静脉分支管壁的坏死，而肝动脉分支不受影响．术后8周原冷冻区的肝动脉、门静脉分支的管腔依然保持通敞，所在肝叶萎缩、纤维化。结论如对第一肝门部进行直接深低温冷冻，应注意避免损伤胆管系统；而机体可耐受对部分肝叶Ghsson氏管道系统二、三级分支区域的直接深低温冷冻，冷冻可造成受冻部位肝实质的坏死，达到外科治疗目的。     

Ischemic arterial complications after liver transplantation in the adult: multivariate analysis of risk factors

HYPOTHESIS: To minimize the incidence of ischemic arterial complications, risk factors should be clearly identified. Knowledge of the predisposing factors for such complications would make possible the institution of strict surveillance protocols that could ensure early detection of complications and so prevent the progression of ischemic damage to graft failure. DESIGN: Retrospective univariate and multivariate analysis. SETTING: University hospital. PATIENTS: Six hundred fifty-three adults who underwent 747 orthotopic liver transplantations. MAIN OUTCOME MEASURES: We used univariate and multivariate analyses to retrospectively assess the role of possible risk factors for early and late HA thrombosis (HAT) and stenosis (HAS), including etiology of liver disease, donor and recipient sex and age (aged < or =60 vs >60 years), cause of donor death, preservation solution, cold ischemic time, previous orthotopic liver transplantation, HA back-table reconstruction, direct arterial anastomosis vs interpositional conduit, experience of the surgeon, intraoperative transfusion requirements, acute rejection, and cytomegalovirus infection. RESULTS: We observed 58 ischemic complications, including 26 early HAT, 13 late HAT, and 19 HAS. Independent predictors of early HAT were donor age greater than 60 years and bench reconstruction of anatomical variants of the HA; of late HAT, arterial anastomosis fashioned using an interpositional graft of donor iliac artery (iliac conduit) and donors who died of cerebrovascular accident; and of HAS, previous orthotopic liver transplantation and cytomegalovirus infection. CONCLUSIONS: Predisposing factors for HAT mostly stem from donor and graft features. Use of iliac conduits should be limited, particularly when using old donors. Frequent screening of the arterial flow to the graft with Doppler ultrasonography is advisable in patients at risk.     

肝移植术后肝动脉狭窄的诊断和治疗

目的：总结肝移植术后肝动脉狭窄的诊治经验。方法：回顾性总结１０６例１０７次肝移植病人的３例肝动脉狭窄的临床资料,结合文献分析了肝动脉狭窄的高危因素及其对肝移植的影响。结果：本组肝动脉狭窄的发生率为２．８％。３例均经彩超检查诊断和肝动脉造影确诊。例１狭窄位于受体肝总动脉起始处,放置血管内支架后血流恢复正常,但术后第１８天死于肝功能衰竭;例２狭窄位于吻合口,不能通过导丝而未行介入治疗,但病人无症状,肝功能良好;例３狭窄位于吻合口近端,经肝动脉重建后血流恢复正常。结论：肝动脉狭窄的早期诊断和及时治疗非常关键,其对移植肝的影响取决于当时的肝功能状态。纠正肝动脉狭窄有助于预防胆道并发症和提高移植物的存活率。     

Dearterialization of the liver causes intrahepatic cholestasis due to reduced bile transporter expression

BACKGROUND: Bile duct injury after hepatic artery thrombosis (HAT) in liver transplantation is believed to be caused by ischemia predominantly. We aimed to define the involvement of bile secretory dysfunction in the pathogenesis of liver injury after HAT. METHODS: In a murine model, the main hepatic artery, the extrahepatic peribiliary plexus, or both arterial connections to the liver were interrupted (n=5 for each group). After 1, 14, or 28 days, hepatobiliary function was assessed by analysis of bile transporter expression, serum bile acids and bilirubin, and hepatic ATP content. In addition, cellular injury was assessed by light microscopy and biochemical markers. RESULTS: There were no signs of hepatobiliary dysfunction or injury in sham-operated animals or in mice with interruption of the hepatic artery or the extrahepatic peribiliary plexus alone. However, as early as 24 hr after complete dearterialization, bile transporter expression was significantly reduced and intrahepatic cholestasis started to progress the following weeks. Histologic studies at 28 days after complete dearterialization showed severe hepatobiliary injury. CONCLUSIONS: This study indicates that arterial blood supply is critical for normal bile secretion. Bile duct injury after complete arterial deprivation is preceded by a loss of bile secretory function and subsequent intrahepatic cholestasis.