肝硬化门静脉高压症不同手术方式与血栓形成

目的分析肝硬化门静脉高压症患者不同手术方式与血栓形成部位及发生率的关系,探讨血栓形成的机制。方法回顾性分析2011年1月至2012年12月间收治的资料完整的72例肝硬化门静脉高压症患者术前术后的临床资料,脾切除＋断流手术25例,选择性断流术15例,脾切除脾肾静脉分流＋断流的联合手术32例,分析术前术后患者的血小板数量、凝血功能、门静脉血流动力学状况与血栓形成的关系。结果①术前在有无门静脉系统血栓形成的两组问各项凝血功能参数差异均无统计学意义,唯门静脉血流速度在血栓组较无血栓组显著减慢（P〈0．05）。②术后有无血栓形成的两组间血小板数量无明显差异,D-二聚体均较正常值为高,但两组间差异无统计学意义。③行断流术的25例患者,在术后2周和2个月时,血栓形成率可达100％,主要为脾静脉血栓,其中12例（48％）合并门静脉主干及分支血栓。④选择性断流术后以脾静脉血栓为主,部分可向门静脉主干或分支蔓延,将胃冠状静脉一食管旁静脉闭塞;部分患者仅显示肠系膜上静脉-胃冠状静脉-食管旁静脉,门静脉主干、分支及脾静脉均闭塞。⑤脾肾静脉分流加断流的联合手术后2个月时血栓形成率最高（75％）,至6个月时下降至41％,为3组中最低（P〈0．01）。主要为门静脉主干和（或）分支血栓,除1例外,肠系膜上静脐-脾静脉-吻合口血流通畅。结论肝硬化门静脉高压症患者的术前、术后门静脉系统血栓形成与凝血功能改变无明显关系。无论何种手术,术后门静脉系统均有血栓形成可能,术式不同其血栓发生的部位可不同,血栓形成主要与门静脉系统血流动力学改变有关。联合手术后,虽门静脉主干及分支内可有血栓形成,但吻合口通畅,基本上无术后再出血,且肝性脑病发生率低、易被处理,应成为首选。     

门静脉高压症外科手术后门静脉系统血栓形成

目的：探讨门静脉高压症外科手术后门静脉系统血栓形成率及原因.方法：回顾性分析我院近8年采用脾肾分流加门奇断流联合手术和门奇断流术治疗233例病人门静脉高压症的临床资料,并应用核磁共振血管造影测量门静脉、脾静脉和肠系膜上静脉流速.结果：断流手术后门静脉系统血栓形成率为91.06%,且均有脾静脉血栓形成,门静脉主干血栓形成占其中25.89%,联合手术后血栓形成率为10.91%.与术前相比,血栓组术后门静脉（PV）和脾静脉（SV）流速下降显著,无血栓组术后PV和SV的流速无显著下降.术后血栓组SV的流速与无血栓组病人比较有非常显著的降低.血栓组和无血栓组在术前和术后的相同时间,病人血小板无显著性差异,PT延长时间两组手术前后及两组间均无显著性差异.结论：门静脉高压症断流手术后门静脉系统血栓形成率高达91.06%,且均有脾静脉血栓形成.门静脉系统血液流速减缓在术后门静脉系统血栓形成中起重要作用.脾切除后病人血小板升高并非是形成血栓的主要原因.脾肾静脉分流联合断流术在减少门静脉系统血栓形成中有很大优势.     

门静脉高压症术后门静脉血栓形成的危险因素分析

目的:分析肝硬化门静脉高压症术后出现门静脉血栓的危险因素。方法 :回顾性分析2008年1月至2010年7月,因肝硬化门静脉高压导致脾功能亢进和消化道出血在我院行手术治疗的92例病人的临床资料。分为血栓组和非血栓组,对可能导致门静脉血栓形成的各种因素进行多因素分析。结果:92例病人中有40例(43.47%)出现门静脉血栓形成。病人的性别、年龄、病因、肝功能Child-Pugh分级、血清总胆红素、白蛋白、凝血酶原时间、门静脉流速及流量、手术方式、手术前后门静脉压力、手术前后血小板数量及术前D-二聚体均不是门静脉血栓形成的危险因素。门静脉直径和脾静脉直径是血栓形成的独立危险因素(P11.65 mm或脾静脉直径>9.5 mm时,术后容易形成门静脉血栓。结论:肝硬化门静脉高压症行手术治疗的病人,术前门静脉直径及脾静脉直径是术后门静脉血栓形成的独立危险因素。     

门静脉高压症手术后门静脉血栓形成的原因

目的 探讨肝硬化门静脉高压症脾切除术后门静脉血栓形成的原因.方法 回顾分析我院2010年2月至2013年2月132例因肝硬化门静脉高压症行脾切除患者的临床资料,包括对年龄、性别、肝功能、血小板、门静脉血流流速的变化等相关指标监测分析.结果 门静脉高压症患者术后门静脉血栓形成率为17.4％ （23/132）,与无血栓组比较,血栓组患者术中门静脉血流速度显著下降（P＜0.05）,年龄、性别、肝功能、血小板等指标差异无统计学意义（P＞0.05）.结论 门静脉血流速度降低可能是门体断流术后门静脉血栓形成的主要影响因素.     

肝炎肝硬化病人脾切除术后门静脉血栓形成的相关因素分析

目的 分析肝炎肝硬化门静脉高压症病人脾切除术后门静脉系统血栓形成的相关因素.方法 我院2000年8月至2007年6月共为226例肝炎肝硬化门静脉高压症病人施行了脾切除或脾切除加断流术.本文对其中154例进行回顾性分析.根据是否形成血栓将病例分为门静脉系统血栓形成和无血栓形成两组.用Logistic回归分析术前术后门静脉压力下降水平、术前凝血酶原比值(PTR)、术前纤维蛋白原水平(FIB)、术前及术后1、7、14 d血小板水平、术前门静脉直径、术前胆红素水平、术中出血量各指标与门静脉系统血栓形成的关系.结果 在154例病人中,门静脉系统血栓形成31例,123例无血栓形成.Logistic单因素分析和多因素回归分析均显示门静脉系统血栓形成与门静脉压力下降水平有关;术前凝血酶原比值(PTR)、术前纤维蛋白原水平(FIB)、术前及术后1、7、14 d血小板水平、术前门静脉直径、术前胆红素、术中出血量水平与门静脉血栓形成无关.结论 术前、术后门静脉压力下降水平可能是影响门脉高压脾切除术后门脉系统血栓形成的重要因素,术后门静脉压力下降越多,门静脉系统血栓形成几率越高.     

可溶性P-选择素对肝硬化门静脉高压术后门静脉血栓形成的影响

目的探讨可溶性P-选择素对肝硬化门静脉高压症术后门静脉血栓形成的影响。方法检测乙肝肝硬化患者在门静脉高压症围手术期血小板的数量及反映血小板功能的可溶性P-选择素水平的动态变化,比较其在有门静脉血栓形成组患者及无血栓形成组患者间的差异。结果血栓形成组患者及无血栓形成组患者间,血小板数量无显著差异,而可溶性P-选择素水平在术后第4～6天有显著性差异(P<0.05)。结论乙肝肝硬化患者在行门静脉高压症手术后,血小板功能的变化对门静脉血栓形成可能起着重要的作用。     

门静脉高压症断流术后并发门静脉系统血栓的治疗体会

目的　探讨门静脉高压症断流术后门静脉系统血栓的成因及防治。方法　对 6例肝硬化门静脉高压症断流术后并发门静脉系统血栓的原因及其防治进行回顾性分析 ,从而制定治疗措施。结果　 3 6例肝硬化门静脉高压症断流术病人 ,门静脉系统血栓发生率 16.7% ,均经彩色多普勒超声证实 ,经早期口服潘生丁 ,静滴低分子右旋糖酐祛聚治疗 ,随诊 3个月 ,血栓无进一步发展 ,也未引起相应其它并发症。结论　肝硬化门静脉高压症断流术后门静脉系统血栓有一定发病率 ,可造成肝功能进一步受损及内脏血流瘀滞 ,甚至肠坏死 ,危及生命 ,所以对其早期防治有重要意义。     

术前门静脉血流速度在门静脉高压症断流术后血栓形成中的预测价值

目的 评价术前门静脉血流速度对乙型肝炎肝硬化门静脉高压症断流术后门静脉血栓形成(PVT)中的预测价值.方法 对2007年1月至2008年7月在四川大学华西医院同一外科小组行脾切除和断流术的连续45例乙型肝炎后肝硬化门静脉高压症患者,运用彩色多普勒超声测量术前1 d门静脉直径、流速以及术后7 d有无门静脉系统血栓形成.同时计算患者术前Child-Pugh评分.术后测量去脾脏血液后的脾脏重量,检测术前1 d、术后7 d凝血酶原时间(PT)和血小板计数(PLT).并将患者分为血栓组与非血栓组、高速组与低速组,分别对上述指标进行统计学对比分析.结果 术后发生门静脉系统血栓13例(28.9%),血栓组(n=13)术前门静脉流速为(19.5±5.3)cm/s,其中12例低于25 cm/s[平均(18.4±3.8)cm/s],1例为32.3 cm/s;非血栓组(n=32)术前门静脉流速为(29.6±8.0)cm/s,两组差异有统计学意义(P<0.01).低速组(n=17)和高速组(n=28)血栓发生率分别为70.6%和3.6%,差异有统计学意义(P<0.01).分别比较两种分组的患者术前Child-Pugh评分、脾脏重量、手术前后PT和PLT,差异均无统计学意义(P>0.05).25 cm/s作为指标预测术后血栓形成的敏感性为92.3%,特异性为70.6%.结论 术前门静脉直径增加及血流速度降低是导致术后门静脉系统发生血栓的主要危险因素,尤其当门静脉流速降低(<25 cm/s)时,断流术后血栓发生率将显著增高.门静脉直径与血流速度存在负相关系,可根据门静脉流速预测门静脉高压症断流术后的血栓的形成.     

肝炎肝硬化脾切除术后门静脉系统血栓形成的相关因素分析和预防

目的分析肝炎肝硬化门静脉高压症脾切除术后门静脉系统形成血栓的相关因素,寻找预防门静脉高压症脾切除术后门静脉系统形成血栓的方法。方法回顾性分析我院1999年3月至2005年6月收治的肝炎肝硬化门静脉高压症行单纯脾切除、脾切除加EVL或脾切除加贲门周围血管断流术的病人132人,用Logistic回归分析分析术前肝功能Child-Pugh分级、门静脉和脾静脉直径、脾脏的大小以及术后血小板的数量与门静脉系统血栓形成的关系;将其中符合要求的112人分为三组,A组56人:术后未用抗凝、祛凝药;B组33人:术后在血小板＞300×109／L时用抗凝、祛凝药; C组23人:术后早期应用抗凝、祛凝药。比较三组门静脉系统血栓的发生率。结果Logistic单因素分析提示门静脉系统的血栓形成与门静脉直径、脾脏的大小、脾脏的厚度、血清总胆红素以及术后血小板的数量有关;多因素回归分析发现门静脉系统的血栓形成与门静脉和脾静脉直径、脾脏的大小和是否行抗凝祛凝治疗有关;A组、B组和C组门静脉系统发生血栓的人数分别为19人、9人和1人,发生率分别为33．9％、27．3％和4．3％,门静脉血栓发生率的比较A组和B组的差异无显著性(x2= 0.427,P=0.514),A组和C组的差异有显著性(x2=7.545.082,P=0.006),B组和C组的差异有显著性(x2=4．856,P=0.028)。结论肝炎肝硬化门静脉高压症脾切除术后门静脉系统血栓的形成与门静脉和脾静脉直径、脾脏的大小和是否行抗凝祛凝治疗有关;早期、全身应用抗凝、祛凝药能有效的预防肝炎肝硬化门静脉高压症脾切除术后门静脉系统血栓的形成。     

门静脉高压症术后门静脉血栓形成相关因素分析

目的探讨门静脉高压症术后门静血栓形成（Portal Vein Thrombosis,PVT）相关因素。方法回顾性分析我院2001年04月至2008年12月采用脾肾分流术加贲门周围血管离断联合手术和贲门周围血管离断术治疗129例肝硬化门静脉高压症患者的临床资料,对患者年龄、性别、门静脉直径、门脉脉直径、门静脉血流流速的变化、门静脉压力变化、血小板数值等相关指标监测分析,评估门静脉高压症患者术后门静者术后门静脉血栓形成相关因素。结果门静脉高压症患者术后门静脉血栓形率为15．50％（20／129）,其中断流手术后门静脉系统血栓形成率为18．18％（16／88）,联合手术后血栓形成率为9．76％（4／41）。血栓组患者门静脉主干直径、脾静脉直径较非血栓组患者增宽,有显著性差异。术后血全组PV、SV的流速下降显著（P〈0．05）。血栓组患者术前、术后门静脉压力均较无血栓组患者低,有统计不差异（P〈0．05）年龄,性别,肝功能child—pugh分级,凝血酶原时间,术后血小板增高等因素不是脾切除术后门静脉血栓形成的危检因素。结论门脉高压脾切除术后门静脉主干直径、脾静直径增宽,门静系统血液流速减缓,门静脉压力降低有显著性差异,是门脉高压脾切除术后门静脉血栓形成的危除因素。进一步的大样本的随机对照临床研究对解决这个问题是必要的和重要的。     

CT门静脉成像的临床解剖学分析

目的 进行CT门静脉成像(computed tomography portal venography,CTPV)的临床解剖学分析,探讨其临床应用价值.方法 选取手术组(实验组)40例门静脉高压症合并上消化道出血患者和20例正常对照组进行CTPV临床读片与影像学测量,包括门静脉主干及其主要侧支血管.对胃左静脉的注入方式进行分类总结.应用直线拟合数学模型处理测量数据.结果 60例均成功进行CTPV摄片.实验组和对照组门静脉主干直径分别为(16.62±4.80) mm、(10.84±2.14) mm,肠系膜上静脉直径分别为(12.36±2.67) mm、(8.79±1.44) mm,脾静脉直径分别为(14.29±4.24) mm、(8.32±1.78) mm.实验组胃左静脉大部分注入脾-门交角和脾静脉.直线拟合11/18=X/30数学公式计算显示,阈值压力下门静脉主干X值=18.33 mm.胃左静脉食管支的显影率为52.38％、胃左静脉胃支显影率66.67％、胃左静脉食管支及胃支同时显影率23.81％,仍有相当一部分门脉高压患者胃左静脉的胃支和食管支显影不良甚至不显影.腹膜后静脉的显影率为25％.结论 应用CTPV在术前对食管胃底周围曲张的门静脉进行形态和功能的详尽评估,指导术者进行区域性断流(regional devascularization,RDV)具有实用价值及临床意义.CTPV显示胃左静脉注入脾-门交角和脾静脉的患者临床上出血的风险大.门静脉主干直径≥18 mm时可能出血,初步定义为CTPV阈值压力.CTPV在胃左静脉胃支/食管支的精细结构显示上仍然具有一定的局限性.CTPV中提高腹膜后静脉显影率应予关注.     

Portal-to-right portal vein bypass for extrahepatic portal vein obstruction

Objective

Rex shunt (mesenteric-to-left portal vein bypass) is considered a more physiologically rational treatment for EHPVO than other portosystemic systemic shunts in children. However, about 13.6% of children with EHPVO do not have usable left portal veins and up to 28.1%. Rex operations in children are not successful. Hence, a Rex shunt in these children was impossible. This study reports a novel approach by portal-to-right portal vein bypass for treatment of children with failed Rex shunts.

Serial measurement of portal hemodynamics after partial portal decompression

In a serial analysis of splanchnic hemodynamics, we compared partial with total portal decompression in 16 alcoholic cirrhotic patients who underwent portacaval shunts for variceal hemorrhage. Partial decompression was achieved with 8 or 10 mm polytetrafluorethylene portacaval H grafts and aggressive collateral ligation. Total decompression was achieved with larger diameter H grafts (12 or 14 mm). Early and follow-up (mean interval, 18 months) postoperative studies of portal hemodynamics included: direct measurement of shunt gradients, scintigraphic quantitation of portal and mesenteric flow distribution to the liver, and a portal and splenic collateral scoring system developed from standardized splenic venography. Partial portal decompression reduced portal pressure by 43% +/- 8% compared with 81% +/- 5% after total decompression (p less than 0.01). Scintigraphy demonstrated that partial decompression provided a greater fraction of portal flow to the liver than did total decompression (57% +/- 9% versus 2% +/- 1% intrahepatic radioactivity) and mesenteric flow distribution (14.5% +/- 5.4% versus 1.2% +/- 0.7%). Only one patient with partial decompression had a significant loss of portal perfusion during the interval studies. Significantly more residual collaterals were visualized in patients with partial decompression than in those with total decompression, and interval studies showed no significant changes from early studies. We conclude that partial decompression maintains higher portal pressures, more residual collaterals, and a greater fraction of portal and mesenteric flow to the liver than does total decompression. A modest but uniform reduction of portal pressure minimizes stimulus for new collateral formation and further shunting of portal flow.     

搏动性门静脉血泵治疗门静脉高压症的实验研究

目的　为解决门静脉高压症向肝血流减少、肝代谢功能下降及侧支循环压力过高、静脉曲张等问题 ,我们研制了搏动性门静脉血泵 ,对丝线栓塞性门静脉高压模型犬进行门静脉外动力泵血的研究。观察入肝血量、肝代谢变化及侧支压力等一系列指标。方法　对杂种犬进行门静脉左右支丝线栓塞术制备门静脉高压动物模型 ;应用高弹力硅胶球囊连接单流向硅胶瓣“T”型管 ,制作搏动性门静脉血泵 ;应用强磁场磁极片及低频振荡交流线圈体外提供动力。将血泵“T”管安置于门静脉主干前壁侧支平面以上 ,测定血泵工作前后的入肝血流量、侧支静脉压力及吲哚氰绿排泄的变化。结果　模型犬血泵平面以上的门静脉压力在泵工作后由 30 3± 4 2cmH2 O升至 49 0± 7 1cmH2 O ;入肝血流量由 2 70± 2 8ml/min升至 396± 2 5ml/min ;血泵平面以下门静脉压由 31 4± 3 1cmH2 O降至18 0± 4 3cmH2 O ;脾静脉压由 36 2± 4 0cmH2 O降至 2 0 5± 3 4cmH2 O ;胃底静脉压由 35 3± 3 3cmH2 O降至 19 3± 4 7cmH2 O ;吲哚氰绿排泄率由 0 0 92± 0 0 0 9升至 0 15 1± 0 0 13 ;15min滞留率由 19 0 3± 8 5 0降至 9 0 4± 2 5 0。结论　搏动性门静脉血泵对增加门静脉入肝血流 ,改善肝代谢功能状态及降低侧支压力具有显著作用。血泵结构     

Mesenterico left portal bypass for variceal bleeding owing to extrahepatic portal hypertension caused by portal vein thrombosis

Background/Purpose

Portosystemic shunt operations are indicated in patients with extrahepatic portal hypertension owing to portal vein thrombosis (EPH-PVT) suffering from recurrent variceal bleeding despite endoscopic sclerotherapy. Mesenterico left portal bypass procedure (MLPB) is an alternative procedure to the portosystemic shunt operations in patients with EPH-PVT. MLPB operation reestablishes hepatopetal portal blood flow. We herein present our experience with MLPB in children with EPH-PVT.

Methods

Six patients were treated for EPH-PVT with recurrent bleeding despite endoscopic sclerotherapy (2 boys and 4 girls) in our unit. All patients were evaluated preoperatively with complete blood count, portal duplex system Doppler ultrasonography, magnetic resonance angiography, and upper gastrointestinal (GI) endoscopy. MLPB operation was performed as described by de Ville de Goyet. During the postoperative period, patients were evaluated with complete blood count, portal duplex system Doppler ultrasonography, upper GI endoscopy, and magnetic resonance angiography.

Results

Six patients were assessed to be candidates for MLPB procedure and were operated to perform the MLPB procedure. Left portal veins were found to be patent during the operation in 4 patients, and the MLPB procedure was performed. Internal jugular vein was used in 3 patients and enlarged inferior mesenteric vein in 1 patient. Left portal veins of the remaining 2 patients were found to be obliterated; therefore, mesocaval shunt was performed. The postoperative course of the patients was uneventful except for 1 patient. During the following period, the leukocyte and the platelet counts were significantly increased in 3 of the 4 patients after the MLPB procedure. Upper GI bleeding occurred in the early postoperative period in 1 patient with MLPB procedure because of prepyloric ulcer that was successfully treated by endoscopic sclerotherapy. Internal jugular vein graft thrombosis was detected on the 10th postoperative day. This patient underwent a second laparotomy, the distal half of the graft was found to be sclerosed and narrowed that the graft was revised with a synthetic allograft.

Conclusions

Based on a review of the literature, the MLPB functions well in patients with portal hypertension caused by portal vein thrombosis and appears to have a physiologic advance over shunts that decompress but do not return blood directly to the liver. Because intra-abdominal veins appear to function well as a conduit in this operation, it may be favored by eliminating additional incision and increased risk in such patients.     

Preduodenal portal vein

Passage of the portal vein anterior to the duodenum is a rare vascular anomaly that is a result of a variation in the normal developmental pattern of the right and left vitelline veins and their three anastomotic channels. In operations on the duodenum or biliary tract in patients with this condition, there is marked danger of inadvertent tearing, division, ligation, or excessive handling causing thrombosis. One case is added to the twenty-five previously reported in the literature.     

Endoscopic ultrasound-guided portal pressure gradient measurement in managing portal hypertension

Portal hypertension (PH) is still a challenging clinical condition due to its silent manifestations in the early stage and needs to be measured accurately for early detection. Hepatic vein pressure gradient measurement has been considered as the gold standard measurement for PH; however, it needs special skill, experience, and high expertise. Recently, there has been an innovative development in using endoscopic ultrasound (EUS) for the diagnosis and management of liver diseases, including portal pressure measurement, which is commonly known as EUS-guided portal pressure gradient (EUS-PPG) measurement. EUS-PPG measurement can be performed concomitantly with EUS evaluation for deep esophageal varices, EUS-guided liver biopsy, and EUS-guided cyanoacrylate injection. However, there are still major issues, such as different etiologies of liver disease, procedural training, expertise, availability, and cost-effectiveness in several situations with regard to the standard management.     

Bilharzial portal fibrosis: an important cause of portal hypertension

Thirty consecutive cases of portal hypertension seen in a surgical unit in Lusaka, Zambia, are reported. Of these cases 70% were due to portal fibrosis caused by Schistosoma mansoni infestation. Portacaval shunting was undertaken in most cases. Patients with portal fibrosis responded more favourably to portal decompression than did patients with cirrhosis. It is probable that the condition is more common than is generally reconigzed in areas where S. mansoni infestation is endemic.