三种不同术式对门静脉血流动力学的观测

目的 :测定分流 (SRS)加断流手术 (PCDV)前后门静脉系统血流动力学变化 ,评价其在门静脉高压症外科治疗中的价值。方法 :应用彩色多普勒检测 99例门静脉高压症病人手术前后对门静脉系统的血流动力学的影响 ,术中动态测量门静脉压力。结果 :①SRS +PCDV组 :术后PVF减少 36 .1 0 %± 7.8% ,FPP下降 33 .99%± 9.53 %。FPP的下降与PVF的减少呈正相关 ,PVF和FPP较术前下降 (P <0 .0 5) ,但维持在正常高限且保持门静脉向肝血流 ;②SRS +PCDV组术后的PVF和FPP均介于断流组与脾肾分流组之间 ,且各组之间有显著差异 (P <0 .0 5)。结论 :分流手术后门静脉血流向肝内高灌注 ,门静脉系统瘀血状态依然存在。分流术后门静脉高压瘀血状态缓解 ;门静脉血流肝内灌注显著减少。分流术后门静脉压力降低 ,加做断流术后门静脉压力有不同程度回升 ,术后的PVF和FPP均介于断流术和分流术之间 ,该术式明显优于单纯分流术或断流术。     

不同术式治疗门静脉高压症的疗效观察

目的　评价不同术式治疗门静脉高压症的疗效。　方法　对比 3 8例脾肾分流 (SRS)加贲门周围血管离断术 (PCDV)即联合术 ,64例单纯贲门周围血管离断术 (PCDV) ,18例脾肾分流术 (SRS)病人临床疗效及手术前后门静脉系统血流动力学变化。　结果　术后三组病人的自由门静脉压 (FPP)均显著性低于术前 ,其中 ,联合手术组的FPP显著高于SRS组 ,但显著低于PCDV组。PCDV组术后门静脉血流量 (PVF)与术前相比无显著性差异 ,其余两组则有显著降低。联合手术组、PCDV组、SRS组术后的再出血发生率分别为 2 .63 % (1/ 3 8)、18.75 % (12 / 64 )、16.67% (3 / 18) ,联合手术组显著低于PCDV组 (P <0 .0 5 ) ;肝性脑病发生率分别为 2 .63 % (1/ 3 8)、6.2 5 % (4 / 64 )、2 7.78% (5 / 18) ,联合手术组显著低于SRS组 (P <0 .0 5 ) ,与PCDV组相近。　结论　联合手术符合门静脉高压症手术要求 ,且疗效好于单纯断流术或分流术。     

门静脉动脉化治疗门静脉高压症的实验研究

目的观察门静脉动脉化 完全门体分流(PACS)术和传统的脾肾分流(SRS)术及贲门周围血管离断(PCDV)术对门静脉血流动力学的影响。方法制备门静脉高压动物模型,PCDV组行脾切除、贲门周围血管离断术;SRS组采用脾切除、远端脾肾分流术;PACS组采用脾切除、门静脉-脾动脉吻合、门静脉-腔静脉吻合。应用彩色多普勒超声及有创性测压管于开腹后即刻、手术完成即刻及治疗后2周测量门静脉血流量(PVF)及门静脉压力(PVP),PACS组包括入肝及入下腔静脉PVF、PVP。手术前、后测定肝功能指标。结果PCDV组术后2周PVF下降约17%,PVP下降约5%;SRS组术后2周PVF下降约51%,PVP下降约51%;PACS组术后2周入肝PVF上升至开腹后即刻的180%,入肝PVP上升至开腹后即刻的196%,入下腔静脉PVF增至开腹后即刻的130%,入下腔静脉PVP保持低压,约为开腹后即刻的46%。术后2周PACS组入肝PVP、PVF及入下腔静脉PVF均明显高于另2组(P<0.05,P<0.01),而入下腔静脉PVP则明显低于PCDV组(P<0.05)。3组中仅SRS组术后2周ALT较术前明显升高(P<0.05)。结论PACS术成功率较高,手术死亡率与SRS术相近,可同时提高入肝血流和降低侧支压力,而且短期内未明显影响肝脏功能,是一种值得尝试和进一步研究的新手术方法。     

不同术式治疗门静脉高压的临床研究

目的探讨不同术式治疗门静脉高压患者的效果及术后远期疗效。方法回顾自2007年1月至2014年1月手术治疗的84例门静脉高压患者,根据术式分为两组,PCDV组:33例患者采用脾切除、贲门周围血管离断术(PCDV),SRS+PCDV组:51例患者采用脾切除、脾肾静脉分流术(SRS)联合贲门周围血管离断术(PCDV)。采用SPSS19.0软件,采用t检验(均数±标准差)对比分析两组患者术中自由门静脉压力(FPP)改变、术前术后门静脉血流速度变化;采用χ2检验对比分析手术病死率和术后流出道阻塞、再出血、门静脉血栓和肝性脑病的发生率。当P﹤0.05时,差异有统计学意义。结果 PCDV组术后FPP较术前有显著变化(t=2.707,P﹤0.05),但门静脉血流速度无明显变化(t=1.191,P﹥0.05);SRS+PCDV组术后FPP、门静脉血流速度均较术前有显著变化(t=6.881、14.183,P﹤0.05),PCDV、SRS+PCDV两组术后FPP比较差异显著,有统计学意义(t=2.452,P﹤0.05)。术后随访中,SRS+PVDV组流出道阻塞、再出血及门静脉血栓的发生率明显低于PCDV组,差异有统计学意义(χ2=6.75、5.33、5.81,均P﹤0.05),术后病死率及远期肝性脑病的发生率较PCDV组无明显变化,差异无统计学意义(P﹥0.05)。结论 PCDV可阻断脾胃区反常血流,但术后血流状态、淤血情况改善不明显;SRS+PCDV联合术既可明显降低门静脉高压又不增加术后再出血和肝性脑病的风险,因此可以作为治疗PHT的首选术式。     

联合术治疗门静脉高压症22例

为观察断流加分流联合术治疗门静脉高压症的效果 ,总结采用联合断流加脾肾静脉分流术(即联合术 )治疗 2 2例门静脉高压症的经验。均行择期手术 ,无手术死亡。术后随访 18例 ,再出血 1例 ,肝性脑病 1例。术前自由门静脉压 (FPP)为 ( 3.96± 0 .39)kPa ,脾肾分流术后FPP为 ( 2 .2 8± 0 .35)kPa ,断流术后FPP为 ( 2 .71± 0 .38)kPa。断流加分流术既保留了断流术的优点 ,又降低了门静脉压力 ,同时还有利于门静脉向肝的血流灌注     

大网膜包肾术自然分流在门静脉高压症治疗中的临床价值

目的　探讨大网膜包肾术 (ORP)对门静脉高压症患者行贲门周围血管离断术 (PCDV )后门静脉血流动力学的影响 ,及其自然分流作用的效率。方法　比较PCDV ,PCDV ORP和PCDV 门腔H型分流术 (PCDV PCS)患者手术后门静脉向肝血流速度 (PFR)和门静脉平均血流量 (PVF )变化 ,以及上消化道再出血、门静脉高压性胃病和肝性脑病的发生情况。结果　PCDV ORP组与PCDV PCS组比较 ,PFR分别为 14 .0 5± 3 .75和 8.64± 2 .86( P <0 .0 1) ,PVF分别为 714 .3 5± 10 2 .65和 42 3 .5 2± 2 82 .61(P <0 .0 1)。PCDV ORP上消化道再出血率与PCDV PCS组比较无显著性差异 ( 5 .5 6%比 4.3 5 % ,P >0 .0 5 ) ;肝性脑病发生率PCDV ORP组与PCDV组比较亦无显著性差异 ( 2 .78%比 3 .2 3 % ,P >0 .0 5 )。术后门静脉高压性胃黏膜损害的发生率PCDV ORP组 ( 2 7.78% )与PCDV组比较( 66.74% )差异显著 (P <0 .0 1)。结论　PCDV ORP手术既能维持手术后门静脉向肝血流 ,又能安全有效地自然分流 ,降低了断流术和分流术的远期并发症 ,具有临床推广价值     

脾肾分流术对肝炎后肝硬变门静脉高压症肠道功能的保护作用

目的探讨脾肾分流术对肝炎后肝硬变门静脉高压症肠道功能的保护作用。方法69例肝炎后肝硬变门静脉高压症并有食道胃底静脉曲张破裂出血病史的病人按入院先后分为脾肾分流组和断流组。术中、术后动态测量自由门静脉压（free portal pressure,FPP）,术后1、3、5、7、9d检测门静脉血内毒素、D-乳酸水平,术前及术后7d尿乳果糖／甘露醇（lactulose／manicol,LAC／MAN）比值。结果近期观测FPP,发现稳定期分流组明显低于断流组（P〈0．05）。分流组脾窝引流液明显少于断流组,体温恢复正常时间、肛门恢复排气及开始进食所需时间明显短于断流组（P〈0．05）。分流组术后1d内毒素、D．乳酸显著低于断流组;且下降较快,术后3d又显著低于术后1d;术后5d进入稳定期（P〈0．05）。而断流组内毒素、D．乳酸下降较慢,术后5d才显著低于术后1d,术后7d进入稳定期（P〈0．05）。分流组术后LAC／MAN比值显著低于断流组（P〈0．05）。结论脾肾分流术既能维持有效的向肝门静脉血流灌注;又能适当降低门静脉压,减轻胃肠血流瘀滞,对肝炎后肝硬变门静脉高压症肠道有明显的保护作用。     

改良脾腔分流联合断流术治疗门静脉高压症的疗效分析

目的 探讨改良近端脾腔静脉分流联合贲门周围血管离断术(分断流联合术)治疗门静脉高压症的疗效及其对门静脉血流动力学和肝储备功能的影响.方法 回顾性分析我院1997-2007年接受分断流联合术治疗的门静脉高压症患者135例和断流术患者120例的临床资料.通过彩色多普勒超声测定门静脉血流量(PVF)及监测术中自由门静脉压(FPP),观察手术前后门静脉系统血流动力学的变化.采用吲哚氰绿排泄实验观察15 min(R_(15))滞留率和肝有效血流量(FHF)的变化.结果 联合组手术死亡率为2.2%,无近期出血病例,远期出血率为5.5%,肝性脑病发生率为6.4%,术后1、3、5、10年生存率分别为96.4%、90.0%、81.3%和62.5%;断流组手术死亡率为4.3%,近期出血率为3.3%,远期出血率为14.1%,肝性脑病发生率为5.4%,1、3、5、10年生存率分别为95.7%、86.7%、75.0%和57.1%.联合组术后FPP、PVF和FHF分别为(32.0 ±1.5)cm H_2O、(880 ±260)ml/min和(430±180)ml/min,较术前均下降(P<0.05).R_(15)为30%±4%,较术前明显增加(P<0.01);断流组术后FPP、PVF和FHF下降(P<0.01),R_(15)增加(P<0.01).与断流组比较,联合组术后FPP下降更为明显(P<0.05),但PVF、FHF和R_(15)之间相比差异均无统计学意义(P>0.05).结论 改良脾腔静脉分流联合断流术的临床疗效满意,血流动力学改变合理,对肝储备功能影响较小,是治疗门静脉高压症的理想术式.     

应用术中FPP监测选择肝硬化门静脉高压症断分流术式的研究

目的 探讨肝硬化门静脉高压症(PHT)最佳的手术方式.方法 对36例PHT患者依据断流术后门静脉压力(FPP)的变化,选择FPP＜32cm H2O的患者22例只施行断流术(断流组),FPP≥32cm H2O的患者14例加行近端脾肾分流联合术(断分流组),并结合术前、术后门静脉血流动力学、断流及断分流后FPP变化及术后随访等,评价两组不同手术对门静脉血流动力学的影响及近、远期效果.结果 断流组断流前后FPP分别为(38.01±1.57)cm H2O和(27.41±1.90)cm H2O,手术前后差异有统计学意义;断分流组断流前后FPP分别为(37.68±1.98)cm H2O和(35.11±2.67)cm H2O,差异无统计学意义,联合分流后FPP降低为(22.86±3.74)cm H2O,差异有统计学意义.随访再出血率:断流组10.53%,断分流组8.33%.结论 根据手术前、后门静脉血流动力学状况和断流术前后的FPP的变化,可以选择最佳的手术方式;如果断流术后FPP下降不明显,或FPP仍≥32cm H2O,则加做分流手术,通过术中FPP监测选择正确的术式可以达到最佳的临床效果.     

门静脉高压症血流动力学变化的临床研究

目的：探讨脾脏体积大小与门静脉系统高动力循环状态及手术前后门静脉体循环分流率，血流动力学变化的关系。方法：利用彩色多普勒复合装置、CT及公式法测量22例肝硬变门静脉高压症行脾切除、贲门周围血管离断术（下简称门静脉奇静脉断流术）患者的血流动力学变化参数、脾体积及门静脉体循环分流率。结果：（1）门静脉血流量（PVF）：对照组为785±144ml/min；实验组为966±125ml/min（t=3.56,P=0.002)。其中实验组的脾静脉血流量／门静脉血流量（SVF／PVF）为77％±17％，实验组的肠系膜上静脉血流量／门静脉血流量（SMVF／PVF）为28％±8％。（2）脾体积与脾静脉血流量、流速、直径显著相关（r=0.793,P<0.001,r=0.471,P<0.05,r=0.494,P<0.02)。（3）术后PVF减少187±87ml/min,SMVF增加100±40ml/min，门静脉体循环分流率减少26％±15％。结论：门静脉高压症时，门静脉系统处于高动力循环状态，对门静脉高压的形成和维持有重要意义。脾脏的高动力循环是门静脉系统产生高动力循环的主要因素。门静脉奇静脉断流术后、门静脉血流量的变化取决于术前脾脏的高动力循环状态，胃脾区的分流程度及术后肠系膜上静脉的代偿能力。     

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     

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.     

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.     

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.