门静脉高压症外科手术后门静脉系统血栓形成的原因及防治

目的　探讨门静脉高压症外科手术后门静脉系统血栓形成的原因及处理。方法　回顾性分析我院 1992～ 2 0 0 1年施行肝炎后肝硬化门静脉高压症手术伴脾切除术 32 9例患者的临床资料 ,对其中 4 3例 (13 1% )术后出现门静脉系统血栓患者的临床资料进行统计和分析。结果　 4 3例门静脉系统血栓患者中 ,1例发生感染性门静脉炎死亡 ,其余均康复出院。单纯行脾切除或脾切除加断流术患者 138例 ,血栓形成 2 6例 (18 8% ) ;行脾切除加分流术患者 191例 ,血栓形成 17例 (8 9% ) ,差异有显著意义 (χ2 =8 4 4 ,P <0 0 1)。结论　门静脉高压症外科手术后门静脉系统血栓形成的主要原因是脾切除术后血小板升高 ,且与选择不同术式导致术后门静脉系统血流动力学改变有关。手术操作规范化、术后动态监测血小板总数、常规彩超检查及早期行抗凝祛聚疗法是防治门静脉高压症术后门静脉系统血栓形成的有效方法。     

门脉高压脾切除术后静脉血栓形成危险因素研究

目的探讨门静脉高压症患者脾切除术后门静脉系统血栓形成的危险因素。方法回顾性分析肝硬化门静脉高压症患者脾切除术300例的临床资料,选取性别、年龄、血小板计数、血小板聚集试验、门静脉血流速变化、脾脏质量及手术方式作为观察指标．对术后40例并发血栓形成的原因进行比较：结果术后门静脉系统血栓形成与血小板计数、血小板聚集试验、门静脉血流速变化及脾脏质量有关（P〈0．05）,与性别、年龄及手术方式无关（P〉0．05）、结论脾切除术后血小板计数、血小板聚集试验、门静脉血流速变化及睥脏质量是门脉高压脾切除术后形成门静脉系统血栓的危险因素     

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.     

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。     

门静脉系统抗凝预防断流术后门静脉系血栓形成

目的 探讨门静脉高压症断流术后门静脉系血栓形成的预防方法。方法 将７１例肝硬化门静脉高压症患者分为２组：Ａ组３６例在断流术中经脾静脉分支插入抗凝管,术后行门静脉系统凝治疗;Ｂ组３５例断流术后未行门静脉系抗凝治疗。结果 术后３个月内彩超检查,Ａ组门静脉系均未见血栓形成,Ｂ组门静脉系血栓形成１３例（３７．１４％）。结论 门静脉系统抗凝治疗是预防门静脉高压症断流术后门静脉系血栓形成的有效方法。     

早期抗凝、祛聚预防门静脉高压症脾切除术后门静脉血栓形成

目的 研究门静脉高压症病人脾切除术后早期接受抗血栓治疗对预防门静脉血栓形成的效果及安全性.方法 将中山大学附属第三医院2003-2005年肝硬化门静脉高压症欲接受脾切除术的病人59例随机分为2组:早期使用抗凝、祛聚药物预防组与同期常规用药组为对照进行对比研究,利用彩色多普勒超声监测门静脉血栓形成情况.结果 52例完成随访6个月以上,随访率88.1%,其中预防组29例,对照组23例.术后对照组10 d内发生门静脉血栓1例,1个月内4例,1月后3例,合计8例(34.8%),1例为复发性血栓.预防组10 d内无一例发生门静脉血栓,1个月内2例,1个月后1例,合计3例(10.3%),两组病例门静脉血栓发病率差异有显著性(X2=4.59,P＜0.05),3例并发上消化道出血.结论 门静脉高压症病人脾切除术后早期接受抗凝、祛聚治疗能降低术后门静脉血栓形成的发生率.     

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.     

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。     

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.     

肝硬化脾切除术后门静脉系统血栓形成的原因分析

目的 探讨肝硬化门静脉高压患者行脾脏切除+贲门周围血管离断术后门静脉系统血栓(portal vein thrombosis,PVT)形成的原因.方法 回顾性分析我院2004年1月至2010年1月204例肝炎后肝硬化门静脉高压症行手术治疗患者的临床资料.结果 其中150例行脾切除+贲门周围血管离断术,54例行脾脏部分切除术+贲门周围血管离断术.术后发生PVT30例,未发生PVT174例;发生PVT患者的门静脉和脾静脉直径、术后门静脉血液流速及术后并发症与未发生PVT患者有显著性差异(P<0.05),脾脏部分切除术后患者PVT的发生率明显比脾脏切除患者低,有显著性差异(P<0.05).结论 门静脉和脾静脉直径、门静脉血液流速及术后并发症是肝硬化门脉高压症脾切+贲门周围血管离断术后PVT形成的危险因素,脾脏部分切除术可有效减少断流术后PVT的发生.     

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.     

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.     

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.     

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.