生长抑素对门静脉高压症患者门静脉血流动力学的影响

目的研究生长抑素对门脉高压症患者门静脉血流动力学的影响和外周静脉血中胰岛素样生长因子(IGF1)、血管内皮素(ET1)、胰高血糖素(GLU)、一氧化氮(NO)浓度变化。方法通过对14例门脉高压症经颈内静脉肝内门体分流术(TIPS)术后患者经颈内静脉留置于门静脉内支架下方的导管,以美国REDMOND,WA太空检测仪直接测压,动态观察门静脉血流动力学改变,同时抽血检测IGF1、NO、ET1、GLU浓度。施他宁(6mg/24h)于TIPS术后24h采用微量泵持续24h经周围静脉输入。分别对患者用药前、用药后8、24h进行检测,结果行交叉自身对照。结果施他宁用药前后门静脉压力最大差值为(9.4±1.0)cmH2O(1cmH2O=0.098kPa),两者差异有非常显著性(P<0.01)。NO、ET1用药前后比较差异无显著性(P>0.05)。IGF1、GLU用药前后比较差异有显著性(P<0.05)。结论生长抑素施他宁(6mg/24h)能显著降低门静脉压力和血中GLU、IGF1水平。其降低门静脉压力的作用机制可能是通过降低GLU、IGF1等激素的分泌和释放,降低肝脏的代谢,减少肝脏的血流量,从而降低门静脉压力。     

门静脉压力改变对门静脉高压症肠道通透性的影响

目的　观察门静脉压力改变对门静脉高压症患者肠道通透性的影响。　方法　门静脉高压症患者 2 0例分为 2组 ,每组 10例 ,A组采用经颈内静脉肝内门体分流术 (transjugularintrahepaticportosystemicshunt,TIPS)加改良Sugiura联合治疗 ,B组行改良Sugiura治疗。分别于术前、TIPS后 2周和改良Sugiura术后 2周行肠道通透性检查 ;2 0例健康志愿者作对照。　结果　门静脉高压症患者较健康志愿者肠道通透性明显升高 (0 132± 0 110vs 0 0 32± 0 0 18,P <0 0 1)。A组患者TIPS术后 2周门静脉压力和肠道通透性均显著降低 (P <0 0 5 ) ;改良Sugiura术后 2周 ,2者无显著变化 ,但较术前明显降低 (P <0 0 5 )。B组患者改良Sugiura术后 2周肠道通透性和术前相比无显著变化。A、B组患者术前肠道通透性相比无显著差异 ,改良Sugiura术后 ,A组明显降低 (P <0 0 5 )。研究还发现门静脉压力与肠道通透性之间有显著相关性 (r=0 6 2 7,P <0 0 1)。　结论　研究表明TIPS加改良Sugiura术降低门静脉压力 ,改善肠道通透性 ,提高临床疗效。     

部分门静脉动脉化重建肝血流的实验研究

目的　了解部分门静脉动脉化重建肝血流对肝脏的影响。方法　建立部分门静脉动脉化重建肝脏血流的大鼠实验模型 ,通过该模型对肝脏的血流量、门静脉压和结构的影响分别进行了为期 1个月和 6个月的观察。结果　大鼠在行部分门静脉动脉化后的肝脏血流量为 (2 5 2± 3 2 )mV、术后 1个月为 (2 3 4± 4 6 )mV与术前 (2 2 6± 2 8)mV相比 ,差异无显著意义 (P >0 0 5 )。术后半年的肝脏血流量 (30 6± 10 8)mV与术前 (2 2 6± 2 8)mV相比 ,差异有显著意义 (P <0 0 5 ) ;术后门静脉压为 (12 9± 1 8)cmH2 O、术后 1个月为 (12 3± 1 4 )cmH2 O与术前 (10 0± 0 4 )cmH2 O相比 ,差异有显著意义 (P <0 0 1) ;术后半年门静脉压 (18 8± 6 3)cmH2 O与术前 (10 0± 0 4 )cmH2 O相比 ,差异亦有显著意义 (P <0 0 1) ;行部分门静脉动脉化后 1个月时肝脏结构无明显变化。术后 6个月时 4只大鼠 (4/ 10 )出现Disse间隙轻度扩张。结论　部分门静脉动脉化术后 6个月可造成较明显的肝脏血流量增加和门静脉压增高 ,但对肝脏结构的损害尚不很明显     

门静脉置管在门奇静脉断流术治疗门静脉高压症中的作用

目的探讨经颈内静脉肝内门体分流术(transjugular intrahepatic porto-systemic shunt,TIPS)途径门静脉置管对门奇静脉断流术治疗门静脉高压症疗效的作用。方法 2011年3月至2015年5月,对60例门静脉高压症病人行门奇静脉断流术治疗,术前采用随机方法分为研究组(门静脉直接抗凝)和对照组,每组各30例。采用直接门静脉造影和测压、门静脉CT血管造影(CTA)检查,观察断流术的彻底性、门静脉血栓发生率和门静脉压力的变化。结果门奇静脉断流术后1周,门静脉CTA显示研究组和对照组门静脉血栓发生率分别为6.7%(2/30)和26.7%(8/30),差异有统计学意义(P0.05);直接门静脉测压示门静脉压力较术前明显下降(P0.05),术后7 d稍有回升。直接门静脉造影示研究组病人冠状静脉和食管静脉曲张显影4例,采用弹簧栓栓塞。两组病人术中失血量、术后并发症发生率差异均无统计学意义。术后随访,研究组和对照组出血复发率分别为3.3%(1/30)和16.7%(5/30)。门静脉CTA复查示研究组病人冠状静脉无显影,对照组病人显示冠状静咏和食管静脉曲张,TIPS治疗成功4例,失败1例。结论经TIPS途径门静脉置管,直接门静脉造影、冠状静脉栓塞以及抗凝可以提高断流术的彻底性、降低门静脉血栓发生率,同时还能动态观察门静脉压力变化。     

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     

用放射性核素显像方法测定分流和断流术前后门静脉压力及其临床价值

目的比较放射性核素显像测定分流、断流术前后门体分流指数和实测门静脉压力的变化 ,探讨其临床应用价值。方法应用放射性核素显像法测定 15例分流术和 2 0例断流术前后门静脉高压症患者的门静脉压力 (H/L PVP) ,并与术中和术后的实测门静脉压力 (PVP)相比较。结果本组 35例手术中实测PVP值为 (37± 4)cmH2 O ,与术前经H/L PVP公式推算值 (36± 4)cmH2 O非常接近 (r =0 81,P <0 0 1)。 15例行分流手术的患者手术前后H/L PVP变化不大 ,而分流术后实测得PVP(2 8± 3)cmH2 O则较分流前的 (37± 5 )cmH2 O显著降低 (P <0 0 5 ) ;2 0例行断流术的患者术后H/L PVP平均下降较多 ,但与术前相比差异无显著意义 (P >0 0 5 ) ,而断流术后测得PVP数据较分散(P >0 0 5 )。结论H/L PVP可以真实反映门静脉高压症患者术前的门静脉压力 ,但对推测分流和断流术后门静脉压力的准确性欠佳     

一氧化氮在门静脉高压症发病中的作用

目的　探讨一氧化氮在门静脉高压症发病中的作用。　方法　 75例门静脉高压症患者 ,术中胃网膜静脉插管测定门静脉压力 ,检测外周动静脉和门静脉血中内毒素和NO2 -/NO3-的含量。　结果　 ( 1)门静脉高压症患者的血中内毒素和NO2 -/NO3-的水平 [( 0 2 4 9± 0 112 )Eu/ml和( 5 5 9± 2 6 2 ) μmol/L]均显著高于对照组 ,且门静脉血中水平最高。 ( 2 )门静脉高压症患者门静脉压力[( 3 5 5± 4 4 )cmH2 O]与门静脉血NO2 -/NO3-的水平呈显著正相关 (n =2 5 ,r =0 5 5 ,P <0 0 1) ,二者在术后的变化量也呈正相关 (r =0 5 7,P <0 0 5 )。 ( 3 )门静脉高压症患者白蛋白水平与NO2 -/NO3-呈负相关 (n =75 ,r=- 0 3 5 ,P <0 0 1) ,且有腹水组的NO2 -/NO3-水平 [( 72 4± 2 0 3 ) μmol/L]较无腹水组 [( 5 0 3± 2 1 0 ) μmol/L]为高。　 结论　门静脉高压症患者血中内毒素和NO的水平升高 ,后者可能参与了门静脉压力的异常升高且与肝功能损害有关。     

门静脉灌注80%乙醇建立猪肝硬化门静脉高压模型

目的探讨门静脉灌注80%乙醇建立猪肝硬化门静脉高压动物模型的可行性。方法选取健康贵州小型香猪13只,随机分为3组:实验1组(5只)、2组(5只)及对照组(3只),实验1、2组门静脉分别灌注80%乙醇5ml及10ml,对照组灌注生理盐水10ml,对所有实验猪于灌注前、灌注后即刻、灌注后6周行直接门静脉造影测量门静脉压力及直径;灌注前及灌注后6h内、术后1~6周行肝组织活检;灌注前及灌注后6周分别行增强CT;灌注后6周解剖所有实验猪,对肝脏各叶标本进行组织学检查。结果实验1组及对照组实验猪灌注前、后门静脉直径及压力的差异无统计学意义(P均0.05)。实验2组灌注后即刻、灌注后6周与灌注前比较,门静脉直径及压力的差异均有统计学意义(P均0.05)。实验1、2组灌注后所有实验猪均形成肝纤维化,灌注后6周实验1组2只、实验2组5只纤维化METAVIR评分达4级。结论经门静脉灌注80%乙醇更适宜构建肝硬化门静脉高压动物模型。     

断流术治疗门静脉高压症的疗效分析

目的　评价断流术治疗门静脉高压症的效果。方法　回顾性分析2 12例门静脉高压症断流术的治疗效果。结果　本组176例(83% )施行Hassab术,36例(17% )施行改良Sugiura术。断流术前后门静脉压力分别为(40±6 )cmH2 O和(36±7)cmH2 O。术后肝功能衰竭发生率为6 % ,其中急诊手术后为2 9 2 % ,择期手术后为3 2 % (P <0 0 1)。手术死亡15例,总手术死亡率为7% ,急诊手术死亡率为33% ,择期手术死亡率为4 % (P <0 0 1)。术后3、5、10年再出血率分别为2 %、6 %、11% ,生存率分别为97%、92 %和89%。结论　断流术止血效果确切,肝功能衰竭和肝性脑病发生率低。急诊手术死亡率高,应尽量避免。断流术引起的门静脉压力下降可能对肝功能造成负面影响。术后肝功能的恶化以及合并原发性肝癌影响患者的长期生存     

经门静脉全胃肠外营养对兔肝再生的影响

目的　探讨经门静脉营养对兔再生的影响。方法　将兔随机分为三组 :Ⅰ组 (对照组 ,n =5 ) ;Ⅱ组 (中心静脉营养组 ,n =10 ) ;Ⅲ组 (门静脉营养组 ,n =10 )。分别切除兔肝左叶。行门静脉或颈内静脉插管后 ,连续胃肠外营养 ,6d后取新鲜肝组织用流式细胞仪分析细胞周期并计算肝细胞增殖指数。结果　Ⅱ、Ⅲ组G0 +G1 期细胞均明显减少 (P <0 .0 1) ,且Ⅲ组减少更明显 (P <0 .0 1)。S期细胞均明显增加 (P <0 .0 1)。G2 +M期细胞Ⅲ组明显高于Ⅰ组和Ⅱ组 (P <0 .0 1)。肝细胞增殖指数Ⅲ组明显高于Ⅱ组 (5 6 .3%对 4 9.3% P <0 .0 1)。结论　经门静脉营养促进肝再生的作用优于经中心静脉营养     

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.     

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.