穿刺肝内支架辅助经颈静脉开通TIPS术后分流道闭塞

目的 观察穿刺肝内支架辅助经颈静脉途径开通TIPS术后分流道闭塞的应用价值。方法 对经单纯颈静脉途径行分流道再通术失败的12例TIPS术后分流道闭塞患者行肝内分流道支架穿刺,辅助经颈静脉通路进行再通,观察术中及术后情况。结果 对12例(12/12,100%)均成功经皮经肝穿刺肝内分流道支架。于10例(10/12,83.33%)实现分流道再通,术前门静脉压力为(29.20±2.04)cmH₂O,术后为(21.70±1.70)cmH₂O;对2例(2/12,16.67%)术前无症状患者未能通过分流道,予口服β受体阻滞剂降低门静脉压力治疗。术中对7例(7/12,58.33%)经肝脏穿刺道置入血管鞘,另5例(5/12,41.67%)仅以导丝穿过闭塞的分流道而未置入血管鞘。术中未发生穿刺道出血等穿刺相关并发症。术后1年,10例成功再通患者TIPS分流道通畅率为90%(9/10)。随访5～60个月期间无肝性脑病、肝性脊髓病或门静脉高压症状复发,无死亡。结论 对于经颈静脉通路再通失败的TIPS术后分流道闭塞患者,经肝穿刺分流道内支架可安全、有效地辅助经颈静脉...     

肝静脉阻塞型布加氏综合征动物模型的制作

目的　探讨肝静脉阻塞型布加氏综合征的发病机制和合理的治疗方案。方法　将2 0条杂种犬随机等分为实验组和对照组,在自动控制X光机监视下,利用介入技术将带侧孔的球囊导管分别放入肝左静脉和肝右静脉,球囊远端阻塞肝静脉远端后,实验组分别注入无水乙醇、明胶海绵和钢丝圈,对照组注入生理盐水。饲养5个月后在全身麻醉下,测定肝功能和门静脉压力,并行肝脏活检,与未行本项操作的家犬门静脉和肝脏组织进行比较。结果　实验组均出现肝静脉闭塞或严重狭窄,出现胃底食管静脉曲张、瘀血性肝硬变,而对照组正常,实验组和对照组总胆红素(TB)分别为(3 1.6±2 .1)和(13 .7±1.1) μmol/L、丙氨酸氨基转移酶(ALT )分别为(15 6.2 3±17.67)和(2 8.44±3 .12 )U /L、碱性磷酸酶(AKP)分别为(177.89±11.2 2 )和(5 8.3 3±17.2 3 )U /L、白蛋白(ALB)分别为(4 0 .3 3±5 .10 )和(5 5 .3 2±4.10 ) g/L及门静脉压力(HPP)分别为(2 5 .68±2 .10 )cmH2 O和(11.5 6±1.70 )cmH2 O ,差异均有统计学意义(P <0 .0 1)。结论　利用介入技术可成功制作肝静脉阻塞型布加氏综合征家犬模型     

经颈静脉肝内门体分流术治疗门静脉海绵样变并发门静脉高压

目的探讨经颈静脉肝内门腔静脉分流术治疗合并门静脉海绵样变的门静脉高压症的疗效。方法 8例反复上消化道出血患者(均有肝硬化、门静脉高压)术前均经B超及CT等影像学证实伴有门静脉海绵样变,门静脉主干及左右支有完全或部分闭塞,对其行TIPS治疗,并评价疗效。结果对7例患者均成功施行TIPS术,1例失败,6例为先经皮穿刺右肝门静脉分支,建立经门静脉右支至主干通道,并行球囊扩张成形治疗。其中4例经常规TIPS途径由肝右静脉穿刺门静脉右支建立门腔静脉分流道,2例由门静脉右支穿刺右肝静脉建立门腔静脉分流道。1例穿刺门静脉右支失败,改由常规TIPS途径穿刺门静脉左支建立门腔静脉分流道。门静脉压力由术前的(33.72±8.35)mmHg降低至术后的(21.43±7.64)mmHg;1例在术后6个月发现分流道狭窄,再次植入支架后恢复通畅。1例术后5个月再发黑便,复查提示分流道堵塞,并门静脉广泛血栓形成,放弃进一步治疗。另5例在12个月随访中分流道通畅,未再发消化道出血。结论 TIPS是治疗伴门静脉海绵样变的门静脉高压症的安全、有效的方法。     

TIPS治疗慢性门静脉血栓伴食管曲张静脉出血的临床疗效

目的:总结经颈内静脉肝内门体分流术(transjugular intrahepatic portosystemic shunt,TIPS)治疗慢性门静脉血栓伴食管曲张静脉出血的临床疗效。方法:对53例慢性门静脉血栓伴食管曲张静脉出血病人实施TIPS治疗。采用经典TIPS、经皮经肝门静脉穿刺TIPS和肝动脉引导门静脉穿刺TIPS完成门静脉开通,建立肝内分流道。结果:TIPS治疗慢性门静脉血栓的技术成功率81.1%。其中,门静脉部分、完全阻塞和海绵状变性病人技术成功率分别为100%、76.5%和60.0%,并发症发生率分别为14.3%、23.5%和46.7%。术后随访(48.0±6.2)个月,门静脉部分、完全阻塞和海绵状变性病人2年分流道通畅率80.0%、61.5%和44.4%,肝性脑病发生率15.0%、15.4%和11.1%,出血复发率15.0%、38.5%和33.3%,死亡率20.0%、23.1%和22.2%。结论:TIPS技术成功率和分流道通畅率与门静脉阻塞的严重程度密切相关,在无其他有效措施治疗慢性门静脉血栓伴食管曲张静脉出血时,可选择TIPS。     

经颈静脉肝内门体分流术后抗凝治疗现状

经颈静脉肝内门体分流术(TIPS)可治疗门静脉高压,但术后常发生分流道狭窄或闭塞。TIPS术后抗凝治疗可预防支架内血栓形成,但同时增加出血风险,且目前尚缺乏统一标准。本文就TIPS术后抗凝治疗现状进行综述。     

小口径人造血管门腔静脉H型分流治疗门静脉高压症

目的　评价小口径人造血管门腔静脉 H型分流治疗门脉高压症的临床效果。方法　 1995年 11月～ 1999年 9月采用小口径 e PTFE(膨化聚四氟乙烯 )人造血管门腔静脉 H型分流治疗 2 3例门静脉高压症患者 ,同时行胃左动脉及冠状静脉结扎 ,2 2例同时切除脾脏。结果　自由门脉压平均由分流前 31.2 7± 4.71cm H2 O降至分流后 16 .82± 3.2 8cm H2 O,门脉向肝血流量较术前减少约 1/ 3。平均随访 2 0 .2月 ,2 3例全部存活 ,均未发生消化道再出血 ,彩超和 /或下腔静脉造影检查示 2 1例分流道通畅 ,2例闭塞 (8.7% ) ,3例发生肝性脑病 (13% )。结论　小口径 e PTFE人造血管门腔静脉 H型分流能有效的降低门脉压力 ,亦能维持大部分门脉向肝血流 ,肝性脑病发生率较低 ,带支持环者通畅率高 ,疗效确切。     

覆膜支架对肝内分流道通畅的影响

经颈内静脉肝内门体分流术(TIPS)已广泛用于治疗门静脉高压症伴食管静脉曲张破裂大出血和顽固性腹水,临床近期疗效十分显著.近十年来,国外采用Viatorr覆膜支架取代裸支架,用于肝内分流道的建立,成功解决了分流道狭窄和阻塞,显著提高了TIPS治疗门静脉高压症的远期疗效[1].我们采用覆膜支架建立肝内门体分流道,并对100例门静脉高压症患者实施治疗,通过超声、CT血管成像(CTA)和直接门静脉造影研究了覆膜支架对肝内分流道通畅的影响.     

肝静脉阻塞型布加综合征的腔内治疗

目的 总结肝静脉阻塞型布加综合征(Budd-Chiari syndrome,BCS)的腔内治疗经验.方法 回顾性分析32例肝静脉阻塞型BCS的临床资料.分别行下腔静脉球囊扩张成形或支架植入术+脾肾静脉分流术;经股静脉或颈静脉入路肝静脉成形术和经皮肝穿刺肝静脉联合颈静脉和/或股静脉入路肝静脉成形术或支架植入术.结果 2例行经皮肝穿刺肝静脉造影时未发现主肝静脉而放弃治疗,其余病例均成功行肝静脉成形和下腔静脉成形术.肝静脉扩张成形前后测肝静脉压力由术前(43±8)cm H_2O降至术后(16±4)cm H_2O(t=21.23,P<0.01).术后1周原有症状明显缓解,腹水消失,腹胀减轻,胸腹壁曲张静脉塌陷.围手术期发生2例穿刺针道出血,经剖腹止血后痊愈.本组随访25例,随访率78.1%.随访时间5～65个月,平均(26.0±2.0)个月.无支架移位及肝静脉再狭窄或闭塞,胸腹擘曲张静脉消失,食道造影见食道静脉曲张明显减轻.本组无肺栓塞及死亡病例.结论 腔内治疗肝静脉阻塞型BCS方法简便、微创、有效,远期疗效尚有待于进一步观察研究.     

腔内治疗肝静脉阻塞型布加综合征

目的 探讨肝静脉型布加综合征(Buddi-Chiari syndrome,BCS)介入治疗方法和疗效的评估.方法 37例肝静脉型BCS患者,术前常规行腹部彩超检查,CT扫描及肝脏血管重建.采用经颈静脉、经股静脉或二者联合途径行肝静脉穿刺造影及闭塞段的开通.术后给予护肝、抗凝、溶栓治疗.结果 手术成功34例,成功率92％,共开通了38条肝静脉.肝静脉开通后,单纯行球囊扩张患者9例;余25例患者置入肝静脉支架27枚,其中2例患者同时置入了右肝静脉和副肝静脉的支架.闭塞的下腔静脉开通后置入国产Z型支架7枚.肝静脉的压力术前24 ～ 48 cm H2O,平均为(36.0±3.4)cm H2O,介入治疗后即刻下降为11～34 cmH2O,平均(21.0±2.3) cm H2O.术后随访3 ～48个月,平均(23.0±2.0)个月,9例单纯行球囊扩张术治疗的患者中,有4例再次发生狭窄或闭塞,均再次行支架置入治疗.行支架置入的患者23例得到了随访,其中6例发生再狭窄或闭塞(6/23,26％).结论 肝静脉型BCS可根据肝静脉闭塞和肝内侧支建立的情况行介入治疗,可显著降低肝静脉和门静脉压力,改善患者的临床症状.     

经颈静脉肝内门体静脉分流术治疗肝硬化门静脉高压症的研究进展

门静脉高压症（ portal hypertension ,PHT）是由于各种原因导致的门静脉及其主要分支压力增高,引起一系列临床症候群,肝硬化是引起PHT最常见的病因。门静脉压力升高可导致食管胃底静脉曲张破裂出血、顽固性肝性腹水、门静脉高压性胃肠病、淤血性脾肿大、肝性脑病、肝肾综合征、肝肺综合征等多种并发症,其中以食管胃底曲张静脉破裂出血最为严重,是导致患者死亡的主要原因。因此, PHT的治疗原则主要是降低门静脉压力和防治并发症。经颈静脉肝内门体静脉分流术（ transjugular intrahepatic portosystemic shunt ,TIPS）利用外科分流术和断流术的基本原理,经颈静脉入路,在肝静脉与门静脉之间建立分流通道,同时栓塞食管胃底曲张静脉,从而预防和治疗上消化道出血。 TIPS具有低侵袭性、无须全麻、操作难度相对低、安全性高、起效迅速、疗效明显等优势,但肝性脑病和术后分流道狭窄仍是亟待解决的难题。本文就TIPS治疗肝硬化PHT的研究进展做一综述,旨在进一步推广该技术的临床应用。     

Treatment of Budd-Chiari Syndrome by Side-to-Side Portacaval Shunt: Experimental and Clinical Results

The Budd-Chiari syndrome caused by occlusion of the major hepatic veins, often of unknown etiology, is typically characterized by massive ascites, hepatomegaly and abdominal pain due to intense congestion of the liver. The outcome has almost always been fatal. This report describes an evaluation of side-to-side portacaval shunt in dogs with experimental Budd-Chiari syndrome and in six patients with hepatic vein thrombosis. In the animal studies, side-to-side portacaval shunt was very effective in relieving massive ascites, hepatomegaly, hepatic congestion and portal hypertension produced by ligation of the hepatic veins. Only one of 24 dogs with side-to-side anastomosis reformed ascites, 67% of the animals survived until the study was concluded after one year, and liver biopsies showed reversal of the severe pathologic abnormalities. In contrast, all 20 control dogs subjected to a sham laparotomy, and all 20 dogs that underwent end-to-side portacaval shunt reformed massive ascites and died within six months with continued hepatic congestion and necrosis.

All six patients with the Budd-Chiari syndrome due to hepatic vein occlusion had massive ascites (4.4-15.9 l), hepatomegaly, abdominal pain and disturbed liver function. In all six, angiography demonstrated occlusion of the hepatic veins with a patent inferior vena cava (IVC) and a normal IVC pressure, and liver biopsy showed intense centrilobular congestion and necrosis. The most valuable diagnostic study was angiography of the IVC and hepatic veins with pressure measurements. Side-to-side portacaval shunt was performed from four to 14 weeks after the onset of symptoms, and produced dramatic and sustained relief of ascites in five of the six patients during follow-up periods of from eight months to seven years. Liver function returned to normal, hepatosplenomegaly disappeared, none of the survivors developed portal-systemic encephalopathy, and follow-up liver biopsies showed disappearance of congestion and necrosis, but mild to moderate fibrosis. One patient died following an emergency IVC thrombectomy and portacaval shunt, which was undertaken when, during the course of his workup, his condition deteriorated suddenly because the thrombotic process extended from the hepatic veins into the IVC. The everpresent risk of this complication, and the dangers associated with delaying operation were emphasized by this case. It is concluded that side-to-side portacaval shunt, which decompresses the liver by converting the portal vein into an outflow tract, provides effective treatment of the Budd-Chiari syndrome when the occlusive process is confined to the hepatic veins.

     

Transjugular intrahepatic portosystemic shunts: An update

Transjugular intrahepatic portosystemic shunts (TIPS) have been used in the treatment of complications of portal hypertension. TIPS is used for the control of acute variceal bleeding and for the prevention of vericeal rebleeding when pharmacologic therapy and endoscopic therapy have failed. Patients with refractory ascites with adequate hepatic reserve and renal function who fail to respond to large volume paracentesis may be reasonable candidates for TIPS. Promising indications for TIPS are Budd-Chiari syndrome uncontrolled by medical therapy, severe portal hypertensive gastropathy, refractory hepatic hydrothorax, and hepatorenal syndrome. TIPS cannot be recommended for preoperative portal decompression solely to facilitate liver transplantation. Special care should be taken to insure proper placement of the stent to avoid increasing the technical difficulty of the transplantation procedure. The major limiting factors for TIPS success are shunt dysfunction and hepatic encephalopathy. Because shunt stenosis is the most important cause of recurrent complications of portal hypertension, a surveillance program to monitor shunt patency is mandatory. The MELD score may be useful in predicting post-TIPS survival, and also in counseling patients and their families. (Liver Transpl 2003;9:207-217.)     

Differential effects on portal and effective hepatic blood flow. A comparison between transjugular intrahepatic portasystemic shunt and small-diameter H-graft portacaval shunt.

OBJECTIVE: This study was undertaken to determine the effects of transjugular intrahepatic portasystemic shunt (TIPS) and small-diameter prosthetic H-graft portacaval shunt (HGPCS) on portal and effective hepatic blood flow. SUMMARY BACKGROUND DATA: Mortality after TIPS is higher than after HGPCS for bleeding varices. This higher mortality is because of hepatic failure, possibly a result of excessive diminution of hepatic blood flow. METHODS: Forty patients randomized prospectively to undergo TIPS or HGPCS had effective hepatic blood flow determined 1 day preshunt and 5 days postshunt using low-dose galactose clearance. Portal blood flow was determined using color-flow Doppler ultrasound. RESULTS: Treatment groups were similar in age, gender, and Child's class. Each procedure significantly reduced portal pressures and portasystemic pressure gradients. Portal flow after TIPS increased (21 mL/second +/- 11.9 to 31 mL/second +/- 16.9, p < 0.05), whereas it remained unchanged after HGPCS (26 mL/second +/- 27.7 to 14 mL/second +/- 41.1, p = n.s.). Effective hepatic blood flow was diminished significantly after TIPS (1684 mL/minute +/- 2161 to 676 mL/minute +/- 451, p < 0.05) and was unaffected by HGPCS (1901 mL/ minute +/- 1818 to 1662 mL/minute +/- 1035, p = n.s.). CONCLUSIONS: Both TIPS and HGPCS achieved significant reductions in portal vein pressure gradients. Portal flow increased after TIPS, although most portal flow was diverted through the shunt. Effective hepatic flow is reduced significantly after TIPS but well preserved after HGPCS. Hepatic decompensation and mortality after TIPS may be because, at least in part, of reductions in nutrient hepatic flow.     

Simultaneous retrohepatic inferior vena cavoplasty and side-to-side portacaval shunt for recurrent thrombosed mesoatrial shunt in the Budd-Chiari syndrome

The Budd-Chiari syndrome is an unusual and often fatal form of portal hypertension caused by hepatic vein occlusion. It comprises less than 5% of surgically correctable causes of portal hypertension and can be one of the most difficult to treat. Recurrent Budd-Chiari syndrome associated with a thrombosed mesoatrial shunt can be an even more vexing problem because of the patient's debilitated condition, hypercoagulable state, and altered anatomy from the previous thoracic and abdominal operations. Although the literature describes numerous surgical methods of treating the Budd-Chiari syndrome, no report specifically addresses the reoperative management of a recurrent thrombosed mesoatrial shunt. We report a patient with a recurrent thrombosed mesoatrial shunt, tightly stenotic retrohepatic inferior vena cava, and occluded hepatic veins with severe portal hypertension. A simultaneous inferior vena cavoplasty and a side-to-side portacaval shunt have produced excellent results with 26-month follow-up. To the best of our knowledge, this method has not been previously described. Other reported surgical methods of treating the Budd-Chiari syndrome are discussed, with emphasis on their relative applicability to the reoperative management of this condition. We submit that this one-stage patch cavoplasty and side-to-side portacaval shunt are the best direct surgical methods to provide immediate and long-term benefit for patients with this most challenging problem.     

Mesoatrial shunt: a surgical option in the management of the Budd-Chiari syndrome

The Budd-Chiari syndrome, arising from hepatic venous outflow obstruction, is frequently complicated by inferior vena caval occlusion or obstruction. Satisfactory decompression of the liver by either portacaval or mesocaval shunts may therefore prove impossible or be prone to failure from shunt thrombosis. The mesoatrial shunt which allows the portal vein to drain directly into the right atrium has previously been advocated in this situation. Five patients with the Budd-Chiari syndrome and caval occlusion and/or obstruction have had mesoatrial shunts constructed using externally supported polytetrafluoroethylene grafts. A single thoracoabdominal incision, incorporating a median sternotomy, was found to provide a satisfactory approach. All patients recovered well with resolution of ascites, diminution in liver size and improvement in inferior vena caval pressure gradients. Furthermore, all shunts have remained patent, as determined by Doppler flow studies and contrast-enhanced computed tomographic scanning, during follow-up periods ranging from 9 to 16 months. If these results are supported by longer term studies, the mesoatrial shunt may become the surgical treatment of choice in patients with hepatic vein occlusion and the Budd-Chiari syndrome associated with inferior vena caval obstruction.     

浅析经颈静脉肝内门体静脉分流术治疗门静脉高压并发症

目的评估经颈静脉肝内门体静脉分流术(TIPS)治疗肝硬化门静脉高压并发症的安全性和有效性。方法自2013年12月至2014年6月,收集31例接受TIPS治疗的肝硬化门静脉高压症的临床资料。术前均接受肝脏CT增强扫描和血管三维重建,了解肝静脉与门静脉的解剖结构关系,以便确定穿刺门静脉分支的靶点,术中,28例栓塞曲张的食管胃底静脉,28例置入巴德公司的一个裸支架加一个Fluency覆膜支架,2例置入单个Fluency覆膜支架。结果 31例患者中30例TIPS操作成功,其中穿刺门静脉右支26例,穿刺门静脉左支4例,成功率为96.8%(30/31);1例因门静脉海绵样变性未成功;无严重并发症发生,近期止血率为100%。结论 TIPS治疗肝硬化门静脉高压并发症是安全和有效的。     

Budd-chiari syndrome and acute portal vein thrombosis: management by a transjugular intrahepatic portosystemic shunt (tips) and portal vein interventions via a tips

Acute portal vein thrombosis (PVT) is a devastating complication of Budd-Chiari syndrome (BCS). Con-servative approach, anticoagulation, systemic or transarterial thrombolysis, and urgent liver transplanta-tion were applied in this scenario but with poor results. We present and discuss an approach to treat BCS complicated by acute PVT. Two young female patients presented with acute liver failure, rapidly pro-gressive tense ascites, renal- and respiratory failure. The diagnosis of chronic BCS complicated by acute PVT was confirmed with ultrasound Doppler. Initial treatment was supportive. Right portal vein local-ization was by transarterial portogram or by computed tomography-guided microcoil placement. Trans-jugular intrahepatic portosystemic shunt (TIPS) was performed and included Wallstents and a Jograft in one case and Viatorr stentgraft that was extended later with a Hemobahn stentgraft in another. Mechan-ical clot removal from the portal system was performed in the primary procedure and in a revision pro-cedure in the following few days. Stents were placed precisely with no extension into the inferior vena cava or deeply into the main portal vein. Patients were fully anticoagulated and patency was assessed by ultrasound Doppler. The procedures were performed on days 5 and 10 following admission. In both cases, successful thrombectomies were reveised and maintained. Partial occlusion of the TIPS and reaccumulation of ascites were reversed with repeated procedure. Both patients were discharged without ascites and normal liver function. In conclusion, urgent TIPS and portal vein thrombectomy via TIPS are emerging therapeutic options that offer a safe and effective treatment to patients with BCS complicated by acute portal vein thrombosis.     

Approach to the spectrum of Budd-Chiari syndrome: Which patients require portal decompression?

Budd-Chiari syndrome (occlusion of the hepatic veins) represents a spectrum disorder. From 1974 to 1984, 20 patients with the syndrome were managed. Eleven required shunt surgery (Group 1) and 5 were managed with nonshunt therapy (Groups 2 and 3). Results have been good. Retrospective review of the liver biopsy specimens showed that Group 1 patients had a greater degree of zone 3 necrosis than Group 2 and 3 patients. We submit that presence of zone 3 necrosis on an initial liver biopsy specimen may define the failing liver of Budd-Chiari syndrome that requires conversion of the portal vein to an outflow tract by shunting.     

A radical operation for the Budd-Chiari syndrome associated with obstruction of the inferior vena cava. A report of six patients

The Budd-Chiari syndrome is caused by an occlusion of the hepatic veins and is often associated with an obstruction in the hepatic portion of the inferior vena cava (IVC). Therefore, the various shunt operations done in an attempt to relieve the portal hypertension are often not effective. By using a radical surgical technique on six patients with Budd-Chiari syndrome, the liver was freed and a wide longitudinal incision was made in the hepatic portion of the IVC. The obstructed hepatic vein was reopened using a Fogarty catheter, and a pericardial patch reinforced with a Teflon prosthesis was secured over the incision. Two patients were still asymptomatic 3 and 4 years after operation. Two patients died postoperatively of pneumonia and hepatic insufficiency. The two other patients were discharged in fair condition, and one died 6 months postoperatively following hepatic failure.