合并静脉血栓形成的布加综合征的介入治疗

目的探讨合并静脉血栓形成的布加综合征的介入治疗。方法回顾性分析我科2005年8月～2012年2月收治的39例合并静脉血栓形成的布加综合征患者的临床资料,其中合并下腔静脉血栓形成18例,合并下肢静脉血栓形成21例。结果 18例经股静脉行置管溶栓术,21例经腘静脉行置管溶栓术,经溶栓治疗后行介入治疗,成功36例,成功率92.3%。26例单纯行下腔静脉球囊扩张术,10例行球囊扩张后置入支架,1例术中出现心包填塞严重并发症,终止手术,转心脏外科开胸行下腔静脉修补术;2例闭塞段较长(>7cm),未开通,放弃介入治疗。33例患者得到随访,平均随访52.6个月。随访期内2例下腔静脉膜性狭窄球囊扩张术后分别于6个月和10个月出现再狭窄,后置入支架,症状改善。其余随访患者下腔静脉通畅,支架无脱落及移位。结论置管溶栓联合血管腔内成形术治疗合并静脉血栓形成的布加综合征微创、有效,中远期效果好,应为首选的治疗方法。     

Budd-Chiari综合征:预开通治疗下腔静脉内陈旧性血栓

目的 探讨预开通技术治疗Budd-Chiari综合征(BCS)合并下腔静脉内陈旧性血栓的临床应用.方法 收集2006年12月-2009年8月采用预开通技术治疗的BCS合并下腔静脉内陈旧性血栓9例,先行下腔静脉造影,而后使用直径12～16 mm的球囊导管预扩张下腔静脉以恢复下腔静脉正向血流;术后给予抗凝、溶栓治疗促进血栓溶解;血栓溶解完全后使用直径25 mm/30 mm的球囊导管扩张下腔静脉以充分开通下腔静脉.术后采用彩色多普勒超声探查血栓溶解情况及下腔静脉通畅情况.结果 9例BCS合并下腔静脉内陈旧性血栓患者均为下腔静脉膜性阻塞,预开通下腔静脉后,除1例因再次阻塞下腔静脉而改行可同收支架治疗外,余8例患者血栓逐渐溶解消失,未出现肺栓塞症状,成功实施下腔静脉球囊扩张成形.术后随访除1例下腔静脉再次阻塞外,余8例下腔静脉血流通畅,无血栓再次形成.结论 预开通技术治疗BCS合并下腔静脉内陈旧性血栓,安全、有效.     

可回收支架治疗下腔静脉阻塞合并血栓形成的中期疗效

目的 观察可回收支架治疗下腔静脉阻塞(BCS)合并血栓形成的中期疗效.方法 8例下腔静脉合并血栓BCS,采用术中抗凝溶栓治疗后,行钝性破膜小球囊预扩张后植入可回收支架,最后使用大球囊充分扩张闭塞膜.术后给予抗凝溶栓治疗,待血栓消失后经颈内静脉将可回收支架取出.其中下腔静脉节段性闭塞合并血栓患者同时置入"Z"型支架.术后用彩色多普勒随访疗效.结果 8例患者均成功实施了介入治疗,血栓均在短期内消失,可回收支架顺利取出,术中未发生肺动脉栓塞和其他并发症.彩色多普勒超声随访3～12个月,2例下腔静脉狭窄,余6例可回收支架置入部位未见血栓形成、局部再狭窄及管壁增厚等情况发生.结论 使用可同收支架治疗下腔静脉阻塞合并血栓形成疗效满意.     

Budd-Chiari综合征:下腔静脉阻塞合并血栓的可回收内支架设计与应用

目的设计可回收内支架以治疗下腔静脉阻塞并血栓型Budd-Chiari综合征(BCS)并观察其临床效果。方法根据下腔静脉合并血栓型BCS病变特点,设计可回收内支架。4例下腔静脉阻塞并血栓型BCS,行钝性破膜小球囊预扩张后置入可回收内支架压迫血栓,再使用大球囊充分扩张闭塞段,完全开通闭塞的下腔静脉。术后给予抗凝溶栓治疗,待血栓消失后经颈内静脉或股静脉将可回收内支架取出。其中下腔静脉节段性闭塞合并血栓者同时在原闭塞段置入“Z”型支架,术后彩超随访。结果4例患者成功介入治疗,血栓短期内消失,可回收内支架顺利取出,术中术后未发生肺动脉栓塞、下腔静脉破裂以及其他并发症。彩超随访3个月,可回收内支架置入部位未见血栓形成、管壁增厚和局部再狭窄。结论应用可回收内支架治疗BCS下腔静脉病变合并血栓安全、有效,对局部血管壁无不良影响,可替代永久内支架置入,值得推广。     

下腔静脉广泛新鲜血栓形成Budd-Chiari综合征的综合介入治疗

目的探讨下腔静脉广泛新鲜血栓形成Budd-Chiari综合征的综合介入治疗的价值。方法15例Budd-Chiari综合征合并下腔静脉广泛新鲜血栓形成患者,综合采取包括大腔导管血栓抽吸、球囊导管扩张、腔静脉临时滤器植入、静脉内插管溶栓以及内支架植入等综合介入治疗。结果经7~10 d的系统治疗,所有病例症状体征消失,下腔静脉完全再通,未出现肺栓塞、出血等严重并发症。结论采取综合介入方法治疗下腔静脉广泛新鲜血栓形成Budd-Chiari综合征疗效确切、安全。     

血管内介入治疗布加氏综合征(附60例分析)

目的：探讨布加氏综合征血管内介入治疗的价值。方法：回顾分析60例病例，在造影明确诊断后行血管内介入治疗。12例行单纯球囊扩张成形术，48例行穿通、球囊扩张成形术 支架置入术。结果：12例行球囊扩张成形术后下腔静脉通畅，48例完全阻塞者开通后置入内支架50枚。全部病例下腔静脉压力减低，随访临床症状缓解。结论：血管内介入治疗布加氏综合征安全有效，应成为治疗本病的首选方法。     

肺癌合并上腔静脉综合征的介入治疗

目的探讨经皮血管内支架植入联合肿瘤供血动脉化疗栓塞治疗肺癌合并上腔静脉综合征的方法及临床价值。方法28例肺癌合并上腔静脉阻塞患者,经螺旋CT和静脉造影明确诊断,以阻塞远侧静脉压大于22mmHg为支架植入适应证,支架植入前明确伴有继发血栓形成患者行抗凝及溶栓治疗,经肘前静脉或股静脉入路,先行狭窄部位球囊扩张术,然后在上腔静脉和头臂静脉狭窄段植入支架,支架植入前后联合支气管动脉栓塞化疗。结果28例患者成功植入支架30枚,3例支架内继发急性血栓形成,经过保留导管溶栓治疗成功溶解血栓,2例术后出现肺栓塞,经过血栓抽吸 抗凝溶栓治疗症状缓解,1例3个月后上腔静脉综合征复发,再次植入1枚支架后上腔静脉重新开通,其余病例在生存期内支架保持通畅。结论上腔静脉支架植入联合支气管动脉栓塞化疗治疗肺癌所致上腔静脉综合征,缓解症状迅速有效、微创、并发症较少,可以明显提高患者的生存质量。     

血管内介入治疗滤器源性下腔-髂静脉长段阻塞8例北大核心CSCD

目的探讨血管内介入治疗滤器源性下腔-髂静脉长段阻塞的可行性和安全性。方法2014年1月至2016年10月采用经皮腔内血管成形术(PTA)和支架植入术治疗8例下腔静脉滤器置入后慢性下腔-髂静脉长段闭塞患者。收集8例患者临床及影像学资料,对血管内介入治疗方法、技术成功率、并发症发生率及随访情况进行统计分析。结果 8例患者闭塞段血管均成功开通。7例球囊成形结合植入支架术后即刻造影显示支架位置良好,支架内血流通畅,侧支血管减少;1例球囊成形结合支架植入术后发生急性支架内血栓形成,经导管直接溶栓2 d后复查造影显示支架内血栓完全溶解,血流恢复通畅。术后随访2~13个月,平均(4.7±3.9)个月。至末次随访,8例患者CT及下肢静脉造影均显示支架在位良好,其中3例支架内可见内膜轻度增生,但血流均通畅。结论滤器长期置入可导致慢性下腔-髂静脉长段闭塞。球囊成形及支架植入可有效开通闭塞血管,是一种安全可行的方法。     

合并血栓形成Budd－Chiari综合征的介入治疗

目的：研究并有血栓形成Ｂｕｄｄ－Ｃｈｉａｒｉ综合征的介入治疗。材料与方法：３例为肝段下腔静脉阻塞并阻塞下方血栓形成。应用导丝对血栓行穿通试验，证实为软血栓后用手推法注入尿激酶溶栓，而后对其阻塞的下腔静脉行穿通术，球囊扩张及内支架置入。结果：３例溶栓及相应介入治疗成功，下腔静脉压力由术前的３．４１ｋＰａ，降至１．７５ｋＰａ。结论：对于软血栓行溶栓治疗后再对阻塞的下腔静脉行ＰＴＡ及内支架置入，可避免肺栓塞发生。对机化血栓直接行穿通术，ＰＴＡ及内支架置入。     

不同类型下腔静脉阻塞型Budd-Chiari综合征的介入治疗

目的探讨不同类型下腔静脉阻塞型Budd-Chiari综合征(BCS)介入治疗方法,评价介入治疗BCS的价值。方法86例BCS患者均由DSA确诊,根据不同类型下腔静脉阻塞采用的介入治疗方法有下腔静脉经皮单纯球囊扩张成形术;球囊扩张术加支架置入术,血栓抽吸和溶栓术。结果56例下腔静脉膜性阻塞中54例完全开通,1例因隔膜太坚硬未能扩开,1例胸段下腔静脉破裂出血。15例下腔静脉节段性阻塞中14例获得良好开通,1例因闭塞段太长(约6 cm)开通未成功。6例下腔静脉内伴有新鲜血栓完全清除后获得开通;11例下腔静脉内伴有陈旧性附壁血栓10例获得开通。介入治疗BCS成功率95.8%(68/71,肝静脉型及混合型BCS除外),死亡率1.4%,复发率4.2%,未发生心包填塞、支架滑移、肺栓塞等严重并发症。结论介入治疗BCS是一种简单、创伤小、见效快的方法,绝大部分可替代外科手术治疗。对不同类型下腔静脉阻塞采用正确的治疗方法可减少并发症和复发率。     

Use of the Arrow percutaneous thrombectomy device and transjugular liver biopsy cannula for mechanical thrombectomy of the inferior vena cava in a patient with Budd-Chiari syndrome

A 33-year-old woman with Budd-Chiari syndrome and hypercoagulability was sequentially treated with the placement of hepatic vein stents and transjugular intrahepatic portosystemic shunts (TIPS), all of which repeatedly thrombosed. Four months after TIPS revision with an endoprosthesis, a large inferior vena cava (IVC) thrombus developed caudal to an IVC stenosis. A percutaneous thrombectomy device was introduced coaxially through a transjugular liver biopsy cannula to extend its effective diameter range of attack and was steered within the IVC to successfully clear the thrombus. The condition recurred 9 months later, and the technique was repeated successfully. At subsequent 12-month follow-up, the IVC remains patient and symptoms resolved. This combination of cannula and percutaneous thrombectomy device proved essential in facilitating successful mechanical thrombectomy of the IVC.     

置管溶栓治疗下腔静脉血栓：附21例报道

目的探讨置管溶栓（catheter-directed thrombolysis,CDT）治疗下腔静脉血栓的安全性和疗效。 方法回顾性分析21例经CDT治疗的下腔静脉血栓患者的临床及影像资料。 结果21例患者均经静脉造影诊断为下腔静脉血栓,同时伴有下肢深静脉血栓。其中下肢深静脉血栓向上延续导致的下腔静脉血栓18例,下腔静脉滤器导致的下腔静脉血栓3例。21例患者均在下腔静脉滤器的保护下成功进行CDT治疗,其中7例患者伴有髂静脉压迫综合征,给予髂静脉支架治疗。随访3～48个月,1例肿瘤患者CDT术后2周再次出现下肢深静脉血栓,给予加强抗凝治疗后好转,其他患者无血栓复发,所有患者无严重并发症的发生。 结论下肢深静脉血栓和下腔静脉滤器均会导致下腔静脉血栓。在下腔静脉滤器的保护下,CDT治疗下腔静脉血栓是安全有效的方法。     

Hepatic inferior vena cava obstructions: clinical results of treatment with percutaneous transluminal laser-assisted angioplasty

Three cases of hepatic inferior vena cava (IVC) obstruction (two segmental and one membranous) associated with Budd-Chiari syndrome were successfully treated with percutaneous transluminal angioplasty (PTA) with use of an Nd-YAG (neodymium-yttrium, aluminum, garnet) laser. The occluded portions were canalized by advancing a ceramic-capped delivery system and delivering intermittent laser emissions. The canal was widened by simultaneous inflation of three or four Gruentzig balloon catheters. In two of the three cases, this procedure was done after unsuccessful canalization of the occluded portions by conventional means. Postoperatively, all patients showed disappearance of Budd-Chiari syndrome. One patient also showed marked regression of a huge intraluminal thrombus. There were no serious complications during and after the procedures. Use of the Nd-YAG laser seems to be of value in PTA for the treatment of hepatic IVC obstructions as well as in treatment of arteriosclerotic lesions.     

Treatment of Budd-Chiari syndrome with urokinase following predilation in patients with old inferior vena cava thrombosis

Purpose

This study was undertaken to evaluate the safety and feasibility of thrombolytic urokinase treatment after predilation in patients with Budd-Chiari syndrome (BCS) with chronic inferior vena cava (IVC) thrombosis.

Materials and methods

Between December 2006 and September 2009, 13 consecutive BCS patients with chronic IVC thrombosis were treated with continuous urokinase infusion after predilation and subsequent (i.e. after thrombus resolution) IVC dilation with a 30-mm dilator. The procedural technical and angiographic, and ultrasonic results, as well as mortality, morbidity and the final clinical outcome, were evaluated immediately after the treatment or at 1 week and 1, 3, 6 and 12 months and then annually thereafter.

Results

The immediate and long-term procedural technical outcome was successful in all patients. Follow-up inferior vena cavagrams demonstrated complete resolution of the chronic IVC thrombi and full IVC patency, without occurrence of pulmonary embolism at any time during the study. Colour-Doppler ultrasound (US) follow-up for 16.92 months (±12.04) showed full patency of the IVC, without thrombosis, restenosis or reobstruction, in all patients and resolution of all clinical symptoms. All patients were alive at the time of this report.

Conclusions

Our preliminary results indicate that thrombolysis with continuous infusion of urokinase after predilation is a safe and feasible approach for treating BCS patients with chronic IVC thrombosis.     

42例Budd－Chiari综合征影像学分析

报告４２例Ｂｕｄｄ－Ｃｈｉａｒｉ综合征．其中膜性梗阻７例，膜性狭窄５例，节段性梗阻１２例，节段性狭窄１４例，下腔静脉正常肝静脉狭窄４例。４２例中９例（２１．４％）合并肾后段下腔静脉瘤。本文着重通过对本组病例超声与下腔静脉造影资料的对比分析，进一步评价超声与下腔静脉造影对本征的诊断价值。本文同时对影响下腔静脉瘤形成的因素进行了详细研究，并对下腔静脉瘤的影像学表现进行了探讨。     

Useful interventional thrombolytic and anticoagulant therapy for thrombosis due to embolization (TAE) in Budd-Chiari syndrome.

Transarterial embolization given for hepatoma in a patient with Budd-Chiari syndrome resulted in hepatic infarction and inferior vena cava thrombosis. Transarterial membranotomy and repeated infusion of thrombolytic agents and anticoagulants directly in the thrombus brought about improvement of the circulation surrounding the liver and IVC, and recovery from hepatic failure.     

Acute thrombosis of the inferior vena cava and hepatic veins in patients with Budd-Chiari syndrome: CT demonstration

We reviewed the CT findings in 17 patients with angiographically proved Budd-Chiari syndrome to determine the ability of CT to show acute thrombosis of the inferior vena cava (IVC) and hepatic veins. In eight patients with membranes (web or band) in the IVC, no thrombus was detected with CT or angiography. In the other nine patients, thrombi in the IVC and/or hepatic veins were seen as intraluminal filling defects that did not change in appearance on precontrast and postcontrast CT scans. Attenuation values of intraluminal filling defects of the IVC ranged from 38 to 42 H in four patients. High-attenuation intraluminal filling defects (60-70 H) of the IVC (five patients) and hepatic veins (one of five patients) were detected. Of these five patients, four had acute symptoms and one had chronic vague symptoms. The underlying disease was a web or band in the IVC and hepatic veins in three patients, invasive hepatocellular carcinoma in one, and injury to the IVC wall during hepatectomy in one. Inferior venacavography showed occlusion of the hepatic segment of the IVC in all five patients. Additional angiograms obtained by injection of contrast medium after a catheter tip was placed in the occluded hepatic IVC showed numerous filling defects suggestive of thrombi of recent onset, which correlated with the high-attenuation thrombi seen on CT scans in two patients. In the remaining three patients, high-attenuation areas in the IVC and hepatic veins also were considered to represent thrombi of recent onset because the attenuation values later decreased to 33-42 H. Spontaneous reduction in diameter of the thrombosed segment of the IVC was observed in four of the five patients. Knowledge of the CT features of acute thrombosis of the IVC and hepatic veins is useful in the early diagnosis of Budd-Chiari syndrome.     

Reconstruction of an inferior vena cava stent occlusion using double-barrel stenting in a patient with Behçet's disease

Symptomatic inferior vena cava (IVC) and iliac vein thrombosis is increasingly being treated with thrombolysis, thrombus retrieval and deep venous stenting. If the IVC stent occludes, endovenous intervention is indicated to restore patency. An 18-year-old male with Behçet''s disease presented with deep vein thrombosis (extending from the IVC to the popliteal segments bilaterally) which was initially treated with thrombolysis and stenting. Fifteen months later, the patient experienced symptomatic deterioration; a chronically-occluded IVC stent was identified and reconstructed using a double-barrel stenting technique. Patient compliance to post-stenting anticoagulation therapy is paramount to maintain stent patency. A multi-disciplinary approach including haematologists can be beneficial for patients with a background of thrombophilic disorders.     

Membranous obstruction of the inferior vena cava with Budd-Chiari syndrome: MR imaging findings.

Membranous obstruction of the inferior vena cava (IVC) is a curable cause of a primary type of Budd-Chiari syndrome. Magnetic resonance (MR) imaging and vena cavography were performed on nine patients with membranous obstruction of the IVC. The MR findings were retrospectively analyzed and compared with computed tomographic findings in seven patients. The morphologic features of membranous obstruction of the IVC on spin-echo MR images were a curvilinear soft-tissue membrane (five cases) or an obliterated lumen of a hepatic segment of the IVC (four cases) in transverse or sagittal views. The lumen below the obstruction revealed flow-related signal (seven cases), intraluminal thrombus (one case), and thrombotic occlusion (one case). The hepatic veins were narrow and disoriented without connection to the hepatic segment of the IVC just below the diaphragm. On T2-weighted images, inhomogeneity with high signal intensity was shown more prominently in the hepatic parenchyma in Simson type II or III membranous obstruction. Other findings were hepatosplenomegaly, enlarged caudate lobe, cirrhotic liver, associated hepatoma, and presence of various collaterals.