经皮经肝组织粘合剂栓塞治疗食管静脉曲张的疗效观察

目的观察经皮经肝组织粘合剂（TH胶）栓塞治疗食管静脉曲张的远期效果。方法经皮经肝TH胶栓塞治疗食管静脉曲张47例，术后定期复查胃镜及CT，了解食管下段曲张静脉内TH胶转归和静脉曲张消失情况。结果45例食管静脉曲张患者术后显效率100％，随访6～52个月，平均（31±22）个月，静脉曲张复发10例；随访过程中出血4例，再出血率8．9％。胃镜及cT随访显示，食管黏膜下曲张静脉内TH胶逐渐脱失，而食管旁和胃底贲门周围静脉内TH胶长期滞留栓塞。结论经皮经肝栓塞术能使TH胶到达食管下段的黏膜下曲张静脉，使曲张静脉长期闭塞，能有效的治疗食管静脉曲张，预防复发。     

TH胶栓塞联合门体静脉小分流治疗肝硬化门脉高压食管胃底静脉曲张出血

目的探讨应用TH胶栓塞联合门体静脉小分流治疗门脉高压食管胃底曲张静脉曲张破裂出血中的应用价值。方法入选41例门静脉高压症并食管胃底静脉曲张的患者,其中21例行TH胶栓塞联合门体静脉小分流术（A组）,另外20例患者行经皮经肝食管胃底曲张静脉栓塞术（PTVE）联合部分性脾栓塞（PSE）（B组）,对比两组患者肝功能、白细胞、血小板改变、食管胃底曲张静脉消失率、再出血率、肝性脑病发生率及门静脉自由压（free portal pressure,FPP）变化。结果 A组曲张静脉消失率、总有效率均高于B组（P〈0.05）,再出血率、肝性脑病发生率均低于B组（P〈0.05）,术后门静脉压力亦明显低于B组（P〈0.01）。两组术后白细胞及血小板、白蛋白较术前明显升高,差异有统计学意义（P〈0.01）,两组之间也存在显著统计学差异（P〈0.01）。结论以TH胶栓塞联合门体静脉小分流治疗门静脉高压症食管胃底静脉曲张安全、有效、并发症少,值得临床应用与推广。     

经皮经肝组织黏合剂栓塞联合部分脾栓塞治疗食管静脉曲张

目的评价经皮经肝穿刺组织黏合剂（TH胶,α-氰基丙烯酸正丁酯）栓塞联合部分脾动脉栓塞（PSE）治疗食管静脉曲张的临床疗效。方法以食管下段曲张静脉和贲门胃底周围血管为靶血管,将TH胶灌注至食管下段及胃底曲张静脉内,使曲张静脉永久性闭塞,并联合PSE治疗食管静脉曲张出血患者84例,18例患者行急诊栓塞治疗。结果（1）81例栓塞成功,成功率96.4%,3例术后1个月因肝功能衰竭、腹腔感染和脑出血死亡。（2）TH胶栓塞到食管下段曲张静脉及胃底周围血管者38例;栓塞冠状静脉及胃底贲门周围曲张静脉但未达食管下段者31例;仅栓塞到胃冠状静脉主干者9例。术后其食管静脉曲张消失率分别为71.1%（27/38）、35.5%（11/31）、0（0/9）,χ^2=18.3105,P〈0.01。（3）随访6～47（31.0±16.5）月,13例患者再出血,总出血率为16.7%。其中食管胃底型栓塞再出血率为7.9%（3/38）;胃底型再出血率为12.9%（4/31）;主干型再出血率为66.7%（6/9）,χ^2值分别为12.6603和8.0765;P值均〈0.01。结论经皮经肝TH栓塞联合部分脾动脉栓塞不仅可控制急症出血,还可预防再出血,是治疗和预防门静脉高压食管静脉曲张出血的有效方法,术中应尽量将TH胶注射到食管下段曲张静脉和贲门胃底周围静脉内,以确保介入栓塞治疗的远期疗效。     

经皮经肝组织粘合剂栓塞联合内镜下套扎治疗食管静脉曲张的临床应用

目的 探讨经皮经肝组织粘合剂(TH胶)栓塞(PTVE)联合内镜下套扎(EVL)治疗食管静脉曲张的合理性和临床疗效.方法 23例食管静脉曲张患者先行PTVE使TH胶栓塞胃冠状静脉主干及胃底贲门周围静脉,1个月后对食管黏膜下曲张静脉行内镜下套扎治疗.结果 该组患者TH胶未栓塞食管下段曲张静脉,PTVE后静脉曲张缓解,但未完全消失;联合EVL后17例患者静脉曲张基本消失,消失率73.9%.21例行1次套扎治疗,2例行2次套扎治疗,平均套扎次数1.1次/例.随访3～31个月(平均19.2个月),静脉曲张复发或加重3例(13.1%),2例(8.7%)患者门脉高压性胃病出现少量出血.结论 经皮经肝TH胶栓塞能阻断冠状静脉主干、食管胃底周围血管等曲张静脉的供血血管,而内镜下套扎治疗则消除食管下段黏膜下曲张静脉,二者联合可优势互补,从而取得更好的远期疗效.     

不同栓塞剂经皮经肝经导管栓塞治疗食管静脉曲张的疗效比较

目的比较经皮经肝α-氰基丙烯酸（TH胶）栓塞与无水乙醇、明胶海绵及金属钢圈栓塞治疗食管静脉曲张的临床疗效。方法将76例食管静脉曲张患者分为经皮经肝TH胶栓塞40例（TH胶栓塞组）和经皮经肝无水乙醇、明胶海绵和金属钢圈栓塞36例（对照组），两组均联合部分脾动脉栓塞（范围50％～80％）。比较两组近期疗效，1、2年静脉曲张复发率、再出血率、死亡率及并发症。结果两组操作成功率及急症止血率均为100％，术后1～2个月TH胶栓塞组和对照组静脉曲张消失率分别为62．5％（25／40）和63．9％（23／36），差异无统计学意义（P〉0．05）。TH胶栓塞组和对照组1、2年静脉曲张复发率分别为12％（3／25）和20％（5／25）、39．1％（9／23）和86．9％（20／23），差异有统计学意义（P〈0、01）。术后2年再出血率TH胶栓塞组为17．5％（7／40），对照组为52．8％（19／36）；两组死亡率分别为17．5％（7／40）和38．9％（14／36）。腹痛、发热、胸腹水、异位栓塞等并发症在两组间差异无统计学意义（P〉0．05）。结论经皮经肝TH胶注射能彻底栓塞食管下段曲张静脉及其供血血管，具有较好的远期效果，优于传统的无水乙醇、明胶海绵和金属钢圈栓塞。     

内镜下套扎联合经皮经肝TH胶栓塞治疗肝硬化食管胃底静脉曲张的临床应用

目的评价内镜下套扎(EVL)联合经皮经肝曲张静脉TH胶栓塞术(PTVE)治疗肝硬化食管胃底静脉曲张出血的远期疗效。方法 44例肝硬化食管胃底静脉曲张出血患者,先行食管曲张静脉的内镜下套扎治疗,1周后再行TH胶PTVE,栓塞食管胃底曲张静脉区域及其来源血管。联合治疗术后定期复查胃镜,观察曲张静脉消失情况,随访治疗后曲张静脉复发率及再出血率。结果 44例食管胃底静脉曲张患者,32例食管曲张静脉基本消失,消失率72.7%;8例胃底静脉曲张基本消失,消失率100%;12例食管静脉曲张程度明显减轻,总有效率100%。随访6~39个月,平均25.6个月,5例食管静脉曲张复发,复发率11.4%;3例再出血,再出血率6.8%。结论内镜下套扎治疗能机械性地消除食管曲张静脉,经皮经肝TH胶栓塞能栓塞食管胃底曲张静脉区域及其供血血管,二者联合能达到协同作用,具有更好的远期疗效。     

Glubran-2胶栓塞术治疗门静脉高压食管胃底静脉曲张

目的观察Glubran-2胶栓塞术治疗门静脉高压食管胃底静脉曲张的疗效。方法中重度门静脉高压食管胃底静脉曲张患者15例,经皮经肝穿刺门静脉造影明确出血曲张静脉后,超选择插管行Glubran-2胶栓塞术治疗。栓塞前后进行CT平扫联合增强扫描,并测定患者门静脉压力。结果 15例患者成功进行胃左静脉、胃后静脉和胃短静脉Glubran-2胶完全性栓塞术。门静脉压力术前为(34.1±7.1)cmH2O、术后为(37.7±4.1)cmH2O,手术前后相比,P<0.05。术后CT增强扫描显示曲张静脉完全栓塞,其内可见高密度铸型。术后随访3～12个月,再出血2例。结论 Glubran-2胶栓塞术治疗门静脉高压食管胃底静脉曲张安全有效,手术前后CT检查可明确诊断及判断疗效。     

经皮经肝组织胶栓塞治疗食管静脉曲张与内镜下套扎治疗的疗效比较

目的比较经皮经肝α氰基丙烯酸正辛酯（TH胶）栓塞术（PTVE）与内镜下食管静脉套扎术（EVL）治疗食管静脉曲张的临床疗效。方法急性及近期食管胃静脉曲张出血的肝硬化患者随机分成PTVE组（52例）及EVL组（50例）进行干预治疗,观察术后上消化道再出血率、食管曲张静脉复发率及生存率。结果随访期间（PTVE组平均24个月,EVL组25个月）两组的上消化道再出血率分别为15．4％（8／52）和42％（21／50）（χ^2=8．87,P=0．005）,其中食管曲张静脉再出血率为5．8％（3／52）和24％（12／50）（χ^2=5．38,P=0．012）,两组食管静脉曲张复发率分别为17．3％（19／52）和52％（26／50）（χ^2=13．61,P〈0．001）,两组生存率相似,（χ^2=3．30,P=0．054）。结论PTVE能使曲张静脉及其穿支静脉和贲门胃底静脉周围静脉一并栓塞,术后食管静脉曲张的再出血率低于EVL治疗,具有较好临床价值。     

经皮经肝胃冠状静脉栓塞术联合脾动脉栓塞术治疗肝硬化食管胃底静脉曲张疗效观察

目的 观察经皮经肝胃冠状静脉栓塞术联合脾动脉栓塞术治疗肝硬化食管胃底静脉曲张的疗效.方法 12例经胃镜明确为食管胃底重度静脉曲张出血的肝硬化患者,择期行经皮经肝胃冠状静脉栓塞术及脾动脉栓塞术,术后定期胃镜检查,观察曲张静脉的动态变化.结果 术后即时食管胃底曲张静脉均消失;随访6～12个月曲张静脉基本消失6例,中度曲张3例,仍为重度曲张者3例,其中2例发生再出血,行胃镜下硬化剂治疗.结论 经皮经肝胃冠状静脉栓塞术联合脾动脉栓塞术是治疗肝硬化食管胃底静脉曲张安全有效的方法.     

胃冠状、胃短静脉栓塞术对胃底静脉曲张出血疗效评价

目的探讨胃冠状静脉、胃短静脉栓塞术对胃底静脉曲张出血治疗的价值。方法32例肝硬化并食管胃底静脉曲张出血经内镜下套扎、硬化治疗后仍有出血的患者，经皮经肝穿刺行胃冠状静脉、胃短静脉栓塞治疗。栓塞剂主要为无水乙醇、钢圈和明胶海绵。均行1次栓塞治疗，并经3～11个月随访，胃镜复查。结果29例复查胃镜，其中21例(72．4％)胃底曲张静脉完全消失，8例(27．6％)胃底曲张静脉明显减轻，无红色征及糜烂。随访期内有1例(3．1％)因门脉高压性胃炎致黏膜糜烂出血。未发现明显并发症。结论经皮经肝穿刺行胃冠状静脉、胃短静脉栓塞治疗具有消除胃底静脉曲张，并可预防出血的作用。     

经皮经肝曲张静脉栓塞治疗断流术后食管胃底静脉破裂出血的疗效

目的 研究以组织胶为主要栓塞材料,采用经皮经肝曲张静脉栓塞术(PTVE)治疗和预防门奇静脉断流术后食管胃底静脉曲张破裂出血的临床疗效.方法 2006年11月至2008年9月,对22例曾行断流术再发食管胃底静脉曲张破裂出血的患者行PTVE组织胶栓塞(n=10)或内镜下硬化剂(EIS,n=12)治疗,随访两组患者治疗后再出血率、死亡率、治疗前后静脉曲张和肝功能以及PTVE治疗组患者在曲张侧支静脉栓塞前后门静脉压力的变化.结果 ①在平均12.5个月的随访期内,PTVE治疗组患者再出血率和死亡率分别为1/10和0;EIS治疗组随访13.4个月,患者再出血率和死亡率分别为7/12和3/12,两组问差异有统计学意义(P<0.05).②PTVE和EIS治疗均可显著减轻食管和胃底静脉曲张程度.③对有门静脉血栓患者,PTVE联合门静脉球囊成形术,可以改善肝脏门静脉血供.④PTVE和EIS治疗均未加重肝功能损伤.结论 对门奇静脉断流术后食管胃底静脉破裂出血的患者,采用以组织胶为主要栓塞材料的PTVE治疗的疗效优于EIS治疗.     

门脉CTA及内镜对胃静脉曲张诊断及疗效评估的比较研究

目的探讨多层螺旋CT血管造影（门脉CTA，简称CTPA）在诊断门脉高压胃静脉曲张及内镜下胃静脉曲张黏合剂联合硬化剂治疗疗效评估中的作用。方法对20例内镜下证实存在胃静脉曲张的患者予以黏合剂联合硬化剂治疗，治疗前后分别进行多层螺旋CT血管门脉造影检查。结果20例门脉CTA检查均发现胃静脉曲张。GOV-型门脉CTA示血流来源以胃左静脉为主，GOV-2型则由胃左静脉、胃短／胃后静脉混合供血，IGV-型以胃短／胃后静脉供血为主，此型分流发生率较高。经内镜下黏合剂联合硬化剂治疗，孤立性瘤状胃静脉曲张（IGV-型）10例，总体有效率为90．00％，而非孤立性瘤状胃静脉曲张（GOV-型和GOV-型）9例，总体有效率为44．45％。结论门脉CTA能准确、直观、立体地显示血管解剖特点，为门脉高压胃静脉曲张的诊断、治疗方案的选择提供重要依据，并且可作为评估内镜下胃静脉曲张黏合剂联合硬化剂治疗疗效的一种重要手段。     

胃冠状静脉栓塞联合部分脾动脉栓塞术在门静脉高压治疗中的评价

目的探讨经皮胃冠状静脉栓塞联合部分脾动脉栓塞术在门静脉高压治疗中的可行性和疗效。方法50例肝硬化食管胃底静脉曲张的患者,用TH胶进行胃冠状静脉栓塞并联合部分脾动脉栓塞术,分析术中造影情况,随访术后反应及并发症、止血效果、血小板及白细胞上升情况。结果经皮胃冠状静脉栓塞联合部分脾动脉栓塞手术成功率100%;栓塞前门静脉压在35～55cmH2O,平均43.2cmH2O,栓塞后门静脉压力在25～38cmH2O,平均28.5cmH2O。栓塞前可看到明显增粗的胃冠状静脉以及曲张静脉团,栓塞后则消失;所有患者中10例有穿刺部位疼痛,穿刺道出血0例。10例出现左上腹脾区隐痛不适,10例出现反应性左胸腔积液,2例出现脾脓肿;18例急性出血者术后出血皆停止,2例6个月内再出血,重行胃短静脉栓塞,术后未再出血;术前血小板50×10^9/L以下12例中2例3个月内没有明显上升,余血小板异常者3个月内均有不同程度上升。结论胃冠状静脉栓塞联合部分脾动脉栓塞术治疗门静脉高压效果显著,是目前值得推广的治疗方案。     

Combination treatment of partial splenic embolization, endoscopic embolization and transjugular retrograde obliteration for complicated gastroesophageal varices

The treatment of complicated gastroesophageal varices with a gastrorenal shunt and portal hypertensive gastropathy has not yet been established. We were able to control a case of complicated large gastroesophageal varices with gastrorenal shunt and portal hypertensive gastropathy using a combination treatment of partial splenic embolization, endoscopic embolization and transjugular retrograde obliteration. We first applied partial splenic embolization to reduce the hyperdynamic cycle of portal hypertension and to treat thrombocytopenia. We secondarily applied endoscopic embolization for the esophageal varices. Transjugular retrograde obliteration was performed for the gastric varices 14 days after endoscopic embolization. The wedged hepatic venous pressure had not changed after transjugular retrograde obliteration. After the combination treatment, the gastroesophageal varices were successfully obliterated, but portal hypertensive gastropathy did not worsen. The platelets count, arterial ketone body ratio and ICGR15 were improved. Partial splenic embolization was useful to protect side effects of endoscopic embolization and transjugular retrograde obliteration. We conclude that the combination treatment of partial splenic embolization, endoscopic embolization and transjugular retrograde obliteration is a rational, effective and safe treatment for complicated gastroesophageal varices with gastrorenal shunt and portal hypertensive gastropathy.     

The natural history of portal hypertensive gastropathy in patients with liver cirrhosis and mild portal hypertension

BACKGROUND: Portal hypertensive gastropathy is a potential cause of bleeding in patients with liver cirrhosis. Studies on its natural history have often included patients submitted to endoscopic or pharmacological treatment for portal hypertension. PATIENTS AND METHODS: A total of 222 cirrhotic patients with mild degree of portal hypertension (i.e., with no or small varices at entry, without previous gastrointestinal bleeding and medical, endoscopic, or angiographic treatment) were followed up with upper endoscopy every 12 months for 47 +/- 28 months. RESULTS: Upon enrollment 48 patients presented portal hypertensive gastropathy (43 mild and 5 severe) and the presence of esophageal varices was the only independent predictor of the presence of this gastric lesion at multivariate analysis. The incidence of portal hypertensive gastropathy was 3.0% (1.1-4.9%) at 1 yr and 24% (18.1-29.9%) at 3 yr, while the progression was 3% (1-6.9%) at 1 yr and 14% (4.2-23.8%) at 3 yr. The presence of esophageal varices and the Child-Pugh class B or C at enrollment were predictive of the incidence of portal hypertensive gastropathy, while only Child-Pugh class B or C was correlated with the progression from mild to severe, at multivariate analysis. During follow-up 16 patients bled from portal hypertensive gastropathy (9 acutely and 7 chronically) and one patient died of exsanguination from this lesion. CONCLUSIONS: The natural history of portal hypertensive gastropathy is significantly influenced by the severity of liver disease and severity of portal hypertension. Acute bleeding from portal hypertensive gastropathy is infrequent but may be severe.     

肝硬化非常见侧支循环临床特点研究

目的 探讨肝硬化患者门体循环之间非常见侧支循环形成的临床特点及意义。方法 对临床确诊为肝硬化的患者运用64排螺旋CT和三维血管成像结合电子胃镜检查,观察其门体循环之间非常见侧支循环的形成。结果 ①700例肝硬化患者中118例(16.86%)存在非常见侧支循环,依次为脾肾静脉分流、胃肾静脉分流、椎旁静脉分流、腹膜后静脉分流、胃脾分流和心膈角静脉分流。②非常见侧支循环形成与肝硬化Child-Pugh分级相关(P<0.01)。③与常见侧支循环形成组比较,非常见侧支循环组较少出现重度食管和(或)胃底静脉曲张、重度门静脉高压性胃病及大量腹水(P<0.01)。④非常见侧支循环组中肝性脑病和慢性血氨升高的发生率高于常见侧支循环组(P<0.01)。结论 ①肝硬化患者中非常见侧支循环并不"非常见";②非常见侧支循环形成与肝功能Child-Pugh分级有关;③非常见侧支循环形成可缓解门静脉高压引起的相关并发症,但增大了肝性脑病和慢性血氨升高的发病率。     

Natural history of portal hypertension

A rise in pressure in the portal vein is a frequent occurrence in patients with cirrhosis. One common manifestation affecting at least 50% of cirrhosis patients is the development of gastroesophageal varices and portal hypertensive gastropathy. Bleeding from gastric or esophageal varices will occur in approximately 1/4 of cirrhotic patients with an associated high mortality. Large esophageal varices that have red color signs and isolated gastric varices in the fundus of the stomach are most likely to hemorrhage. The greatest risk of bleeding is during the first year following the index endoscopy. Once varices have bled they are almost certain to rebleed in the absence of therapy. Similarly, severe portal hypertensive gastropathy is likely to cause chronic blood loss. Knowledge of the natural history of gastroesophageal varices allows for the development of effective treatment strategies.     

胃静脉曲张的病因及临床特点

目的探讨胃静脉曲张的病因及临床特点。方法回顾性分析北京协和医院2000年1月至2005年4月胃静脉曲张患者的病因及并发出血的情况,胃静脉曲张出血与红色征、曲张静脉类型、程度的关系,以及各型曲张静脉发生门脉高压性胃病的情况。结果我院5年间共诊治胃静脉曲张407例,占同期全部食管、胃静脉曲张的47.1%。胃静脉曲张的病因中,肝硬化占74.4%。孤立性胃静脉曲张的病因中脾静脉阻塞占37.2%,肝硬化占33%。407例胃静脉曲张患者中出血121例(29.7%)。在1型和2型胃静脉曲张、1型孤立性胃静脉曲张患者中,出血组红色征的阳性率、静脉曲张的程度均显著高于未出血组(P<0.01)。门脉高压所致的304例胃静脉曲张患者中发生门脉高压性胃病60例(19.7%),与食管静脉曲张发生门脉高压性胃病(22.3%)无差异,但孤立性胃静脉曲张很少出现门脉高压性胃病(9.6%,P<0.05)。结论胃静脉曲张最常见的病因是各种原因引起的肝硬化,而孤立性胃静脉曲张最常见的病因是脾静脉阻塞。红色征、静脉曲张程度是胃静脉曲张出血的危险因素。胃静脉曲张对门脉高压性胃病无影响。     

Treatment of bleeding from portal hypertensive gastropathy by portacaval shunt

Portal hypertensive gastropathy is a vascular disorder of the gastric mucosa distinguished by ectasia of the mucosal capillaries and submucosal veins without inflammation. During 1988 to 1993,12 patients with biopsy-proven cirrhosis (10 alcoholic, 2 posthepatitic) were evaluated and treated prospectively by portacaval shunt for active bleeding from severe portal hypertensive gastropathy. Eleven patients had been hospitalized for bleeding three to nine times previously, and one was bleeding uncontrollably for the first time. Requirement for blood transfusions ranged from 11 to 39 units cumulatively, of which 8 to 30 units were required specifically to replace blood lost from portal hypertensive gastropathy. Admission findings were ascites in 9 patients, jaundice in 8, severe muscle wasting in 10, hyperdynamic state in 9. Child's risk class was C in 7, B in 4, A in 1. Ten of the 12 patients had previously received repetitive endoscopic sclerotherapy for esophageal varices, which has been reported to precipitate portal hypertensive gastropathy. Eight patients had failed propranolol therapy for bleeding. Portacaval shunt was performed emergently in 11 patients and electively in 1, and permanently stopped bleeding in all by reducing the mean portal vein—inferior vena cava pressure gradient from 251 to 16 mm saline. There were no operative deaths, and two unrelated late deaths after 13 and 24 months. During 1 to 6.75 years of follow-up, all shunts remained patent by ultrasonography, the gastric mucosa reverted to normal on serial endoscopy, and there was no gastrointestinal bleeding. Recurrent portal-systemic encephalopathy developed in only 8% of patients. Quality of life was generally good. It is concluded that portacaval shunt provides definitive treatment of bleeding portal hypertensive gastropathy by eliminating the underlying cause, and makes possible prolonged survival with an acceptable quality of life.