门静脉癌栓分型及与食管胃底静脉曲张程度和出血的关系

目的观察不同类型门静脉癌栓患者食管胃底静脉曲张程度、破裂出血发生率及预后,试图建立一种更为科学的门静脉癌栓(PCT)分型方法。方法将2003-07~2004-06山东聊城人民医院消化内科76例原发性肝癌并PCT患者,按PCT是否超过胃冠状静脉门静脉入口,将PCT分为两型。所有患者长期随访至死亡,随访期间多次行胃镜及超声检查,观察PCT不同分型患者食管胃底静脉曲张程度及预后。结果两组患者食管胃底静脉曲张的程度比较差异无显著意义;Ⅰ型PCT患者破裂出血发生明显高于Ⅱ型PCT患者,主要死亡原因为上消化道出血;Ⅱ型PCT患者主要死亡原因为肝功能等多脏器衰竭。结论门脉癌栓生长迅速,短时间内对静脉曲张的程度影响不大,不同的类型PCT患者预后不同。本文PCT分型,可较简便地预测患者预后,并为不同PCT患者治疗方案的选择提供理论根据。     

胃底静脉曲张诊断治疗进展

胃底静脉曲张(gastric varices,GV)是各种原因引起的门脉高压症导致的胃底部位侧枝循环建立的病理表现.各种病因引起的门脉高压症中,胃静脉曲张的发生率为10%～50%,大多为食管及胃静脉曲张并存,单独发生胃静脉曲张的仅占5%～12%.虽然胃静脉曲张破裂出血发生率较食管静脉曲张破裂出血发生率低,约10%～36%,但一旦破裂出血发生风险大,死亡率高.因此,胃静脉曲张的诊断和治疗一直是临床关注的课题.     

经胃镜注射硬化剂联合组织粘合剂治疗肝硬化胃底静脉曲张患者的临床研究

<正>食管胃底静脉曲张破裂出血是门脉高压症最严重的并发症之一[1-5],同时也是上消化道出血的主要原因[6],其首次出血的病死率可达30%,反复出血的发生率达50%~80%,再出血的病死率可达30%~70%,及时、有效的治疗可以降低患者的病死率,并可预防再出血[7]。由于胃底静脉曲张破裂出血较食管静脉曲张破裂出血更凶险,所以患者常在短时间内死于大出血。目前对于肝硬化胃底静     

血清-腹水白蛋白梯度与食管-胃底静脉曲张破裂出血的关系

目的 探讨血清-腹水白蛋白梯度（Serum-ascites albumin gradient,SAAG）与门脉高压的关系,评价SAAG对预测门脉高压性食管-胃底静脉曲张破裂出血的价值.方法 测定29例肝硬化腹水患者SAAG值并行胃镜检查以了解有无食管-胃底静脉曲张,以11 g/L为界将29例患者分为高SAAG组及低SAAG组,采用Pearson相关分析法分析SAAG与食管-胃底静脉曲张之间的关系.29例患者中并发食管-胃底静脉曲张破裂出血者8例,非出血者21例,测定两组患者的SAAG值并进行比较.结果 26例高SAAG患者中17例有食管-胃底静脉曲张,而3例低SAAG患者均无食管-胃底静脉曲张.SAAG与食管-胃底静脉曲张存在正相关关系（r=0.40,P＜0.05;r=0.84,P＜0.01）;8例出血组患者其SAAG值为（24.24±7.18）g/L,21例非出血组患者其SAAG值为（18.27±6.06）g/L,两组比较差异有显著性（P＜0.05）.结论 SAAG与门脉压力密切相关且对预测门脉相关性食管-胃底静脉出血有一定临床价值.     

内镜下组织胶注射联合套扎治疗急性胃食管静脉曲张出血的临床应用

目的探讨内镜下组织胶注射联合套扎治疗急性胃食管静脉曲张出血的临床价值。方法23例临床确诊为肝硬化急性胃食管静脉曲张破裂出血患者,均于出血稳定12h内采用胃曲张静脉三明治法组织胶注射后联合食管曲张静脉套扎治疗,术后2周、3个月进行内镜随访。观察治疗后再出血率、死亡率、食管胃静脉曲张程度。结果所有患者均一次成功止血。6例患者于术后2周,再次行EVL术。食管胃静脉曲张程度明显减轻,食管静脉治疗有效率95．65％,胃底静脉曲张治疗有效率91．30％。随访期3个月内无一例再出血及死亡病例。结论内镜下组织胶注射联合套扎是治疗胃食管静脉曲张急性出血一种安全可靠的方法。     

肝硬化上消化道出血92例临床分析

目的探讨肝硬化上消化道出血的原因及其与肝功能损害程度的关系。方法对92例肝硬化上消化道出血患者行急诊胃镜检查,发现病因。结果在92例肝硬化并发上消化道出血患者中,食管胃底静脉曲张破裂出血占52．2％,门脉高压性胃病出血占22．8％,肝源性溃疡出血占20．7％;肝功能A级与B级和C级患者出血原因差异显著。结论食管胃底静脉曲张破裂出血是肝硬化上消化道出血的主要原因,门脉高压性胃病和肝源性溃疡也是不可忽视的出血原因。     

经皮经肝TH胶灌注栓塞术与内镜下注射TH胶术治疗食管胃底静脉曲张的对照研究

目的比较α-氰基丙烯酸正辛酯(TH胶)作为栓塞材料行经皮肝穿刺门静脉胃冠状静脉栓塞术(percutaneous transhepatic varices embolization,PTVE)和内镜下食管胃底静脉注射TH胶术的远期疗效及可行性。方法将150例门脉高压食管静脉曲张破裂出血患者随机分为2组,分别行经皮肝TH胶灌注胃冠状静脉栓塞术联合部分脾脏栓塞术和内镜下食管胃底静脉注射TH胶术。结果所有患者均手术成功,止血率达100%。随访3年,行PTVE的患者食管胃底静脉曲张再出血率为25.00%,而内镜下食管胃底静脉注射TH胶术的患者的再出血率为53.24%。结论 PTVE手术安全,创伤小,止血率高,再出血率低,是治疗门脉高压并食道胃底静脉曲张的理想方法。     

肝硬变患者B超与内镜检查对预测门脉高压性上消化道出血的临床价值

目的为探讨B超与内镜检查对预测门脉高压性上消化道出血的临床价值.方法将入选的54例肝硬变患者均经B超与内镜检查,以了解门静脉的内径大小及食管胃底静脉曲张程度.结果门静脉内径大小及食管胃底静脉曲张程度呈正相关(相关系数R=0.411,P<0.05),门脉扩张程度及食管胃底静脉曲张程度与上消化道出血呈正相关(相关系数R=0.377,P<0.05).结论B超门静脉的内径大小与内镜检查食管胃底静脉曲张程度可作为门脉高压性上消化道出血的预测标志.     

晚期血吸虫病并发食管及胃底静脉破裂出血的急诊处理

食管及胃底静脉曲张破裂出血是晚期血吸虫病(下称晚血)门脉高压主要的并发症，首次出血病死率约为20％～40％，2年内再出血率高达70％。因此，晚血食道及胃底静脉曲张破裂出血是病人死亡的主要原因，如何有效控制出血和预防反复出血是一个重要的临床课题。目前认为，食管和(或)胃曲张静脉内压力升高是静脉破裂出血的重要因素，迅速准确确定出血部位和病因并及时作出正确处理，对预后有重要意义。     

急诊内镜治疗食管贲门胃底静脉曲张活动出血200例

目的:探讨急诊内镜治疗食管贲门胃底静脉曲张活动出血的疗效. 方法:内镜下套扎、硬化和栓塞等治疗手段治疗200例食管贲门胃底静脉曲张活动出血.结果: 200例食管贲门胃底静脉曲张活动出血患者, 经急诊内镜治疗仅4例术中死亡, 止血成功率98%. 术后2 wk内因为各种原因死亡32例, 病死率16%. 结论:食管静脉破裂出血, 贲门静脉曲张破裂出血, 套扎效果好. 胃底静脉曲张出血应首选注射人体组织胶栓塞.     

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。     

位置、直径、出血风险在食管胃底静脉曲张破裂出血患者分型中应用初探

目的 初步探讨应用静脉曲张位置、直径、出血风险对食管胃底静脉曲张破裂出血患者进行分型(LDRf分型)的可行性.方法 回顾分析381例因食管胃底静脉曲张破裂出血行内镜下急诊治疗患者,对静脉曲张位置、直径和出血危险因素进行分析,并尝试进行LDRf分型.结果 食管胃底静脉出血好发于食管中下段,不同直径的曲张静脉均有出血,曲张静脉多见有红色征.所有患者均可进行LDRf分型,食管静脉曲张破裂出血患者中,Rf1共计 133 例(45.4%),Rf2共计 160 例(54.6%);胃静脉曲张破裂出血患者中,Rf1共计47例(53.4%),Rf2共计41例(46.6%).结论 LDRf可用于食管胃静脉曲张的分类并对诊断治疗有一定指导意义.     

经内镜栓塞术联合套扎术治疗食管胃底静脉曲张出血的疗效观察

目的探讨胃底静脉曲张栓塞术联合内镜下食管静脉曲张套扎术（EVL）治疗肝硬化上消化道出血的疗效。方法经急诊胃镜检查发现活动性胃底静脉曲张出血合并Ⅱ°以上食管静脉曲张且排除其他病因的上消化道出血患者共156例,分为治疗组和对照组,治疗组胃底静脉曲张组织粘合剂栓塞同时食管静脉EVL治疗;对照组胃底静脉曲张组织粘合剂栓塞治疗2个月后行食管静脉EVL。结果两组均未发生与治疗相关的并发症。止血成功率治疗组为96．3％（77／80）,对照组为97．4％（74／76）,（P〉0．05）;近期再出血率治疗组为6．4％（5／78）,对照组为21．3％（16／75）,两组差异有统计学意义（P〈0．05）;两组患者随访6个月,再出血率分别为13．0％（9／69）、25．4％（17／67）,差异有统计学性意义（P〈0．05）。胃底静脉曲张改善总有效率治疗组和对照组分别为61．6％、59．1％,食管曲张静脉改善总有效率为74．0％、67．9％,差异均无统计学意义。结论胃底静脉曲张栓塞联合EVL是治疗肝硬化胃底静脉曲张出血并食管静脉曲张的安全有效方法,同时联合治疗更能降低再出血率。     

Prevalence, classification and natural history of gastric varices: a long-term follow-up study in 568 portal hypertension patients.

To determine the prevalence and natural history of gastric varices, we prospectively studied 568 patients (393 bleeders and 175 nonbleeders) with portal hypertension (cirrhosis in 301 patients, noncirrhotic portal fibrosis in 115 patients, extrahepatic portal vein obstruction in 117 patients and hepatic venous outflow obstruction in 35 patients). Primary (present at initial examination) gastric varices were seen in 114 (20%) patients; more were present in bleeders than in non-bleeders (27% vs. 4%, respectively; p < 0.001). Secondary (occurring after obliteration of esophageal varices) gastric varices developed in 33 (9%) patients during follow-up of 24.6 +/- 5.3 mo. Gastric varices (compared with esophageal varices) bled in significantly fewer patients (25% vs. 64%, respectively). Gastric varices had a lower bleeding risk factor than did esophageal varices (2.0 +/- 0.5 vs. 4.3 +/- 0.4, respectively) but bled more severely (4.8 +/- 0.6 vs. 2.9 +/- 0.3 transfusion units per patient, respectively). Once a varix bled, mortality was more likely (45%) in gastric varix patients. Gastric varices were classified as gastroesophageal or isolated gastric varices. Type 1 gastroesophageal varices (lesser curve varices) were the most common (75%). After obliteration of esophageal varices, type 1 gastroesophageal varices disappeared in 59% of patients and persisted in the remainder; bleeding from persistent gastroesophageal varices was more common than it was from gastroesophageal varices that were obliterated (28% vs. 2%, respectively; p < 0.001). Type 2 gastroesophageal varices, which extend to greater curvature, bled often (55%) and were associated with high mortality. Type 1 isolated gastric varices patients had only fundal varices, with a high (78%) incidence of bleeding.(ABSTRACT TRUNCATED AT 250 WORDS)     

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。     

益生菌在食管胃静脉曲张破裂出血初级预防中的作用

目的探讨益生菌对肝硬化食管胃静脉曲张患者1年内出血风险的影响。方法选取2008年2月—2017年2月于首都医科大学附属北京地坛医院住院且随访时间超过1年的肝硬化食管胃静脉曲张患者692例,其中346例患者在1年的随访期内接受了益生菌治疗(益生菌组)队列,随后采用1∶1倾向评分的方法通过校正Child-Pugh分级、静脉曲张分度、红色征为其匹配346例未接受益生菌治疗的患者(非益生菌组)。所有入选患者均按照指南推荐的初级预防策略进行管理,而益生菌队列则在此基础上辅助了益生菌治疗,观察两个队列1年内静脉曲张出血发生率的差异。计量资料两组间比较采用t检验或Mann-Whitney U检验;计数资料两组间比较采用χ^2检验;食管胃静脉曲张破裂出血影响因素的筛选采用向后的Cox单因素和多因素回归分析;Kaplan-Meier对两个队列EVB的累积发生率进行分析,并用log-rank进行比较。结果益生菌治疗是肝硬化食管胃静脉曲张破裂出血的独立保护因子(校正危险比=0.510,95%CI:0.299~0.870,P=0.013)。共61例患者在1年的随访期内发生了EVB事件,其中益生菌组23例,非益生菌组38例,益生菌组1年内EVB的累积发生率明显低于非益生菌组(6.6%vs 11.0%,χ^2=4.045,P=0.042),且益生菌组基线时至发生出血的中位时间晚于非益生菌组[137.0(85.0~258.0)d vs 123.0(72.5~206.5)d,Z=-1.101,P=0.271]。结论益生菌能有效降低肝硬化食管胃静脉曲张患者1年内出血事件的发生率,并有延缓出血事件发生时间的趋势。     

肝硬化患者中性粒细胞及白细胞与胃食管静脉曲张破裂出血的关系

目的探讨肝硬化患者中性粒细胞及白细胞与胃食管静脉曲张破裂出血的关系。方法回顾性对比分析151例肝硬化胃食管静脉曲张破裂出血患者与347例肝硬化未出血患者中性粒细胞相对值及白细胞计数。结果中性粒细胞相对值、白细胞计数不同的患者出血率有差别(P<0.05),大于正常值的患者出血率高。肝硬化胃食管静脉曲张破裂出血患者中性粒细胞相对值及白细胞计数高于未出血患者(P<0.05)。单因素非条件Logistic回归分析中性粒细胞相对值(OR=1.074,P=0.000)和白细胞计数(OR=1.112,P=0.000)与出血呈正相关。结论中性粒细胞相对值、白细胞计数为肝硬化胃食管静脉曲张破裂出血的危险因素。     

Endoscopic variceal ligation plus propranolol versus endoscopic variceal ligation alone in primary prophylaxis of variceal bleeding

BACKGROUND AND AIMS: The role of propranolol in addition to EVL in the prevention of first variceal bleed has not been evaluated. This prospective randomized controlled trial compared endoscopic variceal ligation (EVL) with propranolol and EVL alone in the prevention of first variceal bleed among patients with high-risk varices. PATIENTS AND METHODS: One hundred and forty-four consecutive patients with high-risk varices were randomly allocated to EVL plus propranolol (Gr I, n = 72) or EVL alone (Gr II, n = 72). EVL was done at 2-wk interval till obliteration of varices. In Gr I, incremental dosage of propranolol (sufficient to reduce heart rate to 55 beats/min or 25% reduction from baseline) was administered and continued after obliteration of varices. The endpoints of the study were bleeding and death. RESULTS: The two groups of patients had comparable baseline characteristics; follow-up (Gr I: 13.1 +/- 11.5 months, Gr II: 11.2 +/- 9.9 months), number of cirrhotic and noncirrhotic portal hypertension patients [Gr I 64 (88.6%) and 8 (11.4%), Gr II 63 (87.5%) and 9 (12.5%)], and frequency of Child's A (15 vs 18), B (38 vs 35), and C (19 vs 19). The mean daily propranolol dose achieved in Gr I was 95.6 +/- 38.6 mg. Eleven patients had bleeds, 5 in Gr I and 6 in Gr II. All patients bled before the obliteration of varices, the actuarial probability of first bleed at 20 months was 7% in Gr I and 11% in Gr II (p= 0.72). Six patients died in the combination and 8 in EVL group. All deaths in Gr I were due to nonbleed-related causes, while in Gr II, 2 deaths were bleed related, the actuarial probability of death at 20 months was 8% and 15%, respectively (p= 0.37). The probability of bleed-related death was comparable (p= 0.15). At the end of follow-up, 4 patients in Gr I and 11 in Gr II had recurrence of varices (p= 0.03). Side effects on propranolol were seen in 22% patients, in 8% it had to be stopped. There were no serious complications of EVL. CONCLUSIONS: Both EVL plus propranolol and EVL alone are effective in primary prophylaxis of bleed from high-risk varices. Addition of propranolol does not decrease the probability of first bleed or death in patients on EVL. However, the recurrence of varices is lower if propranolol is added to EVL.     

Development of Gastroesophageal Varices and Risk of Variceal Bleeding in Patients With Cirrhosis

Abstract: We studied the relationships between portal pressure measured using the portal venous pressure gradient, the development of gastroesophageal varices, and the risk of variceal bleeding in 56 patients with cirrhosis. Portal pressure was higher in patients with varices than in those without (P>0.01), and 11 mmHg was the lowest portal pressure measured in the patients with varices. The size of the varices was not associated with the portal pressure. There was no difference in the value of portal pressure measurements for the patients with variceal bleeding and those without and there was no linear-relationship between the degree of portal hypertension and the rate of variceal bleeding. 12 mmHg was the lowest portal pressure measured in the patients with variceal bleeding. The size of the varices was related to the rate of variceal bleeding (P>0.05). We conclude that (a) a portal pressure of 11 mmHg is necessary for the formation of varices, (b) 12 mmHg of portal pressure is necessary for variceal bleeding to occur but the degree of portal hypertension has no predictive value for the risk of variceal bleeding, and (c) the size of the varices does not depend on the degree of portal hypertension but is associated with the risk of variceal bleeding.