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1.
目的探讨超声内镜对肝硬化并发食管胃底静脉曲张破裂出血的诊断价值,为临床预防及治疗措施提供参考。方法选取肝硬化伴食管胃底静脉曲张的患者164例,依据是否并发出血,分为病例组(并发出血组)和对照组(无并发出血组)。分析2组患者的一般临床资料以及超声内镜指标等。结果 (1)超声内镜对EV的诊断率是82.93%,对GV的诊断率为76.83%,对EGV的诊断率为46.34%,均高于常规胃镜检查(依次为71.34%、48.17%和31.09%,P0.05)。(2)病例组在食管曲张静脉总横断面表面积、胃左静脉直径、肠系膜上静脉直径、脾静脉直径、门静脉直径高于对照组,在曲张静脉壁厚度低于对照组,P0.05,差异均有统计学意义。结论超声内镜对肝硬化并发食管胃底静脉曲张破裂出血具有较高的诊断价值,食管曲张静脉总横断面表面积、胃左静脉直径、肠系膜上静脉直径、脾静脉直径、门静脉直径是出血的危险因素,曲张静脉壁厚度是出血的保护因素,对出血风险均有预测作用。  相似文献   

2.
目的:探讨内镜下治疗食管胃底静脉曲张出血的临床疗效.方法:随机抽取2012-05/2014-11湟中县第二人民医院收治的84例食管胃底静脉曲张出血患者的临床资料.对患者进行常规内镜检查,了解食管胃静脉曲张程度、位置、糜烂情况、出血情况等.对于存在出血情况的患者,了解出血部位,明确治疗措施.手术时采取"三明治"夹心法,手术后,患者进行常规处理.观察患者内镜下治疗再出血发生情况,食道静脉曲张治疗效果,胃底静脉曲张治疗效果,静脉曲张分级情况,胃底曲张静脉直径改变情况,并发症发生情况,治疗前后门静脉及其属支直径、流速、流量变化情况.结果:84例患者经内镜下治疗后,再出血发生12例,发生率为14.29%,无死亡病例.食道静脉曲张治疗效果:显效52例(61.90%)、有效24例(28.57%)、无效8例(9.52%),总有效率为90.48%.胃底静脉曲张治疗效果:显效48例(57.14%)、有效32例(38.10%)、无效4例(4.76%),总有效率为95.24%.患者经治疗后,静脉曲张分级情况得到明显改善胃底曲张静脉直径显著缩小,与治疗前比较,差异有统计学意义(P0.05).患者主要发生的并发症包括发热10例(11.90%),排胶出血2例(2.38%),胸骨后隐痛不适24例(28.57%);无异位栓塞、食管狭窄、吞咽困难等情况发生.患者经内镜下治疗后,患者门静脉血管内径无显著改变,与治疗前比较,差异无统计学意义(P0.05);患者门静脉、脾静脉平均流速、血流量参数显著增大,与治疗前比较,差异有统计学意义(P0.05).结论:内镜下治疗食管胃底静脉曲张出血临床疗效显著,可有效改善患者食道静脉曲张情况和胃底静脉曲张情况,并发症以发热、胸后隐痛为主,患者门静脉、脾静脉平均流速、血流量参数有明显增大.  相似文献   

3.
[目的]探讨超声内镜(EUS)对肝硬化并发食管胃底静脉曲张(EGV)破裂出血的诊断价值,为临床上对高危患者采取积极的预防及治疗措施提供参考。[方法]采用病例对照研究,选取2014年8月~2018年8月我院住院确诊肝硬化伴EGV的患者164例,依据是否并发出血,分为病例组(并发出血组)和对照组(没有并发出血组)。分析2组患者的一般临床资料以及EUS指标等。[结果]EUS对食管静脉曲张(EV)的诊断率是82.93%,对胃底静脉曲张(GV)的诊断率为76.83%,对EGV的诊断率为46.34%,均高于常规胃镜检查(依次为71.34%、48.17%和31.09%),差异有统计学意义(P0.05)。病例组在食管曲张静脉总横断面表面积、胃左静脉直径、肠系膜上静脉直径、脾静脉直径、门静脉直径高于对照组,在曲张静脉壁厚度低于对照组,差异均有统计学意义(P0.05)。[结论]EUS对肝硬化并发EGV破裂出血具有较高的诊断价值,食管曲张静脉总横断面表面积、胃左静脉直径、肠系膜上静脉直径、脾静脉直径、门静脉直径是出血的危险因素,曲张静脉壁厚度是出血的保护因素;对出血风险均有预测作用,并为临床上对高危患者采取积极的预防及治疗措施具有重要作用。  相似文献   

4.
目的探讨肝硬化食管胃静脉曲张内镜特征和分型与肝静脉压力梯度(hepatic venous pressure gradient,HVPG)的相关性。方法 45例肝硬化食管胃静脉曲张患者,通过颈静脉或股静脉途径插管球囊测压法进行HVPG测定。分别采用LDRf分型、Mc Cormick分度、丰永分型评估内镜下食管胃静脉曲张严重程度。同时收集患者人口学资料、临床表现、肝功能分级等。应用单因素和多因素统计方法分析临床和内镜特征与HVPG的相关性。结果单因素分析显示,食管胃静脉曲张的直径、危险度分级、丰永分型、Child-Pugh评分和分级与HVPG呈正相关(P0.05)。多因素回归分析显示,仅有丰永分型(β=0.537)和LDRf分型中的危险度分级(Rf,β=0.368)是HVPG的独立预测因素(P0.05),其预测模型为HVPG=丰永分型(Grade1,2,3)×3.97+Rf(0,1,2)×4.51+4.19。结论内镜下门脉高压性胃病严重程度和食管胃静脉曲张破裂出血危险度能较好地预测肝硬化门脉高压严重程度。  相似文献   

5.
目的探讨经皮经肝食管胃底曲张静脉栓塞术(PTVE)在肝硬化断流术后并发食管胃底静脉曲张破裂再出血治疗中的应用,评价其治疗效果及优势。方法收集2007年1月-2013年6月响水县人民医院消化内科收治的34例肝硬化断流术后食管胃底静脉曲张破裂再出血患者的临床资料,所有患者均行PTVE,术后定期复查胃镜,观察患者术后疗效、并发症以及再出血情况。结果 34例行PTVE治疗的患者急性期止血良好,有效率97%(33/34);术后2周曲张静脉均消失或明显减轻者29例(85.3%),随访2年食管胃底静脉曲张好转及消失者30例(88.2%);随访的2年内共6例(17.6%)出现上消化道出血。所有病例均未出现明显严重并发症。结论 PTVE治疗肝硬化断流术后静脉曲张再出血患者疗效显著,创伤小,并发症少,可防止新的侧支循环血管形成,是治疗肝硬化断流术后食管胃底静脉曲张破裂再出血的有效方法。  相似文献   

6.
目的评价急诊内镜下组织粘合剂(α-氰丙烯酸烷基脂)注射联合套扎治疗食管胃底静脉曲张破裂出血的临床疗效。方法2008年1月至2009年1月间21例食管胃底静脉曲张破裂出血患者接受急诊内镜下胃底曲张静脉组织粘合剂注射联合食管曲张静脉套扎(EVL)治疗,对其治疗疗效进行回顾性分析。结果21例患者的急诊止血有效率达95%(20/21),未出现严重并发症。结论急诊内镜下组织粘合剂注射联合套扎治疗食管胃底静脉曲张破裂出血,止血疗效确切,并发症发生率低,值得推广。  相似文献   

7.
目的 评价以医用胶为栓塞剂的经皮经肝胃底曲张静脉栓塞术(PTVE)治疗和预防肝硬化患者瘤样胃底静脉曲张破裂出血的临床疗效.方法 回顾性分析24例采用医用TH胶完成PTVE治疗的肝硬化胃底静脉曲张破裂出血患者的病例资料,比较治疗前后胃底静脉曲张程度的变化情况,统计术后再出血率及死亡率.结果 治疗前24例患者胃底曲张静脉团直径均在20 mm以上,治疗后胃底静脉曲张程度显著减轻,其中20例(83.3%)曲张静脉团直径减至5 mm以下或消失,4例(16.7%)曲张静脉团直径减至5 ~10 mm.在术后1~36个月,平均16.6个月的随访期内,再出血率和病死率分别为12.5%和12.5%,其中l例死于肝癌,另外2例死于慢性肝功能衰竭.结论 对于肝硬化瘤样胃底静脉曲张破裂出血的患者,行医用胶为栓塞剂的PTVE治疗具有良好的临床效果.  相似文献   

8.
目的:评价生物蛋白胶在经皮经肝食管胃底曲张静脉栓塞术治疗胃底食管静脉曲张破裂出血中的可行性和临床价值.方法:60例肝硬化、食管静脉曲张破裂出血的患者,分为经皮经肝胃底曲张静脉栓塞组(percutaneous transhepatic obliteration,PTO)30例和食管曲张静脉套扎组(esophageal varices ligation,EVL)30例,PTO组是在X线透视下经皮经肝穿刺进入上消化道出血责任血管,用弹簧钢圈和生物蛋白胶栓塞曲张的食管和胃底静脉,比较两组治疗方法的急诊止血率和术后累计无出血率.结果:PTO组中28例门脉穿刺及曲张静脉栓塞手术均获成功,1例造影示为门静脉海绵样变,进入责任血管困难,无法进行栓塞治疗,1例行门静脉造影未见明显胃底曲张静脉,栓塞成功率为96.6%(28/29),其余病例术后48h止血率达100%.EVL组急诊止血率为93.3%(28/30).在12-50mo随访期内的患者中,PTO组再出血10例,EVL组再出血17例,PTO组和EVL组的6mo累计无出血率分别为89.3%vs80%,1年累计无出血率为85.7%vs56.7%,PTO组术后累计无出血率明显高于EVL组(?2=5.314,P<0.05).结论:经皮经肝食管胃底静脉栓塞中应用生物蛋白胶治疗上消化道出血安全有效,创伤小、止血效果肯定,在急诊止血方面更具优势,值得推广应用.  相似文献   

9.
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。  相似文献   

10.
目的 探讨LDRf分型方法是否能覆盖食管胃静脉曲张以外的消化道异位静脉曲张(EcV)的内镜下分型.方法 参考相关文献,采用LDRf分型方法对消化道EcV患者914例进行内镜下分型,统计病变位置(L)、血管直径(D)、危险因素(Rf).检查门静脉高压(PH)病因,予相应治疗并随访.结果 EcV按部位进行内镜下LDRf分型,包括:十二指肠198例、空肠回肠93例、胆管105例、结肠65例、直肠453例.各部位EcV血管直径为0.3 ~3.5 cm,危险因素表现亦有不同.PH病因:肝硬化伴门静脉高压者630例(68.9%),其中自身免疫性肝病肝硬化及门静脉海绵样变性各3例(0.6%),伴食管胃静脉曲张252例(27.6%),脾切除者4例(0.5%).EcV患者治疗315例,其中组织胶治疗43例、硬化剂治疗76例、套扎治疗74例、介入治疗52例、外科剖腹探查术70例.共19例因EcV出血死亡.内镜检查随访13~36个月,无静脉曲张复发,1年生存率100%.结论 LDRf分型方法适合于全消化道静脉曲张,其对治疗方法与时机的选择具有明显指导作用,且简便、规范、统一,适合临床推广.  相似文献   

11.
目的探讨十二指肠静脉曲张内镜下诊断及治疗方法。方法对2000年11月至2008年8月93283例内镜检查发现的26例十二指肠静脉曲张的内镜下表现,采用位置(L)、直径(D)、危险因素(跗)即LDRf分型方法进行分型,观察依照分型对十二指肠静脉曲张治疗的效果,并进行随访。结果内镜下分型:Ld1 5例(19.2%),Ld1.2 22例(7.7%),Ld2 19例(73.1%);D。0例,D0.5 2例,D1 10例,D2 13例,D3 1例;Rf0 23例,Rf1 0例,Rf2 3例。其中伴食管及(或)胃底静脉曲张18例。17例住院患者中乙型肝炎肝硬化9例(52.9%)。对其中的3例Rf2患者行内镜下治疗,1例活动出血者(Ld:D,Rf2)行组织粘合剂治疗后即刻止血,1例(Ld2D2Rf2)行组织粘合剂治疗,另1例患者(Ld2D1Rf2)进行了套扎治疗,随后进行了平均14.6个月的随访,3例患者在治疗后1.0~3.5个月内静脉曲张消失,且无复发;其余患者未行内镜治疗,对其中11例进行随访,未发现静脉曲张出血,有2例患者因其他原因死亡。结论LDRf内镜下分型能基本反映十二指肠静脉曲张的内镜特点,依照该分型选择十二指肠静脉曲张内镜治疗方法是安全可行的。  相似文献   

12.
目的 分析总结30岁以下食管胃静脉曲张(GOV)患者的临床特点。方法 2015年1月~2020年12月解放军总医院第一医学中心消化内科医学部收治的61例30岁以下GOV患者,提取、分析和总结其临床资料。结果 在61例GOV患者中,肝硬化门静脉高压症27例(44.3%),其中隐源性肝硬化占40.7%,乙型肝炎肝硬化占33.3%,和非肝硬化性门静脉高压(NCPH)34例(55.7%),其中以门静脉海绵样变占61.8%;基于内镜下静脉曲张LDRf分型,在位置方面主要以Le/g型多见(77.1%),在直径方面,D1.0占41.0%,在出血风险方面,Rf1分级占77.1%;针对GOV治疗,以二级预防治疗为主(85.7%),多采用组织胶或硬化剂注射或套扎联合治疗(66.1%);NCPH患者GOV再出血比例为11.8%,显著低于肝硬化组的29.6%(P<0.01)。结论 30岁以下人群GOV患者以NCPH居多,其中以各种原因引起的门脉海绵样变最多见。NCPH患者并发GOV经内镜治疗后再出血发生率显著低于肝硬化患者。  相似文献   

13.
门静脉癌栓与食管胃底静脉曲张程度及出血的关系   总被引:1,自引:0,他引:1  
观察不同类型门静脉癌栓(PCT)患者的食管胃底静脉曲张程度、破裂出血发生率及最终死亡原因.76例原发性肝癌并门脉癌栓患者,按门脉癌栓的分布及部位被分为两型.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患者破裂出血的发生明显高于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.门脉癌栓生长迅速,短时间内对静脉曲张的程度影响不大,但明显影响患者静脉曲张破裂出血发生率及死亡原因.门脉癌栓分型为患者治疗方案的选择提供了理论依据.  相似文献   

14.
Endoscopic classification of gastric varices   总被引:13,自引:0,他引:13  
Endoscopic observations of gastric varices in 124 patients were classified according to form, location, and color. Form was classified into three types: tortuous (F1), nodular (F2), and tumorous (F3). Location was classified into five types: anterior (La), posterior (Lp), lesser (Ll) and greater curvature (Lg) of the cardia, and fundic area (Lf). Color was white (Cw) or red (Cr). Glossy, thin-walled focal redness on the varix was defined as red color spot (RC spot). Stepwise logistic regression analysis for multivariate adjustments was performed for all of the endoscopic covariates, and four risk factors (La, Lg, F2, RC spot) that affect bleeding from gastric varices were independently identified. This classification should aid in assessing gastric varices observed by fiberoptic endoscopy and help design appropriate treatment.  相似文献   

15.
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)  相似文献   

16.
Gastric Varices: Profile, Classification, and Management   总被引:7,自引:0,他引:7  
Development of gastric varices is an important manifestation of portal hypertension. In segmental portal hypertension, gastric varices originate from short gastric and gastroepiploic veins. In generalized portal hypertension, intrinsic veins at cardia participate in the formation of gastric varices. Endoscopy and/or splenoportovenography and a high index of suspicion are required for the diagnosis of gastric varices. The incidence of gastric varices in patients with portal hypertension has been variably reported (2-70%), probably due to difficulties in diagnosis. In a small proportion of patients with gastric varices, chronic portal-systemic encephalopathy or significant variceal bleeding develops. Gastric varices can be classified, depending on their anatomical location, into gastroesophageal varices (a continuation of esophageal varices) or "isolated" gastric varices (fundal or ectopic varices). This distinction is necessary for management. Whereas surgery is recommended for bleeding fundal varices, in acute bleeding from gastroesophageal varices, sclerotherapy could be attempted successfully. In more than a quarter of patients, gastric varices disappear after obliteration of esophageal varices. Prophylactic sclerotherapy of gastric varices is not recommended.  相似文献   

17.
Background  Mucosal breaks induced by gastroesophageal reflux of gastric contents were more frequently found on the right anterior wall of the lower esophagus. Bleeding from esophageal varices may be also derived from gastroesophageal reflux. The circumferential location of the ruptured esophageal varices was evaluated to elucidate the relationship between gastroesophageal reflux and variceal rupture. Methods  Between January 2004 and December 2006, 26 patients who had primary bleeding from esophageal varices and 74 patients without evidence of bleeding with positive red color signs on varices were enrolled in this study retrospectively. Locations of bleeding spots and nonbleeding red color signs of esophageal varices were retrospectively evaluated by endoscopic photographs, and the relationship between the location of red color signs and the risk of bleeding was evaluated. Other possible predictors for bleeding were also investigated by multivariate regression analysis. Results  Red color signs were frequently found in the right posterior wall of the lower esophagus. However, bleeding spots of esophageal varices were more frequently seen in the right anterior side (64.0%) than in others. The positive predictor for bleeding from esophageal varices was the presence of red color sign in the right anterior wall of the esophagus, and the administration of proton pomp inhibitor was the negative predictor. Conclusions  Gastroesophageal acid reflex may be a risk factor of bleeding from esophageal varices. Attention should be paid to the circumferential location of red color signs in endoscopic screening of patients with esophageal varices to predict future bleeding.  相似文献   

18.
Hemorrhage from esophageal varices in cirrhotics is a frequent event with high mortality in spite of therapy. Preventive sclerotherapy seems to be beneficial only if the patient's bleeding risk is higher than 40 to 50% a year. A series of 320 patients with esophageal varices without previous bleeding was studied prospectively; the varices were classified according to three widely used endoscopic classifications. During follow-up (6 to 36 months, average 14 months), hemorrhage occurred in 49 patients (15.3%) of whom 30 (61.2%) bled from varices (8.2 and 11.0% at 12 and 24 months, respectively). At the same time intervals, mortality of the entire population studied was 18.0 and 23.8%, respectively, of which one third was directly due to hemorrhage. With all three classifications, the higher the degree of bleeding risk, the greater the actual percentage of hemorrhages recorded; however, it never reached 40% a year. In predicting the bleeding event, Dagradi's classification proved more sensitive than JRSPH or NIEC, but the latter classifications were more specific and assessed a higher predictive value for a positive test. Endoscopic observation probably needs integration with other methods if a reliable bleeding prediction is to be made.  相似文献   

19.
目的依据曲张静脉LDRf分型理论,探讨离体猪食管曲张静脉压力和直径对完全套扎度的影响。方法选取实验用猪静脉血管制成离体猪不同静脉压力血管模型,按预设定压力分成3组(A组25~30cmH20,B组35~40cmH20,C组45~50cmH20,1cmH20=0.098kPa),再选取猪食管进一步制成离体猪食管静脉曲张模型,根据所测直径分成3组(D1组0.4~1.0cm,D:组〉1.0~1.5cm,D,组〉1.5~2.0cm),采用单因素和多因素分析方法统计压力和直径对完全套扎度的影响。结果按压力分组时,A组完全套扎18个(56.25%,18/32),B组完全套扎12个(37.50%,12/32),C组完全套扎11个(33.33%,11/33),各组完全套扎率差异无统计学意义(χ2=3.6126,P=0.0573),但P值接近0.05,预示曲张静脉压力是完全套扎度的干扰因素;按直径分组时,D,组完全套扎35个(94.59%,35/37),D2组完全套扎6个(16.67%,6/36),D3组无一个完全套扎,各组完全套扎率差异有统计学意义(χ2=38.0014,P=0.0000),提示曲张静脉直径对完全套扎度影响较大。多因素非条件Logistic回归分析结果显示,食管曲张静脉压力、曲张静脉直径是完全套扎度的独立危险因素(P=0.000)。结论猪食管静脉曲张血管直径在0.4—1.0cm或血管压力在25—30cmH:0时完全套扎率高,套扎效果确实、完全,使用静脉曲张LDRf分型指导内镜下套扎猪食管静脉曲张是科学和可行的。  相似文献   

20.
胃静脉曲张的病因及临床特点   总被引:3,自引:0,他引:3  
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。  相似文献   

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