门静脉高压症并发上消化道出血的急诊手术治疗

门静脉高压症并发食管及胃底曲张静脉破裂大出血患者29例,均接受急诊手术治疗。断流＋分流术11例,术后门静脉压平均降低7．9cmH2O,发生肝昏迷先兆2例、再出血1例,死亡2例;仅行断流术18例,术后门静脉压平均降低2．1cmH2O,发生再出血4例,元手术死亡者。认为肝硬化门静脉高压症并发上消化道大出血者应不失时机实施手术治疗。延误时机只会使患者全身状况进一步恶化,手术死亡率上升。断流＋分流术降压更明显,再出血率低,但术后脑病发生率及手术死亡率高于断流术;断流术后再出血率较高,但术后脑病发生率及手术死亡率较低,适用于术前肝功能较差的患者。     

门静脉高压症上消化道出血25例外科治疗

目的 探讨门静脉高压症上消化道出血恰当的手术治疗时机和围手术期处理的重要性。方法 1995—01／1998—12收治门静脉高压症上消化道出血病人25例。全组病人均施行脾切除及门奇断流术。其中急诊手术3例，相对择期手术于止血后1周内手术11例，2周内8例，3周内3例。结果 全组病人近期止血率100％，肝功能均有不同程度改善，无手术死亡病例。结论 门静脉高压症上消化道出血病人选择恰当的手术时机和稳妥的围手术期处理是提高救治成功率的关键。     

肝硬化门静脉高压症及上消化道出血治疗方法的临床选择

目的 探讨老年肝硬化门静脉高压症及上消化道出血患者的最佳临床治疗方式.方法 回顾分析1990～2006年临床治疗的340例肝硬化门静脉高压症、上消化道出血患者,其中内科保守止血治疗199例,经颈内静脉肝内门体分流术(TIPSS)治疗32例,双介入即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)治疗109例.结果 内科保守治疗组和TIPSS组治疗有效率明显低于双介入治疗组(P＜0.05),一年内再出血率明显高于双介入治疗组(P＜0.05);双介入治疗组白细胞在术后2 w恢复到正常水平,与术前比较差异有显著性(P＜0.05),门脉压力下降,与术前比较差异有显著性(P＜0.05),术后3个月内肝功转氨酶及总胆红素有所升高,但3个月以后各项指标逐渐降至正常范围,与术前比较有显著性差异(P＜0.05).结论 双介入治疗老年肝硬化门静脉高压症、上消化道出血是目前最好的临床选择.     

双介入术治疗肝硬化门静脉高压症并上消化道出血128例临床观察

目的 探讨双介入术即经皮肝穿食管胃底曲张静脉栓塞术（PTVE）联合部分性脾栓塞术（PSE）治疗肝硬化门静脉高压症并上消化道出血的临床效果. 方法 对128例老年肝硬化门静脉高压症并上消化道出血患者行PTVE联合PSE治疗,观察止血有效率、1 a内再出血率及介入术前后自由门静脉压（FPP）、WBC、PLT及肝功能指标变化.结果 117例（91.4%）止血有效,随访观察1 a仅15例（12.8%）发生再出血;余11例疗效欠佳,治疗后仍有活动性出血;术前、PTVE及PSE后FPP分别为（38.76±8.78）、（42.78±9.51）、（4.08±5.72）cmH2O,后两者与术前比较均有显著差异（P＜0.05）;术后2周WBC即恢复至正常,且与术前比较有显著差异（P＜0.05）;术后3个月内ALT及总胆红素水平均显著高于术前（P＜0.05）,但其后均逐渐降至正常.结论 PTVE联合PSE双介入术治疗肝硬化门静脉高压症并上消化道出血具有近期止血效果确切、再出血率低及操作简单、便于推广等特点,尤其适用于病史长、病情重、体质差、耐受性差的老年患者.     

老年肝硬化门静脉高压并发上消化道出血的相关因素

目的探讨老年肝硬化门静脉高压并发上消化道出血的相关因素。方法肝硬化门静脉高压患者395例,研究其合并上消化道出血的发生情况。单因素和多因素Logistic回归分析影响老年肝硬化门静脉高压并发上消化道出血的危险因素。结果肝硬化门静脉高压合并上消化道出血214例,占54. 18%。单因素分析结果表明,性别、肝功能分级、肝硬化病因与是否合并上消化道出血无关(P>0. 05);上消化道出血患者食管胃底静脉曲张多于无上消化道出血患者、门静脉内径高于无上消化道出血患者、不良饮食习惯多于无上消化道出血患者,且有统计学差异(P<0. 05)。将单因素分析具有统计学差异的因素纳入多因素回归分析,食管胃底静脉曲张、门静脉内径和不良饮食习惯为影响肝硬化门静脉高压合并上消化道出血的独立危险因素。结论肝硬化门静脉高压合并上消化道出血相关影响因素中,食管胃底静脉曲张、门静脉内径和不良饮食习惯为其独立危险因素。     

门静脉高压上消化道出血52例分析

我院自1994年以来对52例肝硬化门静脉高压伴有上消化道出血患者,进行急诊胃镜检查,结合临床有关资料,将其出血病因分析探讨如下.对象和方法对象 本组52例中男42例,女10例;年龄20～68岁.52例均在出血后4～8h内经内镜证实有食管、胃底静脉曲张.52例中血吸虫肝硬化22例,肝炎肝硬化20例,原因不明肝硬化8例,酒精性肝硬     

门静脉高压症合并上消化道出血非手术治疗的护理体会

门静脉高压症合并上消化道出血临床常见，一旦发生常危及生命，精心护理有重要意义。1998年2月～2003年12月，我们对35例门静脉高压症合并上消化道出血患者采用非手术治疗，效果满意。现将护理体会报告如下。临床资料：本组男25例，女10例；年龄35～71岁，平均46．2岁；病毒性肝炎病史1～20年。35例均有食管胃底静脉曲张，肝功能分级：Child B级5例，Child C级30例；首次出血23例，2次出血11例，3次出血1例；合并肝性脑病7例。本组人院后均予禁食、卧床休息、输鲜血、静滴垂体加压素、置三腔管压迫止血和防治肝性脑病等治疗。结果治愈33例，死亡2例。     

三种微创方式治疗门静脉高压上消化道出血73例临床分析

目的比较三种微创方式治疗门静脉高压急性上消化道出血的止血效果及并发症情况,为临床选择合适治疗方式提供参考。方法收集浙江大学金华医院2013-02~2017-12因门静脉高压导致急性上消化道出血入院的患者共73例,依据治疗方式不同分为腹腔镜组(16例)、内镜组(31例)、经颈静脉肝内门体分流术(TIPS)组(26例),比较三组患者的一般情况、术后住院时间、术后并发症、围术期死亡情况及术后再出血情况。结果内镜组平均住院时间最短(P0.05),住院费用最少(P0.05),腹腔镜组术后腹腔感染发生率最高(P0.05),TIPS组术后肝性脑病发生率最高(P0.05),腹腔镜组再出血率最低(P0.05)。结论三种微创方式治疗门静脉高压急性上消化道出血各有优势,应综合考虑患者情况、医师的经验以及医院的技术条件,选择合适的治疗方法。     

186例肝硬变门脉高压症患者上消化道出血原因分析

本文对180例肝硬变门脉高压症患者上消化道出血的原因作了分析,结果显示:首次出血的原因主要是胃十二指肠病变(66.7％),而多次出血的主要原因是食管曲张静脉破裂出血(56.4％)。胃十二指肠病变所致出血的病死率为11.3％(14/124),而食管曲张静脉破裂出血的病死率高达40.5％(34/84)。提示,肝炎肝硬变患者的门脉性胃病的发生率较高,因而应引起临床的足够重视。     

断流术治疗门脉高压症上消化道出血疗效分析

目的 探讨采用贲门周围血管断流术治疗肝硬化门脉高压并食管胃底静脉曲张破裂出血的效果及预后.方法 对我院3年间行经腹贲门周围门奇血管断流术治疗门脉高压症并发上消化道出血47例及20例保守治疗患者近、远期疗效进行对比分析.结果 手术组除1例近期死亡外,总体效果满意.近期出血5例,远期出血2例,再出血率14.9%,全组无肝性脑病发生.保守治疗组死亡2例,近期出血4例,远期出血6例,1例发生肝性脑病,再出血率50%.结论 规范而彻底的贲门周围血管断流术治疗门脉高压并上消化道出血创伤小,止血率高,肝性脑病等并发症发生率低,便于开展与推广.     

Conservative treatment of upper gastrointestinal bleeding in portal hypertension.

The main aim of conservative treatment of upper gastrointestinal bleeding in portal hypertension is aim to treat and prevent esophageal variceal hemorrhage. Controlled trials show that the hemostasis rate following vaso-active therapy (vasopressin and analogues, somatostatin) is only slightly superior to the spontaneous hemostasis rate. Complications caused by vasopressin treatment can be avoided by concomitant application of nitroglycerin or by alternative treatment with somatostatin. Balloon tamponade is slightly superior to vasopressin for arresting variceal hemorrhage. Injection sclerotherapy influences acute bleeding most positively. Analysis of controlled trials favors sclerotherapy for prophylaxis of rebleeding, but beta-adrenoceptor blockers appear to be almost equally good.     

Pharmacologic therapy for gastrointestinal bleeding due to portal hypertension and esophageal varices

Cirrhosis results in portal hypertension in many patients. The major complications of portal hypertension include development of ascites and esophageal or gastric varices. Varices lead to hemorrhage and death in a significant proportion of patients. This review focuses on the pharmacologic approach to management of portal hypertension in patients at risk of variceal hemorrhage, or those who have already had variceal bleeding. Pharmacologic therapy is used for 1) primary prevention of bleeding, 2) management of acute bleeding, and 3) prevention of recurrent bleeding (secondary prophylaxis). For acute esophageal variceal hemorrhage, a variety of pharmacologic agents are used, including somatostatin, octreotide, vapreotide, lanreotide, terlipressin, and vasopressin (with nitrates). For primary and secondary prevention of esophageal variceal hemorrhage, a-blockers remain the mainstay therapy.     

Development of a scoring system to predict mortality from upper gastrointestinal bleeding

Despite the widespread application of endoscopy in acute upper gastrointestinal bleeding, there is little evidence of improved survival among those who undergo the procedure. To select high-risk patients who might benefit most from diagnostic and therapeutic endoscopy, the authors developed and validated a scoring system based on prognostic indicators of increased mortality. The scoring system was developed from the best clinical predictors of mortality, determined in a prospective study of consecutive bleeding patients. The model was then tested in a prospective validation phase at three hospitals. Three main factors in the model predict mortality: bleeding, including hematochezia, drop in hematocrit of 5%, short duration of bleeding, absence of melena, and hypotension; liver disease, manifested by prolonged prothrombin time and encephalopathy; and renal disease. Patients determined to be at high risk for death using the scoring system might be candidates for aggressive management and for therapeutic endoscopy.     

Congestive gastroenteropathy--an extension of nonvariceal upper gastrointestinal bleeding in portal hypertension

Three cirrhotic patients with acute and chronic gastrointestinal blood loss are described. All had extensive gastric mucosal changes on endoscopy consistent with congestive gastropathy and also had extensive duodenal and jejunal changes consisting of multiple friable punctate areas of erythema. Two patients had esophageal varices from which bleeding could not be documented. The mucosal abnormalities seen in the small intestine of all three patients were similar to those within the stomach and are thought to represent an extension of congestive gastropathy and to be contributing to the blood loss. We propose that the term "congestive gastropathy" be replaced by a more comprehensive term, "congestive gastroenteropathy." The cause of these mucosal abnormalities remains unclear. Attempts at endoscopic therapy of these extensive abnormalities should be avoided until a greater understanding of the underlying pathophysiology is reached.     

Validation of the Rockall risk scoring system in upper gastrointestinal bleeding

BACKGROUND: Several scoring systems have been developed to predict the risk of rebleeding or death in patients with upper gastrointestinal bleeding (UGIB). These risk scoring systems have not been validated in a new patient population outside the clinical context of the original study. AIMS: To assess internal and external validity of a simple risk scoring system recently developed by Rockall and coworkers. METHODS: Calibration and discrimination were assessed as measures of validity of the scoring system. Internal validity was assessed using an independent, but similar patient sample studied by Rockall and coworkers, after developing the scoring system (Rockall's validation sample). External validity was assessed using patients admitted to several hospitals in Amsterdam (Vreeburg's validation sample). Calibration was evaluated by a chi2 goodness of fit test, and discrimination was evaluated by calculating the area under the receiver operating characteristic (ROC) curve. RESULTS: Calibration indicated a poor fit in both validation samples for the prediction of rebleeding (p<0.0001, Vreeburg; p=0.007, Rockall), but a better fit for the prediction of mortality in both validation samples (p=0.2, Vreeburg; p=0.3, Rockall). The areas under the ROC curves were rather low in both validation samples for the prediction of rebleeding (0.61, Vreeburg; 0.70, Rockall), but higher for the prediction of mortality (0.73, Vreeburg; 0.81, Rockall). CONCLUSIONS: The risk scoring system developed by Rockall and coworkers is a clinically useful scoring system for stratifying patients with acute UGIB into high and low risk categories for mortality. For the prediction of rebleeding, however, the performance of this scoring system was unsatisfactory.     

Hyponatremia in patients treated with terlipressin for severe gastrointestinal bleeding due to portal hypertension

Terlipressin is frequently used in acute variceal bleeding due to its powerful effect on vasopressin V1 receptors. Although terlipressin is also a partial agonist of renal vasopressin V2 receptors, its effects on serum sodium concentration have not been specifically investigated. To examine the effects of terlipressin on serum sodium concentration in patients with acute portal-hypertensive bleeding, 58 consecutive patients with severe portal-hypertensive bleeding treated with terlipressin were investigated. In the whole population, serum sodium decreased from 134.9 ± 6.6 mEq/L to 130.5 ± 7.7 mEq/L (P = 0.002). Thirty-nine patients (67%) had a decrease in serum sodium ≥ 5 mEq/L during treatment: in 18 patients (31%), between 5 and 10 mEq/L and in 21 patients (36%), greater than 10 mEq/L. In this latter group, serum sodium decreased from 137.2 ± 5 to 120.5 ± 5 mEq/L (P < 0.001). In multivariate analysis, the reduction in serum sodium was related to baseline serum sodium and Model for End-Stage Liver Disease (MELD) score; patients with low MELD and normal or near-normal baseline serum sodium had the highest risk of hyponatremia. Serum sodium returned to baseline values in most patients shortly after cessation of therapy. Three of the 21 patients with marked reduction in serum sodium developed neurological manifestations, including osmotic demyelination syndrome in one patient due to a rapid recovery of serum sodium (serum sodium in these three patients decreased from 135, 130, and 136 to 117, 114, and 109 mEq/L, respectively). CONCLUSION: An acute reduction in serum sodium concentration is common during treatment with terlipressin for severe portal-hypertensive bleeding. It develops rapidly after start of therapy, may be severe in some patients and is associated with neurological complications, and is usually reversible after terlipressin withdrawal.     

胰源性区域性门脉高压症合并上消化道出血的诊治分析

目的探讨胰源性区域性门脉高压症合并上消化道出血的诊断和治疗方法。方法回顾分析我院2000年1月至2011年2月收治的14例胰源性区域性门脉高压症合并上消化道出血患者的诊疗措施和随访资料。结果14例患者中胰体尾占位6例,胰腺假性囊肿4例,慢性胰腺炎4例。均有呕血或（和）黑便史,其中4例有失血性休克表现。所有患者均无肝硬化、腹水及肝功能异常等表现。胃镜和超声胃镜提示14例患者均有胃底静脉曲张,2例同时合并食管下段静脉曲张。8例患者有脾肿大和脾功能亢进的表现。14例患者均采用手术治疗。9例患者获得随访,曲张静脉明显改善或消失,随访5月～8年均无出血复发。结论孤立性胃底静脉曲张、脾肿大和脾功能亢进、无肝硬化和肝功能正常以及胰腺疾病病史是诊断胰源性区域性门脉高压症的基本要点。该疾病可通过脾切除术或联合胃底周围血管离断术治愈,应同时重视对胰腺原发疾病的治疗。