外科治疗在急性胃粘膜病变所致上消化道大出血治疗中的地位

经确诊为急性胃粘膜病变所致上消化道大出血１９６例，其中出血性胃炎１３７例，应激性溃疡５９例。其治疗应首先去除与本病有关的致病因素，纠正循环量的不足，控制胃内ｐＨ值，增强胃粘膜的防御能力，经非手术治疗无效者则行手术治疗。应激性溃疡手术组死亡率为６．３％，出血性胃炎组为３３．３％。因此，对出血性胃炎的手术应持慎重态度，对应激性溃疡大出血的手术治疗则应持积极态度。     

急性胃粘膜病变致上消化道大出血190例分析

急性胃粘膜病变致上消化道大出血１９０例分析华西医科大学附属一院普外科（６１００４１）郑吉祥，吕青，彭德恕我院近１０年来经纤维胃镜或手术探查证实为急性胃粘膜病变而致大出血者１９０例，其中出血性胃炎１３７例，应激性溃疡５３例。本文就其病因和治疗进行分析，...     

应激性溃疡大出血的治疗体会

目的 总结外科手术后应激性溃疡大出血的临床特点和治疗经验。方法 回顾分析1997～2003年期间我院治疗的32例应激性溃疡大出血患者的临床资料。结果 28例患者采用非手术治疗，其中12例患者接受急诊胃镜检查；手术治疗4例。奉组患者总的治愈率为87．50％．死亡率为15．62％。结论 急诊胃镜检查有助于明确诊断及止血治疗，应激性溃疡大出血首选非手术治疗，无效者可选择于术治疗。     

烧伤后上消化道应激性溃疡大出血手术治疗

目的　探讨烧伤后上消化道应激性溃疡大出血手术治疗的效果。方法　烧伤后上消化道应激性溃疡大出血患者１５ 例，烧伤面积（３８ ±１５） ％ ，出血部位１２ 例位于十二指肠，３ 例位于胃。手术时间在伤后４ ～１２ 天，手术方式为缝扎止血、幽门成形、选择性迷走神经切断、溃疡外旷置术或胃大部分切除术。结果　１５ 例中１３ 例治愈，２ 例死亡，其中１ 例死于术后败血症，另１ 例死于再出血并多器官功能衰竭。结论　手术治疗是烧伤后上消化道应激性溃疡大出血的有效治疗方法，对符合手术治疗的患者应尽早手术，以免延误时间，造成严重后果。     

人工关节置换术后并发应激性溃疡大出血(附2例报告及文献复习)

目的：探讨人工关节置换术后并发应激性溃疡大出血的预防及治疗经验。方法：1997年9月－2001年9月行人工关节置换术589例，对术后出现应激性溃疡大出血的2例临床资料进行回顾性分析并复习相关文献。结果：本组患者合并有高血压，长期服用激素和非甾体类消炎药物（NSAIDs)，1例患者抗凝治疗，人工关节置换术后并发应激性溃疡大出血的发生率为0．34％，临床表现为排柏油样大便，呕血、低血容量休克、贫血，急诊胃镜显示胃十二指肠粘膜糜烂，弥散性出血，结论：人工关节置换术后并发应激性溃疡大出血是一种严重的并发症，治疗在于有效控制出血，补充血容量，同时注意对重要脏器的保护，非手术治疗无效时，应外科手术治疗。对长期服用容易引起胃粘膜损害药物的患者，围手术期应使用抑制胃酸分泌的药物，预防应激性溃疡的发生。     

急性胃粘膜损害并发大出血的治疗体会

<正> 急性胃粘膜损害(Acute gastric mucosal lesion,AGML)亦称应激性溃疡、急性出血性胃炎、应激性胃粘膜病变等。多继发于严重创伤、大面积烧伤、颅脑损伤、多器官功能衰竭(MOF)、休克、严重感染以及胃肠道接触某些有害物质等。其主要表现为胃粘膜广泛糜烂、溃疡和出血;多发生于胃底及胃体部,也可侵及食管下段和十二指肠粘膜。临床上主要症状为上消化道出血,其中约5％的病人可合并大出血。1990年～1997年间我们共收治了36例急性胃粘膜损害合并大出血的病人,现报告如下。     

手术治疗应激性溃疡顽固性大出血19例体会

目的 探讨应激性溃疡顽固性大出血的手术治疗方法。方法 对19例应激性溃疡顽固性大出血采用胃大部血流阻断术治疗并观察疗效。结果 19例病人治愈17例(占90％)。治愈率与传统手术治疗方式的50％相比有显著性差异(P<0.01)。结论 胃大部血流阻断术治疗应激性溃疡顽固性大出血效果显著,可靠,可作为该类疾病的首选术式。     

急性胃粘膜病变

急性胃粘膜病变(Acute gastric mucosal Lesions)又称应激性溃疡(Stress ulceration)或出血性胃炎(Haemorrhagic gastritis)、急性糜烂性胃炎(Acute erosive gastritis)，是指机体在严重创伤、大面积烧伤、严重感染和休克等严重应激状态下，胃粘膜的完整性受到损害，胃近端发生急性多发性浅表性胃粘膜糜烂和溃疡。但严格地说，应激性溃疡并非就是急性胃粘膜病变。而是急性胃粘膜病变的其中一种类型。     

烧伤后应激性溃疡出血的手术治疗

烧伤后应激性溃疡出血的手术治疗游贵芳我院自１９８６年以来，对２５例烧伤后消化道大出血，经内科止血无效的病例，进行手术治疗。取得良好效果。临床资料本组男１９例，女６例。年龄１～５２岁，６岁以下２０例。烧伤面积１２％～７０％，平均３２％±１８％，Ⅲ度１０...     

胃应激性溃疡的近况

胃应激性溃疡(Stress ulcer)是指各种原因所致的休克、烧伤、感染以及某些药物等因素引起的急性胃粘膜糜烂或溃疡。为了正确地解释该病的病因和病理变化,文献多称此类病变为急性胃粘膜糜烂(Acute erosive gastritis),或急性胃粘膜病变(Arute gastric mucosal lesion),包括应激性溃疡(Stress ulcer),出血性胃炎,硷性反流性胃炎,药物性胃炎,Cushing溃疡以及Curling溃疡。     

胃癌及癌前病变组织中幽门螺杆菌感染与NOD2和TLR9蛋白表达的相关性

目的 研究NOD2和TLR9蛋白在胃癌及癌前病变组织中的表达情况以及幽门螺杆菌(Hp)感染对该蛋白表达的影响.方法 用C13呼气试验和快速尿素酶试验确定感染情况,用免疫组化法测定40例慢性浅表性胃炎,84例慢性萎缩性胃炎,48例胃溃疡,80例胃腺癌组织中NOD2和TLR9蛋白的表达情况.结果 在慢性浅表性胃炎、慢性萎缩性胃炎、胃溃疡、胃腺癌中NOD2阳性表达率分别为35%、21%、33%、40%.TLR9阳性表达率分别为15%、12%、21%、22%.在同一病变中Hp阳性组NOD2及TLPO表达强于Hp阴性组,其中Hp阳性的慢性浅表性胃炎、胃溃疡、肠上皮化生、中重度不典型增生和胃癌组织中NOD2表达与Hp阴件组比较差异有统计学意义(P<0.05).结论 胃腺癌、癌前病变以及幽门螺杆菌感染能增强胃上皮细胞中NOD2和TLPO蛋白的表达,提示二者在胃黏膜天然免疫过程中可能起到重要作用.     

良性和恶性病因术后残胃黏膜组织学变化特征及幽门螺杆菌感染状况

目的分析良性和恶性病因术后残胃黏膜组织学变化特征与幽门螺杆菌感染状况的关系。 方法回顾性分析2014年2月至2019年2月于四川省石棉县人民医院因良性和恶性病因行胃部手术治疗患者共80例,其中36例为良性消化性溃疡患者（良性组）,44例为早期胃患癌者（胃癌组）,两组患者术后均行黏膜组织学与胃镜检测。分析入组患者病例资料（首次行胃大部切除手术时年龄、性别、术后病程、行胃镜检测年龄、幽门螺杆菌感染、手术病因、病理和胃镜检测结果和手术方式等）,观察患者胃黏膜病变[慢性萎缩性胃炎（CAG）、肠化生（IM）和异型增生（DYS）发生率]、幽门螺杆菌感染率与胃黏膜炎症与活动性异常等,比较两组患者中幽门螺杆菌感染者与未感染者胃黏膜的病理特征。 结果良性组患者手术年龄为（40.46 ± 6.71）岁,低于胃癌组[（54.08 ± 8.17）岁],胃镜检测年龄及术后病程分别为（67.78 ± 11.36）岁、（27.26 ± 8.87）年,高于胃癌组[（61.99 ± 11.03）岁和（8.04 ± 6.57）年],差异均有统计学意义（t = 10.419、P < 0.001,t = 3.102、P = 0.003,t = 13.964、P < 0.001）;良性组患者幽门螺杆菌感染和胃黏膜活动性异常比例分别为47.22%（17/36）和66.67%（24/36）,均显著高于胃癌组[31.82%（14/44）和40.91%（18/44）],差异有统计学意义（χ² = 4.147、P = 0.039,χ² = 8.239、P = 0.003）。良性组、胃癌组患者中幽门螺杆菌感染者胃黏膜活动性异常、CAG及癌前病变比例均高于无幽门螺杆菌感染者,而NAG比率低于无幽门螺杆菌感染者,差异均有统计学意义（P均< 0.05）。 结论胃大部切除手术后残胃黏膜病变与进展和幽门螺杆菌感染存在一定关系,为预防残胃黏膜癌变可在幽门螺杆菌检测基础上加强胃镜随访。     

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目的 总结23例腹膜后脓肿诊断和治疗的经验,认识其易致多器官功能障碍综合征（MODS）的重要性。方法 对1993－1999年诊治的23例腹膜后脓肿的临床资料进行回顾性总结。结果 经腹部腹膜后脓肿引流20例,手术1－6次不等,B超引导下经后腰部穿刺置管引流3例。术后合并应激性胃粘膜损害发生消化道出血6例,成人呼吸窘迫综合征（ARDS）5例,急性肾衰2例,腹腔内出血1例,小肠瘘3例,空肠结肠瘘1例,霉菌感染3例。全组平均住院72天。死亡4例,其中因ARDS、ARDS并应激性胃粘膜损害大出血、ARDS并腹腔内血管破裂出血分别死亡1例,应激性胃粘膜大出血并空肠结肠瘘死亡,结论 作为术后并发症,腹膜后脓肿常易致MODS,对其及时诊断,充分有效的引流是预防MODS的关键。     

Current management of upper gastrointestinal bleeding.

Over a four-year period, 585 patients were hospitalized for massive upper gastrointestinal bleeding. Endoscopy diagnosed the cause of bleeding in 80% of 200 patients so studied. Selective angiography localized the bleeding site in 12 of 20 patients, and infusion of vasopressor stopped hemorrhage in six. Barium studies was 90% accurate in diagnosing ulcer disease but failed to detect gastritis. One hundred thirty (22%) patients were operated upon for medically uncontrolled bleeding. The proportion of patients requiring surgery fell from 33% in year one to 13% in year four. Benign ulcer disease caused bleeding in 51% of surgical patients, while gastritis was found in 20%, esophageal varices in 15% and stress ulcer in 8%. Overall operative mortality was 29%. Among 38 duodenal ulcer patients, mortality was 18%. Vagotomy and pyloroplasty were more effective than resection in this group. Resection for distal gastric ulcers in 22 patients resulted in a mortality of 14% and no rebleeding. While V&P controlled bleeding in 12 alcoholics with gastritis, five (42%) died postoperatively. Mortality among 20 patients with esophageal varices was 35%, although all five survived who had porto-caval shunts. Eight of 10 patients operated upon for stress ulcer bleeding died. Postoperative rebleeding occurred in 14 patients, eight of whom were again operated upon. In all but one a new lesion was found to be responsible for hemorrhage. Increasing use of gastroscopy and selective angiography can be expected to improve diagnostic capabilities in patients with upper gastrointestinal bleeding. Infusing vasopressor into selected arteries should reduce the need for surgical control of gastritis, variceal and stress ulcer bleeding, conditions poorly managed by current operative techniques.     

Acute gastric ulcerations in rats with obstructive jaundice--with special reference to gastric mucosal blood flow

The mechanism of acute gastric ulcerations in rats with obstructive jaundice was investigated in terms of the changes in the gastric mucosal blood flow. Further, the effect of vagotomy with or without obstructive jaundice was examined. One hundred and eighty-eight Sprague-Dawley rats weighing about 250 g were prepared and divided into 4 groups as follows; sham operation (control group), ligation of the bile duct (jaundiced group), vagotomy with pyloroplasty (vagotomized group), ligation of the bile duct and vagotomy with pyloroplasty (jaundiced and vagotomized group). After two weeks, water immersion and restraint stress procedures were performed in these 4 groups. The gravity of the gastric ulcerations was calculated by ulcer index. The gastric mucosal blood flow was measured by hydrogen clearance technique. The following results were obtained. The control group showed increased ulcer index and decreased gastric mucosal blood flow after the stress procedures. The jaundiced group showed significantly higher ulcer index and early, significant decrease of gastric mucosal blood flow compared to the control group after the stress procedures. The vagotomized group showed significantly decreased ulcer index after stress procedures compared to the control group, however, the gastric mucosal blood flow were unchanged between both groups before and after the stress procedures. The jaundiced and vagotomized group showed significant decrease of ulcer index and improvement of decrease of gastric mucosal blood flow compared to the jaundiced group. These data suggested that the significant decrease of gastric mucosal blood flow during the stress procedures was one of exacerbating factors of the acute gastric ulcerations in rats with obstructive jaundice, and vagotomy might prevent them by maintaining the gastric mucosal blood flow in obstructive jaundice.     

应激状态下胃黏膜损伤与胃排空及胃酸分泌的关系

目的 研究胃黏膜损伤的确切原因和具体过程,为临床防治胃黏膜损伤、胃炎、胃溃疡及胃癌提供新的理论依据.方法 以水浸-束缚应激(WRS)大鼠的方法,将144只Wistar大鼠随机分为9组,每组16只,A、B、c 3组用放射性核素99mTc灌胃测定大鼠胃液相排空率;D、E、F 3组采用手术清除胃内容物并幽门结扎测定胃酸分泌率;G、H、I 3组为手术不清除胃内容物并幽门结扎,评估胃黏膜损伤溃疡指数(UI);分析胃排空率、胃酸分泌和胃黏膜损伤之间的关系.结果 随着wRs时间延长,大鼠胃排空速率明显下降,B组(WRS 2 h)和c组(WRS 4 h)的胃排空速率与A组(正常对照组)相比,差异均有统计学意义(P＜0.01);C组与B组比较,差异有统计学意义(P＜0.01).大鼠胃酸分泌受到显著抑制,E组(WRS 2 h)和F组(WRS 4 h)的胃酸分泌率与D组(正常对照组)相比,差异均有统计学意义(P＜0.01);F组与E组比较,差异无统计学意义(P＞0.05).胃黏膜损伤随着应激时间的延长而加重,清除胃内容物可以有效防治应激引起的胃黏膜损伤,手术对本实验无明显影响.B、C组与A组的胃黏膜损伤UI比较,差异有统计学意义(P＜0.01);C组与B组比较,差异也有统计学意义(P＜0.01);A、D、E、F、G组大鼠未出现胃黏膜损伤,H与E组比较,差异有统计学意义(P＜0.01);I与F组比较,差异也有统计学意义(P＜0.01);A、D、E、F、G组间比较,差异无统计学意义(P＞0.05).H组与B组之间和I组与C组之间比较,差异有统计学意义(P＜0.01).结论 WRS可导致胃排空障碍、胃酸分泌减少和胃黏膜损伤.     

Gastric devascularization: a useful salvage procedure for massive hemorrhagic gastritis.

Due to poor results with conventional operative therapy for diffuse hemorrhagic gastritis (DHG), a prospective evaluation of gastric devascularization was performed on 21 patients. Sepsis, alcoholism, and steroid abuse were the common etiologic factors. In spite of the fact that these were all critically ill patients, all stopped bleeding with this operation and only two rebled (9%). The average operating time was 84 minutes. There were two operative complications and gastric necrosis did not occur. The mortality was high (38%) due to the primary disease. Gastric devascularization is a useful salvage procedure for the patient with DHG because it can be accomplished rapidly, with few complications, has a low rebleed rate, and causes no permanent sequelae. Since this procedure causes severe gastric mucosal ischemia, it casts doubt only on the importance of this mechanism alone as the cause of "stress ulceration."     

Haemorrhagic gastritis. Incidence, etiological factors, and prognosis

Etiological factors and prognosis were analyzed in 78 patients with haemorrhagic gastritis admitted to an intensive care unit during 8 years. These patients constituted 11.4% of a total of 684 cases with massive upper gastrointestinal haemorrhage admitted during the same time period. The annual incidence of haemorrhagic gastritis was 6.5/100,000 inhabitants. Most frequently, the bleeding episode was associated with intake of alcohol (35%) or anti-inflammatory drugs (23%). Only 4 patients (5%) had classical stress ulcers. Due to massive bleeding, surgery was necessary in 5 patients. Non-resectional surgery was carried out with no postoperative mortality. Six patients (8%) died (age 72-92 years), one as a direct cause of bleeding and five in severe associated disease, haemorrhagic gastritis being more or less a terminal event. Thus, in the great majority of unselected patients with haemorrhagic gastritis bleeding ceases on conservative treatment. In a minor fraction surgical treatment is a last resort but the method of choice is debatable. We propose that gastric resection should be avoided.     

A study on the mechanism of development of acute gastric ulcer in hemorrhagic shock--with special reference to the relation of PGE2 and noradrenaline levels in the gastric mucosa and changes in gastric mucosal blood flow

Changes in gastric mucosal blood flow in acute gastric ulceration associated with hemorrhagic shock were investigated for their relationship to gastric mucosal PGE2 and NA in rats which were deprived of 24 ml/kg of blood. The results were: 1. Gastric mucosal blood flow and NA were decreased by 65% and 25% respectively at 30 minutes after hemorrhage. Gastric mucosal PGE2 was 26% increased at 30 minutes after exsanguination and then showed a marked decrease. 2. Administration of NA resulted in an 100% increase of gastric mucosal PGE2. However, animals receiving NA at 20 or 50 minutes after hemorrhage gave values for gastric mucosal PGE2 which were not different from those of non-NA-treated animals at 30 and 60 minutes after hemorrhage. 3. Pre-treatment with PGE2 suppressed the reduction in both gastric mucosal blood flow and NA and the development of ulcer, whereas pre-treatment with indomethacin accelerated them. These results suggest that the increase in gastric mucosal PGE2 in early shock might represent a phenomenon of adaptation to decreased blood flow, implicating adrenergic activation as one of causative factors, and the decrease in gastric mucosal PGE2 in late shock might be construed as the result of impaired synthesis of PGE2 due to persistent hypoxia and be one of the possible factors for ulcers.     

应激状态下胃黏膜损伤与胃排空及胃酸分泌的关系

目的研究胃黏膜损伤的确切原因和具体过程，为临床防治胃黏膜损伤、胃炎、胃溃疡及胃癌提供新的理论依据。方法以水浸-束缚应激（WRS）大鼠的方法，将144只Wistar大鼠随机分为9组，每组16只，A、B、C3组用放射性核素99m^Tc灌胃测定大鼠胃液相排空率；D、E、F3组采用手术清除胃内容物并幽门结扎测定胃酸分泌率；G、H、I3组为手术不清除胃内容物并幽门结扎，评估胃黏膜损伤溃疡指数（uI）；分析胃排空率、胃酸分泌和胃黏膜损伤之间的关系。结果随着WRS时间延长，大鼠胃排空速率明显下降，B组（WRS2h）和C组（WRS4h）的胃排空速率与A组（正常对照组）相比，差异均有统计学意义（P〈0．01）；C组与B组比较，差异有统计学意义（P〈0．01）。大鼠胃酸分泌受到显著抑制，E组（WRS2h）和F组（WRS4h）的胃酸分泌率与D组（正常对照组）相比，差异均有统计学意义（P〈0．01）；F组与E组比较，差异无统计学意义（P〉0．05）。胃黏膜损伤随着应激时间的延长而加重，清除胃内容物可以有效防治应激引起的胃黏膜损伤，手术对本实验无明显影响。B、C组与A组的胃黏膜损伤UI比较，差异有统计学意义（P〈0．01）；C组与B组比较，差异也有统计学意义（P〈0．01）；A、D、E、F、G组大鼠未出现胃黏膜损伤。H与E组比较，差异有统计学意义（P〈0．01）；I与F组比较，差异也有统计学意义（P〈0．01）；A、D、E、F、G组间比较，差异无统计学意义（P〉0．05）。H组与B组之间和I组与c组之间比较。差异有统计学意义（P〈0．01）。结论WRS可导致胃排空障碍、胃酸分泌减少和胃黏膜损伤。