胃手术后胃植物石的预防及护理

胃植物石的发生并不少见,但胃手术后胃植物石的形成鲜有文献报道.我院从2000年1月-2003年12月共收治12例胃手术后因进食柿子而引发的胃内结石,现报道如下.……     

5例胃手术后残胃功能性排空障碍的护理体会

胃手术后残胃功能性排空障碍是指不伴有吻合口或输出空肠袢等机接性梗阻因素的残胃无力、排空迟缓，经保守治疗可以恢复的一种胃手术后并发症。我院自1992年1月-2002年12月共遇到5例胃手术后发生功能性排空障碍的患者，经精心治疗和护理均痊愈出院，现将护理体会总结如下。     

腹腔非胃手术后胃瘫综合征患者的观察与护理

胃大部切除术后残胃胃瘫综合征在临床上常可遇到，但发生于腹腔非胃手术后的胃瘫综合征（gastroparesis syndrome aftemongastrectomy，GSNG）较少。我院1972—2006年共诊治胃瘫综合征72例，其中50例为胃切除术后残胃胃瘫综合征，22例为GSNG，前者与后者之比为2．3：1．0。本文对GSNG患者的观察与护理要点进行总结，现报道如下。[第一段]     

腹部手术后胃瘫的观察与护理

胃瘫是指腹部手术后非机械性梗阻因素引起的以功能性胃排空障碍为主要征象的胃动力紊乱综合征。胃部手术后约有5％-40％的病人会发生不同程序的胃瘫。自2004年1月至2007年12月我科行腹部手术后共发生23例胃瘫，均经保守治疗恢复了胃肠功能，无一例需行再次手术，现总结报告如下。     

胃术后胃无力症10例诊治体会

胃无力症是胃手术后一种并发症，亦可称为术后胃瘫。主要表现为胃排空延迟（DGE）。它常见于胃癌或溃疡病的大部分切除。近年来，逐渐被人们所认识。我院近10年共发生10例，现对病因和治疗方法进行初步探讨。     

胃术后胃瘫综合征16例诊断与治疗体会

目的：探讨胃手术后胃瘫综合征（stomach postsurgical gastroparesis syndrome,SPGS)发生的病因，寻找诊断与治疗措施。方法：回顾性总结1992年7月－2000年5月间16例SPGS患者的诊断过程和治疗效果，对其发生时间、临床表现及诱发因素进行分析。结果：SPGS临床表现为患者在胃手术后改饮食呕吐胃 内容物，量≥800ml/d，无明显腹痛，肛门排气正常，胃肠X 线动态检查可见胃潴留、胃蠕动差，胃镜检查吻合口通畅，核素 标记胃排空时间延长；所有病例经禁食、胃肠减压、营养支持、维持水电解质及酸碱代谢平衡，以及用促进胃肠动力药治疗，4周内痊愈。结论：SPGS的 要依据临床表现，胃镜、胃肠X线动态检查、核素标记残胃排空时间测定对SPGS有诊断价值；治疗采用综合措施、避免再次手术。     

我院胃手术后病人的饮食护理

胃的手术包括全胃切除术、胃大部切除术、胃部分切除术、胃空肠吻合术等，胃肠吻合又分毕氏Ⅰ式和毕氏Ⅱ式，全胃切除后则多为食管空肠吻合即空肠袢代胃术。在临床工作中，胃手术后往往因进饮进食不合理或饮食不节引起呕吐、上腹部憋胀、倾倒综合征、吻合口出血、吻合口瘘等并发症，给病人带来了不应有痛苦。为了减少胃手术后并发症的发生，使病人顺利度过术后恢复期，促进病人康复，正确合理的饮食护理在整个治疗和康复过程中起着非常重要的作用。现就胃手术后，针对不同术式，怎样做好饮食护理等问题介绍如下。     

腹部手术后胃无力症30例临床分析

目的探讨腹部手术后胃无力症的发生原因、机制、诊断和治疗方法。方法对1993年1月～2005年1月收治的30例腹部手术后胃无力症病人的临床资料进行回顾性分析。结果腹部手术后胃无力症均发生于腹部于术后3～12d,29例经非手术治疗后,3～6周逐渐恢复,可正常进食。1例病人拒绝治疗而死亡。结论腹部手术后胃无力症的病因是多因素的,消化道造影及胃镜检查是诊断胃无力症的主要手段。采用非手术治疗可治愈胃无力症应尽量避免再手术。     

腹部术后胃瘫综合征

术后胃瘫综合征是包括胃术后胃瘫在内的腹部手术后并发的以胃排空障碍为主要征象的胃动力紊乱综合征，其特点是在腹部手术后出现的非机械性梗阻所引起的胃排空障碍症候群，属功能性疾患。1998年2月至2006年12月本科共收治42例胃术后胃瘫及2例其他腹部手术后发生的胃瘫，报告如下。     

1例肠瘘闭瘘术后合并胃瘫的护理

胃瘫是指以胃排空障碍为主要征象的胃动力紊乱综合征，直接影响手术后效果。我科于2003年10月收治1例因多处外伤后肠瘘的病人，在全身麻醉下行闭瘘手术后出现胃瘫，经非手术治疗和精心护理，痊愈出院。现将护理报告如下。     

血清胃蛋白酶原与良、恶性溃疡

目的通过检测血清胃蛋白酶原Ⅰ(PGI)、血清胃蛋白酶原Ⅱ(PGII),探讨胃溃疡及胃癌患者血清PGI、血清PGII及血清PGI/血清PGII的变化规律。方法研究了2005年5月至2006年1月在我院消化内镜中心行胃镜检查者171例,并设正常人对照12例:用免疫放射法(IRMA)测定了其血清PGI及PGII并计算PGI/PGII即PGR。171例胃病患者分组情况:①消化性溃疡组105例;②胃癌组66例。结果①消化性溃疡患者血清PGI及PGII升高(P<0.05)。在溃疡组的分层研究中,血清PGI及PGII升高在活动组更为明显,而在愈合组变化无统计学意义。②胃癌患者血清PGI降低、PGR降低(P<0.01)。在胃癌组的分层研究中:早期胃癌患者PGI及PGR明显降低;进展期胃癌患者PGI及PGR亦降低,两者间无统计学差异(P>0.05)。结论测定血清PGI、PGII水平及PGR值对胃溃疡及胃癌患者的鉴别诊断具有重要的参考意义。     

Near-total gastric necrosis caused by acute gastric dilatation

Gastric dilatation caused by psychogenic polyphagia or bulimia may, under extreme circumstances, progress to total gastric necrosis. We have described a patient in whom acute abdominal symptoms and signs developed while he was receiving psychiatric treatment. Laparotomy showed massive gastric dilatation with near-total infarction. Total gastrectomy with cervical esophagostomy, feeding and decompressing jejunostomies, and wide drainage of the gastric bed were done. After staged reconstruction, recovery was uneventful.     

胃部手术患者经不同侧鼻孔安置胃管的对比研究

目的 探讨不同侧鼻孔置人胃管对术中胃管调整的影响.方法 将200例胃部手术患者随机分为两组.对照组术前经右鼻孔插人胃管,实验组术前经左鼻孔插入胃管,观察两组患者术中发生胃管调整困难的差异.结果 经左鼻孔插入胃管术中发生胃管涮整困难的患者为1例,经右鼻孔插人胃管术中发生胃管调整困难的患者为24例.对经右鼻孔插入胃管术中发生胃管调整(向里插入一部分)困难的患者实施拔除胃管改为经左鼻孔插入后,成功23例.不同侧鼻孔安置胃管术中发生胃管调整困难的百分率差异有统计学意义(X2=24.18,P<0.05).结论 对行胃部手术的患者,术前经左鼻孔留置胃管可有效降低术中胃管调整的困难,减轻患者鼻咽部及食道黏膜的损伤.     

胃手术后并发胃瘫综合征的诊断和治疗

目的 探讨胃手术后胃瘫综合征的诊断及治疗。方法 回顾性分析21例胃手术后胃瘫综合征的临床资料。结果 本组胃瘫综合征发生率3．9％，诊断主要依据患者的临床症状、上消化道造影和胃镜检查，经保守治疗痊愈。结论 综合保守治疗是胃瘫综合征较为理想的治疗方法。     

Endosonography in gastric lymphoma and large gastric folds.

To establish a correct preoperative differential diagnosis between gastric lymphoma and cancer is essential but can be difficult as endoscopic biopsies can sometimes provide a low diagnostic yield. By EUS, infiltrative carcinoma tends to show a vertical growth in the gastric wall, while lymphoma tends to show mainly a horizontal extension. EUS provides an accurate staging of gastric lymphoma, showing the exact level of infiltration and the presence of perigastric lymph nodes, thus the physician can obtain an accurate prognosis for each patient and select the best form of treatment accordingly. The response to chemoradiotherapy can also be investigated very accurately by EUS. Large gastric folds are seen in a great number of benign and malignant conditions. Diagnosis represents a clinical challenge because etiology may be extremely varied and standard biopsies are often inconclusive. Different diseases show different levels of infiltration of the gastric wall, thus a characteristic echo-pattern helps for the differential diagnosis. Endosonography, used always in combination with biopsy, allows to rule out malignancies and to select the most appropriate treatment for each patient (medical or surgical).     

Acrylonitrile-induced gastric mucosal necrosis: role of gastric glutathione

Acrylonitrile [vinyl cyanide (VCN)] induces acute hemorrhagic focal superficial gastric mucosal necrosis or gastric erosions. In this report the authors have studied the mechanism of the VCN-induced gastric erosions. VCN-induced gastric lesions are coupled with a marked decrease of gastric reduced glutathione (GSH) concentration. Pretreatment of rats with various metabolic modulators (cytochrome P-450 monooxygenase and GSH) before VCN demonstrated that there is an inverse and highly significant correlation between gastric GSH concentration and the VCN-induced gastric erosions. Pretreatment of rats with sulfhydryl-containing compounds protected against the VCN-induced gastric necrosis and blocked the VCN-induced gastric GSH depletion. Furthermore, pretreatment of rats with atropine, which blocks muscarinic receptors, protected rats against the VCN-induced gastric erosions. The working hypothesis is that depletion and/or inactivation of critical endogenous sulfhydryl groups causes configurational changes of cholinergic receptors and increases agonist binding affinity, which, among other actions, leads to the causation of gastric mucosal erosions.     

Delayed gastric emptying and gastric autoimmunity in type 1 diabetes

OBJECTIVE: Delayed gastric emptying and/or gastrointestinal symptoms occur in 30-50% of diabetic patients. Known contributing factors are autonomic neuropathy and acute hyperglycemia, but the role of gastric autoimmunity has never been investigated, although 15-20% of type 1 diabetic patients exhibit parietal cell antibodies (PCAs). We studied gastric motility in diabetes in relation to PCA status, autonomic nerve function, HbA(1c), thyroid-stimulating hormone (TSH), Helicobacter pylori (HP), acid production, and gastric histology. RESEARCH DESIGN AND METHODS: Gastric emptying of solids and liquids (measured by (13)C-octanoic acid and (13)C-glycine breath tests, respectively) was tested in euglycemic conditions in 42 type 1 diabetic patients (male/female: 29/13; 15 PCA+; mean age 40 +/- 15 years; mean HbA(1c) 7.8 +/- 0.9%). Gastrointestinal symptoms, autonomic nerve function (Ewing tests), PCA status (indirect immunofluorescence), gastric histology, and acid secretion (pentagastrin) were assessed. RESULTS: Solid gastric emptying was delayed in 40% and liquid emptying in 36% of patients. Gastric motility did not correlate with symptoms. PCA status, gastric morphology, and acid secretion were similar in those with and without gastroparesis. HbA(1c) level (beta = 1.34, P = 0.011) was the only risk factor for delayed solid emptying in a logistic regression model testing HbA(1c), autonomic nerve function, PCA, HP status, age, sex, diabetes duration, and TSH. Half-emptying time for liquids correlated with TSH level (r = 0.83, P < 0.0001) and autonomic neuropathy score (r = -0.79, P = 0.001). CONCLUSIONS: We found that approximately 50% of type 1 diabetic patients studied had delayed gastric emptying that did not correlate with symptoms. Gastric autoimmunity did not contribute to diabetic gastroparesis. Metabolic control was worse in patients with delayed solid emptying.