肝脏切除术后并发胃瘫综合征的护理

目的 探讨9例肝脏切除术后胃瘫综合征的护理.方法 对9例PGS患者保守治疗的同时,采取系统的护理措施.结果 9例患者通过综合保守治疗胃瘫恢复良好,没有其他严重并发症.结论 加强心理护理,有效的胃肠减压,充分的营养支持以及正确运用胃动力药物对PGS的康复至关重要.     

胆道术后胃瘫综合征12例的观察及护理

总结12例胆道术后胃瘫综合征的护理。护理重点为加强胃瘫早期症状的观察及处理,做好心理护理、胃肠减压护理、胆汁回输护理,加强肠外营养及肠内营养支持治疗,注重药物护理,以促进胃肠功能的恢复。12例患者均经保守治疗13-52d恢复,无其他严重并发症发生。     

52例腹部手术后胃瘫综合征的护理

目的 探讨52例腹部手术后胃瘫综合征(PGS)的护理.方法 给予相应的心理护理、持续胃肠减压、肠外与肠内营养支持等护理措施,增强胃蠕动,促进胃动力功能的恢复.结果 51例患者胃瘫恢复良好,没有其他严重并发癌发生;1例术后确诊为输出襻梗阻并再次手术,术后仍有胃瘫,保守治疗22d痊愈出院.结论 PGS的临床护理工作至关重要,应该贯穿于治疗的全过程.     

时间护理对胃瘫综合征患者疗效的影响

目的:研究时间护理对胃瘫综合征患者疗效的影响。方法:将64例腹部手术后胃瘫综合征患者随机分为观察组和对照组,其中观察组34例,对照组30例。对照组患者按常规进行护理,观察组患者给予时间护理。观察两组患者胃瘫综合征恢复时间及恢复率。结果:观察组比对照组恢复所需时间显著降低(P<0.05);在1～3周内观察组与对照组比较其恢复率显著提高(P<0.05,P<0.01);在观察组内非胃手术后胃瘫综合征患者恢复时间比胃手术后胃瘫综合征患者要短(P<0.05)。结论:在治疗胃瘫综合征患者过程中时间护理提高了胃瘫综合征的疗效,缩短了恢复时间,对胃瘫综合征患者的治疗是有积极意义的。     

腹部手术后胃瘫综合症非手术治疗的护理体会

目的探讨腹部手术后胃瘫综合征非手术治疗的护理方法。方法回顾性分析了13例腹部手术后胃瘫综合症患者非手术治疗的经过和护理措施。结果 13例患者均保守治疗获痊愈,无1例患者需再次手术。结论注重心理沟通,胃肠减压,加强营养支持,密切观察,配以必要的药物干预是提高腹部手术后胃瘫综合症护理质量的关键。     

胃癌术后胃瘫综合征的护理体会

[目的]探讨胃癌术后胃瘫综合征的护理措施,提高治疗效果。[方法]回顾性分析30例胃癌术后发生胃瘫综合征病人的护理资料。[结果]所有病人均采用保守治疗,同时给予心理护理、有效的胃肠减压、肠内营养护理、严密监测病人的电解质等,均取得了满意疗效。[结论]胃癌术后胃瘫综合征病人采用合理的护理措施,可以促进临床保守治疗效果,避免再次手术,减少病人的身心痛苦。     

胃手术后胃瘫综合征患者的护理

目的总结20例胃手术后发生胃瘫综合征的护理体会。方法回顾性对500例胃手术后出现胃瘫综合征的20例患者的临床资料进行分析总结。对20例患者加强心理护理,给予有效地胃肠减压,正确使用胃动力药物,给予合理的营养支持。结果20例患者中,7例9～14d胃肠功能恢复,13例15-21d胃肠功能恢复,住院21～34d痊愈出院。结论对于胃瘫综合征患者,严密观察病情、积极药物治疗同时给予心理治疗和护理,是促进患者早日康复的关键。     

上腹部手术后胃瘫综合征的原因分析及护理

[目的]探讨腹部手术后并发胃瘫综合征的原因及护理。[方法]回顾性分析7例胃、胰、胆术后并发胃瘫病人的临床资料,对病人采取保守治疗和综合护理干预。[结果]胃瘫多发生在术后5 d~10 d,经肠内外营养支持、胃肠减压、胃动力药的使用,配合护理,病人在2周~6周内胃动力恢复。[结论]采用合理的保守治疗和综合护理方法,可以显著改善病人的愈后。     

腹部手术后胃瘫综合征的诊治

目的:探讨腹部手术后胃瘫综合征的发病因素、诊断及治疗方法.方法:回顾性分析32例腹部术后胃瘫综合征病例的临床资料.结果:32例胃瘫综合征患者均保守治疗成功.胃瘫综合征发病机制尚不明确,以腹胀、呕吐为主要表现.胃管引流量>800 mL/d,且持续>10 d为主要诊断依据.上消化道碘造影、胃镜检查是诊断胃瘫综合征的有效方法.经综合治疗后胃肠动力一般可在<6周恢复.结论:综合性保守治疗是胃瘫综合征的有效治疗手段,应避免盲目手术治疗.     

胃术后胃瘫的观察与护理

目的介绍胃手术后胃瘫的发病机制、临床观察和护理经验。方法针对患者的病情遵医嘱进行专科护理。结果18例患者经过保守治疗和护理均取得满意疗效。结论胃术后胃瘫采用对症保守治疗和护理均能获得满意疗效，可以避免不必要的再次手术增加病人的经济和心理负担。     

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.