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连续性肾脏替代治疗患者的体温变化及其护理干预
连续性肾脏替代治疗(continuous renal replace-ment therapy,CRRT)广泛用于急性肾功能衰竭(acute renal failure,ARF)全身炎症反应综合征(systemic inflamatory response syndrome,SIRS)、多器官功能障碍综合征(multiple organ dysfunction syndrome,MODS)、急性重症胰腺炎(severe acute pancreatitis,SAP)的救治,与呼吸机、全静脉营养支持一起成为ICU的三大支柱<'[1]>.我们于2008年1~12月对CRRT患者治疗中的体温变化进行了观察和护理,报告如下.
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Objective. To evaluate the effects of epidermal growth factor (EGF) on intestinal permeability and bacterial translocation in rats with acute pancreatitis during total parenteral nutrition (TPN). Methods. Thirty-two male Sprague-Dawley rats that underwent injection of 3.5% sodium taurocholate solution into the pancreatic duct were randomly divided into one of the following two groups: (1) received only TPN (control group) or (2) received TPN with EGF at a dose of 0.2 mg· kg-1· day-1 (Egf group). On fifth day of total parenteral nutrition, samples from mesenteric lymph nodes, pancreas, liver and spleen were harvested for cultures. Water, protein and DNA content in jejunal mucosa were determined. D-xylose and fluorescein isothiocyanate (FITC)-dextran were instilled into the lumen of a ligated segament of small intestine. Thirty minutes later, superior mesenteric vein D-xylose and plasma FITC-dextran concentration were measured. Results. Positive cultures in liver and spleen, as well as FITC-dextran concentration in the Egf group were significantly lower than in the control group. Protein and DNA content in jejunal mucosa in the Egf group were significantly higher than in the control group. Conclusion. The results indicate that EGF may prevent increased intestinal permeability and bacterial translocation in rats with acute pancreatitis during TPN.
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Objective. To evaluate the effects of epidermal growth factor (EGF) on intestinal permeability and bacterial translocation in rats with acute pancreatitis during total parenteral nutrition (TPN). Methods. Thirty-two male Sprague-Dawley rats that underwent injection of 3.5% sodium taurocholate solution into the pancreatic duct were randomly divided into one of the following two groups: (1) received only TPN (control group) or (2) received TPN with EGF at a dose of 0.2 mg· kg-1· day-1 (Egf group). On fifth day of total parenteral nutrition, samples from mesenteric lymph nodes, pancreas, liver and spleen were harvested for cultures. Water, protein and DNA content in jejunal mucosa were determined. D-xylose and fluorescein isothiocyanate (FITC)-dextran were instilled into the lumen of a ligated segament of small intestine. Thirty minutes later, superior mesenteric vein D-xylose and plasma FITC-dextran concentration were measured. Results. Positive cultures in liver and spleen, as well as FITC-dextran concentration in the Egf group were significantly lower than in the control group. Protein and DNA content in jejunal mucosa in the Egf group were significantly higher than in the control group. Conclusion. The results indicate that EGF may prevent increased intestinal permeability and bacterial translocation in rats with acute pancreatitis during TPN.
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重症急性胰腺炎肠外、肠内营养支持
随着对重症急性胰腺炎(Severe acute pancreatitis,SAP)发病机制、病程演变的深入研究,急性胰腺炎诊断、治疗原则渐趋一致,多种临床先进治疗技术介入的综合治疗使SAP病死率降至20%以下,其中营养支持具有重要作用,营养支持虽然不能完全改变SAP病程进展,但通过改善患者整体营养状态,提高免疫功能,有助于减少并发症的发生,提高治愈率.早期研究对SAP主要采用肠外营养,近年来肠内营养受到重视,本文就与SAP的肠外、肠内营养有关问题综述如下:
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儿童急性胰腺炎的诊治
儿童急性胰腺炎(child acute pancreatitis,CAP)的发病率低,但病情凶险,病死率高.近年来,CAP在临床上有增多趋势,但其相关诱因、临床表现、诊断和治疗与成年人不尽相同.
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重症急性胰腺炎肠内营养的应用
重症急性胰腺炎(sevel'e acute pancreatitis,SAP)是一种非常凶险的疾病,占胰腺炎发病率的20%~30%,可引起重要脏器功能衰竭和局部并发症,病程较长,病死率为27%~45%.同时SAP是一种全身性的消耗性疾病,患者存在蛋白质分解、糖原异生和脂肪动员增强为特征的超高代谢反应和严重应激反应,可迅速出现全身内环境紊乱、免疫功能减退和不同程度的营养不良.
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重症急性胰腺炎营养支持治疗的研究进展
重症急性胰腺炎(severe acute pancreatitis,SAP)非手术治疗已成为目前的主要治疗手段,SAP时机体处于高分解代谢状态,能量消耗大,加之禁食、疼痛的消耗,故营养支持成为治疗计划中的重要环节[1],利用营养支持治疗可以保护肠黏膜屏障功能,降低全身炎性反应综合征、急性呼吸窘迫综合征、感染等并发症的发生率[2].
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胰酶的激活在急性胰腺炎肺损伤发生机制中的作用
急性胰腺炎(acute pancreatitis,AP)是外科常见急腹症之一.病理上分为急性水肿性胰腺炎和急性出血坏死性胰腺炎,后者病情危重,病死率高,常伴有远隔器官的损伤或功能衰竭,其中急性肺损伤较为常见,表现为低氧血症、急性呼吸窘迫综合征(ARDS)、肺膨胀不全等.
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急性胰腺炎相关性肺损伤的发病机制
重症急性胰腺炎(severe acute pancreatitis,SAP)具有发病急、病程进展快、病死率高等特点.SAP除引起胰腺局部损伤外,尚可出现胰外多器官的损伤.急性肺损伤(acute lung injury,ALI)和急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)是常见的一种早期并发症.
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急性胰腺炎肺损伤的诊治ⅡASC与重症急性胰腺炎肺损伤
重症急性胰腺炎(severe acute pancreafitis,SAP)发病早期即可伴有严重的重要脏器功能损伤,其中急性肺损伤极为常见,其发病机制尚未完全明了.
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NF-κB炎性反应信号通路在急性胰腺炎肺损伤发病机制中的作用
急性胰腺炎(AP)相关性肺损伤(acute pancreatitis associated lung injury,APALI)是AP高病死率的主要原因.其发病机制错综复杂,迄今尚未完全阐明.
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急性胰腺炎相关性肺损伤的中西医结合治疗
急性胰腺炎(AP)是外科临床常见急腹症之一,尤其是重症AP(SAP)更是急危重症之一,发病急,变化快,并发症多,病死率高.
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急性胰腺炎并发肠粘膜屏障损害机制与作用
急性胰腺炎(acute pancreatitis,AP)并发症多,病死率高,发病机制复杂,继发的细菌感染、内毒素血症亦是其危险因素.近年来,随着对急性胰腺炎中MODS、细菌移位、肠源性感染等的深入研究,肠道的粘膜屏障功能逐渐被人们所重视.肠粘膜屏障能起到防止肠道内致病细菌、毒素等有害物质透过肠壁到达肠外,以及保持机体内环境的稳定等重要作用[1~3].在重症急性胰腺炎(severe acute pancreatitis,SAP)、创伤、手术、放化疗、严重感染等应激状态下,肠粘膜的结构和功能会受到损害,表现为电镜下发现肠粘膜微绒毛部分上皮脱落、减少;绒毛高度、宽度显著减低,面积减少;细胞紧密连接破坏[4~5];凋亡细胞增加;肠道粘膜通透性(intestinal permeability,IP)出现病理性升高.
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急性胰腺炎并发肝损伤机制及治疗研究现状
急性胰腺炎(acute pancreatitis,AP)是一种发病急、进展快,易导致多脏器损伤,且病死率较高的常见急腹症[1,2].近年来临床研究发现,AP并发肝损伤的发生率为40.1%~56.6%,而重症急性胰腺炎(severe acute pancreatitis,SAP)并发肝损伤者高达88.9%[3].
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急性胰腺炎病因学变化趋势和对策的研究进展
急性胰腺炎(acute pancreatitis,AP)是由于各种病因,包括胆道梗阻、酒精和高脂血症等引起的胰腺自身消化性疾病.急性胰腺炎的临床表现差异较大,轻症胰腺炎(mild acute pancreatitis,MAP) 患者预后良好;小部分为重症胰腺炎 (severe acute pancreatitis,SAP) 患者,常伴有多器官功能衰竭或胰腺坏死感染等全身或局部并发症,仍然缺乏有效的治疗手段,治疗费用高,并发症率和病死率很高(8%~20%),其主要原因是发病机制和病理生理过程不清,针对病因治疗重视不够.
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中药对急性胰腺炎实验动物多脏器细胞凋亡的影响
急性胰腺炎(acute pancreatitis, AP)尤其是重症急性胰腺炎(severe acute pancreatitis, SAP)是消化系统疾病中较为凶险的急腹症,严重的会发展成全身炎症反应综合征(SIRS)和多器官功能不全综合征(MODS).细胞死亡包括细胞坏死与细胞凋亡,凋亡与坏死的本质区别在于凋亡不释放细胞内容物和炎症介质,不起炎症反应.凋亡过程紊乱与许多疾病的发生有关,如肿瘤、自身免疫性疾病等.除了胰腺本身外,在实验性AP动物引起的全身并发症中,已经证实心、肝、肺、肠、胸腺等多脏器均存在细胞凋亡.AP属中医"腹痛"、"结胸"、"阳明腑实证"范畴,一些通里攻下、活血化瘀、清热解毒的中药可以通过抑制胰酶、抑制细胞因子、清除氧自由基等机制改善预后.近年来,中药对实验性AP动物多脏器细胞凋亡的影响也受到关注,本文将对此做一综述.
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中药治疗重症急性胰腺炎机制研究进展
急性胰腺炎(acute pancreatitis,AP)是临床常见的急腹症,重症急性胰腺炎(severe acute pancreatitis,SAP)亦称急性坏死性胰腺炎(acute necrotic pancreatitis,ANP),病死率较高,约有20%[1].
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急性胰腺炎与细胞因子
不少急性胰腺炎(acute pancreatitis,AP)患者症状轻微,病情呈自限性,但对于重症急性胰腺炎(severe acute pancreatitis,SAP)患者确有接近30%的病死率,继发感染时则更高.近年来,随着对AP发病机制研究的深入,细胞因子在AP发生、发展过程中起的作用愈来愈受到重视.本文就近几年来细胞因子在AP发病机制中的作用做一综述.
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Toll样受体在急性胰腺炎中的作用
急性胰腺炎(acute pancreatisis, AP)是临床常见疾病,多年来一直是医学领域的研究热点.轻症急性胰腺炎(miid acute pancreatitis, MAP)可为自限性疾病,而重症急性胰腺炎(severe acute pancreatitis, SAP)进展迅速,甚至出现多器官功能衰竭,病死率较高[1,2].
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重症急性胰腺炎并发多器官损伤时的病理改变
重症急性胰腺炎(severe acute pancreatitis,SAP)病情危重、发展快,常并发全身炎症反应综合征(SIRS)和多器官功能障碍综合征(MODS),终导致多器官衰竭(MOF),这是SAP患者早期死亡的主要原因[1],病死率高达20%~40R%[2].目前,通过动物模型来研究SAP的报道较为深入全面,本文就实验性SAP动物并发多器官损伤时的病理改变进行综述.