综合性医院妇产科医院感染的危险因素分析与护理对策

目的调查和分析综合性医院妇产科医院感染发生状况,并制定相应的护理措施来控制和降低医院感染的发生率。方法采用回顾性调查方法,对2005年1月至12月3150侧妇产科出院患者（妇科1910例;产科1240例）进行院内感染的调查、统计和分析。培果妇科发生院内感染57例,感染率为2．98％。妇科病房中高龄患者、化疗患者是医院感染的高危人群;住院时间越长感染率越高。常见感染部位依次为呼吸道、泌尿道、胃肠道等。产科发生院内感染10例。感染率为0．81％。妊娠合并并发症的患者是高危人群,常见感染部位依次为呼吸道,泌尿道,宫腔等。结论严格执行无菌操作。加强病房管理、基础护理和健康教育,缩短留置尿管时间和住院天数。可以降低妇产科的医院感染。     

高原地区65岁以上老年患者医院感染特点分析及护理

目的 分析高原地区65岁以上老年患者医院感染的临床特点,以制定有效的护理对策.方法 对2005年1月-2010年5月期间230例并发医院感染的≥65岁住院患者进行回顾性分析,内容包括医院感染发生率、感染部位、病原菌,并探讨护理对策.结果 ≥65岁老年住院患者发生医院感染230例,发生率11.06%;感染部位依次为上呼吸道、下呼吸道、手术切口、胃肠道、泌尿道、皮肤软组织及其他;病原菌以革兰氏阳性菌为主(73.6%),依次为溶血性链球菌(28.3%)、金黄色葡萄球菌(17.9%)、肺炎链球菌(14.2%);手术切口感染以革兰氏阴性杆菌为主,依次为大肠埃希菌、铜绿假单胞菌.结论 高原地区≥65岁老年住院患者医院感染发生率较高,病原菌菌群分布不同于平原地区,高原缺氧、干燥、寒冷环境是主要因素.提出高原地区医院感染患者应合理给予氧疗,加强呼吸道护理、饮食护理,严格消毒等护理对策.     

158例骨科患者医院感染的调查分析与护理对策

目的探讨骨科患者医院感染的特点与护理对策。方法采用目标性监测方法分析2005年10月～2008年9月本院骨科患者的医院感染情况。结果本院骨科3025例患者共发生医院感染158例(5.22%);感染部位以手术切口为主(40.51%),其次为呼吸道和泌尿道,其中呼吸道感染和泌尿道感染与侵入性操作有相关性。引起医院感染最常见的病原菌以大肠埃希菌为主(21.43%),其次为铜绿假单胞菌、不动杆菌、克雷伯菌属、金黄色葡萄球菌、表皮葡萄球菌、肠球菌及白色念珠菌等。结论骨科医院感染的发生是多种因素所致,重视加强护理工作,提高患者机体抵抗力,严格执行无菌技术,规范侵入性操作,可降低骨科患者医院感染发生率。     

脑梗死患者医院感染因素分析及护理干预

目的探讨降低脑梗死患者医院内感染发生率的护理干预措施。方法对1 945例脑梗死患者住院期间发生医院内感染的资料进行回顾性分析。结果采取护理干预前脑梗死患者972例发生医院内感染114例次,医院内感染发生率为11.6%,发生的首要部位是下呼吸道、泌尿道和上呼吸道;护理干预组脑梗死患者973例,感染73例次,感染率7.4%,明显低于护理干预前(P<0.01)。结论有效的护理干预可减少脑梗死患者医院内感染的发生。     

住院产妇医院感染情况调查

目的了解住院产妇医院感染现状,探讨控制医院感染的措施。方法用回顾性调查方法,对该医院2007-2009年期间30 315例分娩产妇医院感染发生状况进行了调查。结果连续3年住院产妇中发生医院感染203例,感染发生率为0.67%,总体呈逐年下降趋势。产妇医院感染发生部位依其发生率高低依次为:上呼吸道、宫腔、皮肤软组织、泌尿道、手术切口感染。结论该医院住院产妇医院感染发生率较低,且呈逐年降低趋势。     

脑卒中卧床患者医院内感染情况分析与护理对策

目的 分析脑卒中卧床患者医院内感染的发生情况,制定相应护理对策.方法 回顾调查389例脑卒中卧床患者住院期间发生医院内感染的资料进行分析.结果 389例脑卒中卧床患者中,发生医院感染108例,医院感染发生率为27.76%;前3位感染部位为下呼吸道58例次,占53.7%;泌尿道29例次,占26.85%;上呼吸道16例次,占14.81%;医院内感染与患者意识障碍、吞咽困难、留置尿管、长期卧床有关.结论脑卒中卧床患者是医院感染的高发人群,加强基础护理和病房管理,采取有效的护理对策,以降低医院感染的发生率.     

妇科老年患者术后感染相关因素分析

分析老年妇科患者术后感染的相关因素,提出有效防控措施。采用回顾性调查方法,对2010年12月-2013年12月的218例妇科老年手术患者临床资料进行分析,掌握术后感染发生率及相关因素,并进行统计分析。结果 老年妇科患者发生术后感染23例,感染率为10.55%;医院感染部位以呼吸道为主,其次为泌尿道和手术切口等;患者年龄、伴有基础疾病和手术方式等是发生医院感染的危险因素。结论 老年妇科患者术后医院感染发生受多种因素影响,需采取针对性措施进行预防。     

神经内科医院感染病例分析

目的了解神经内科住院患者医院感染构成特点和分布情况,为制定感染控制方案提供依据。方法采用回顾性调查方法,对神经内科住院患者医院感染现状进行了调查与分析。结果调查该医院神经内科住院患者8 913例,发生医院感染患者419例、432例次,医院感染发生率为4.70%、例次感染率为4.85%。医院感染部位以呼吸道感染居首位,构成比占88.43%;其次是泌尿道感染。高龄患者、脑出血患者和导管留置为主要感染因素。结论该医院神经内科住院患者医院感染部位以呼吸道感染构成比最高,应加强机械通气相关肺炎防控措施。     

老年痴呆患者发生医院感染的相关因素及护理对策

目的总结分析老年痴呆患者医院感染的相关因素和护理对策.方法回顾调查352例老年痴呆患者资料.结果 352例老年痴呆患者中,发生医院感染133例,医院感染发生率为37.8%;医院感染159例次,医院感染例次发生率为45.2%;前3位感染部位为下呼吸道71例次、泌尿道36例次和上呼吸道19例次;病原体前3位为真菌感染31例次、大肠埃希菌感染30例次、肺炎克雷伯菌24例次;抗生素使用一联28%、二联60%、三联12%.结论老年痴呆患者是医院感染的高发人群,要采取有效的护理对策,以降低医院感染的发生率.     

神经内科ICU医院感染因素及护理干预

目的探讨神经内科ICU医院感染特点及护理干预措施。方法采用回顾性调查的方法,对124例神经内科ICU出院患者中的医院感染病例进行了分析。结果124例神经内科ICU住院患者中发生医院感染21例,感染率为16.93%。老年重症患者是医院感染的高危人群,重症脑血管疾病医院感染率最高;常见感染部位依次是呼吸道、胃肠道和泌尿道等。感染原因与创伤性操作增加、机体抵抗力降低、不合理使用抗生素有关,另外医护人员缺乏交叉感染意识也是发生感染的因素之一。结论神经内科ICU病人医院感染发生率较高,应加强对老年病人的关注,对重症病人呼吸道、胃肠道和泌尿道的护理干预,限制抗生素的使用和创伤性操作。     

Migraine and genetic and acquired vasculopathies

It is remarkable that migraine is a prominent part of the phenotype of several genetic vasculopathies, including cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL), retinal vasculopathy with cerebral leukodystrophy (RVCL) and hereditary infantile hemiparessis, retinal arteriolar tortuosity and leukoencephalopahty (HIHRATL). The mechanisms by which these genetic vasculopathies give rise to migraine are still unclear. Common genetic susceptibility, increased susceptibility to cortical spreading depression (CSD) and vascular endothelial dysfunction are among the possible explanations. The relation between migraine and acquired vasculopathies such as ischaemic stroke and coronary heart disease has long been established, further supporting a role of the (cerebral) blood vessels in migraine. This review focuses on genetic and acquired vasculopathies associated with migraine. We speculate how genetic and acquired vascular mechanisms might be involved in migraine.     

Fibrinogen and fibrin structure and functions

Fibrinogen molecules are comprised of two sets of disulfide-bridged Aalpha-, Bbeta-, and gamma-chains. Each molecule contains two outer D domains connected to a central E domain by a coiled-coil segment. Fibrin is formed after thrombin cleavage of fibrinopeptide A (FPA) from fibrinogen Aalpha-chains, thus initiating fibrin polymerization. Double-stranded fibrils form through end-to-middle domain (D:E) associations, and concomitant lateral fibril associations and branching create a clot network. Fibrin assembly facilitates intermolecular antiparallel C-terminal alignment of gamma-chain pairs, which are then covalently 'cross-linked' by factor XIII ('plasma protransglutaminase') or XIIIa to form 'gamma-dimers'. In addition to its primary role of providing scaffolding for the intravascular thrombus and also accounting for important clot viscoelastic properties, fibrin(ogen) participates in other biologic functions involving unique binding sites, some of which become exposed as a consequence of fibrin formation. This review provides details about fibrinogen and fibrin structure, and correlates this information with biological functions that include: (i) suppression of plasma factor XIII-mediated cross-linking activity in blood by binding the factor XIII A2B2 complex. (ii) Non-substrate thrombin binding to fibrin, termed antithrombin I (AT-I), which down-regulates thrombin generation in clotting blood. (iii) Tissue-type plasminogen activator (tPA)-stimulated plasminogen activation by fibrin that results from formation of a ternary tPA-plasminogen-fibrin complex. Binding of inhibitors such as alpha2-antiplasmin, plasminogen activator inhibitor-2, lipoprotein(a), or histidine-rich glycoprotein, impairs plasminogen activation. (iv) Enhanced interactions with the extracellular matrix by binding of fibronectin to fibrin(ogen). (v) Molecular and cellular interactions of fibrin beta15-42. This sequence binds to heparin and mediates platelet and endothelial cell spreading, fibroblast proliferation, and capillary tube formation. Interactions between beta15-42 and vascular endothelial (VE)-cadherin, an endothelial cell receptor, also promote capillary tube formation and angiogenesis. These activities are enhanced by binding of growth factors like fibroblast growth factor-2 (FGF-2) and vascular endothelial growth factor (VEGF), and cytokines like interleukin (IL)-1. (vi) Fibrinogen binding to the platelet alpha(IIb)beta3 receptor, which is important for incorporating platelets into a developing thrombus. (vii) Leukocyte binding to fibrin(ogen) via integrin alpha(M)beta2 (Mac-1), which is a high affinity receptor on stimulated monocytes and neutrophils.     

Telemedicine and teleradiology technologies and applications

Summary. Telemedicine and teleradiology hold the key for improving future health care delivery. In this paper we first review current communication and computer technologies used in telemedicine and teleradiology. Five examples in teleradiology applications are given including hospital-integrated picture archiving and communication systems, tele-neuro-imaging, telemammography, university consortium teleradiology service, and teleradiology for second opinion. Parameters important to teleradiology applications like costs, image quality, system reliability, and turn around time are considered. Data security is discussed, including patient confidentiality and image authenticity-which will be a major issue in future teleradiology applications.     

创伤高血糖与感染和MODS早期诊断和干预

本文详细介绍了创伤后血糖应激适度理论,以及高血糖与感染和多器官功能不全综合征的关系;提出涉及胰岛B细胞功能不全的MODS实验诊断新方案和极化液个体化干预新措施,可早期发现创伤MODS、降低感染率及MODS发生率和病死率。     

腹膜后纤维化与肾积水发生关系的临床研究

目的：探讨腹膜后纤维化（RPF）导致肾积水的原因及诊治经验。方法：回顾分析2004年1月—2010年12月24例腹膜后纤维化致肾积水患者的诊治资料。结果：（1）RPF患者常见首发症状为腰背痛或腹痛（69.2%）;（2）红细胞沉降率（ESR）增快和血清IgG4升高最常见。超声检查仅提示上尿路积水。RPF的静脉肾盂造影（IVP）和CT尿路成像（CTU）表现具有特征性。IVP肾盂输尿管显影不良时,CTU能较清晰的显示上尿路影像。CT扫描发现腹膜后软组织肿块9例（37.5%）,优于超声检查;（3）输尿管松解和腹腔化手术治疗22例;行肾切除术1例;行输尿管置双J管术1例。最终确诊为继发性RPF8例,其中4例为术前诊断,3例为术中腹膜后软组织肿块冷冻活检证实,1例为术后病理证实;（4）特发性RPF手术后肾积水均获长期缓解,而继发性RPF的预后取决于原发疾病及其治疗方案。结论：影像学检查是诊断RPF的重要手段,CTU优于超声检查和IVP。输尿管松解和腹腔化手术可以使特发性RPF输尿管梗阻得到长期的缓解,术中对肿块进行冷冻活检有助于鉴别特发性和继发性RPF,及时调整治疗方案。     

探讨儿童慢性顽固性咳嗽与支原体感染的关系及临床治疗观察

目的探讨儿童慢性顽固性咳嗽与肺炎支原体（MP）感染的关系及临床疗效观察。方法采用回顾性研究方法对于现将2005年3月至2008年3月在我院的55例确诊慢性顽固性咳嗽患儿,主要表现为肺炎支原体感染为临床特点进行分析,并进一步临床治疗研究。结果①临床特点：在55例确诊慢性咳嗽的患儿中,以慢性顽固性咳嗽为主要症状。58％（32／55）的病例无肺部体征;②外周血：85％（47／55）的病例外周血变化不大,WBC（4—10）×10 9／L之间,嗜酸性粒细胞增多;③特别检查：47．27％（26／55）肺炎支原体IgM（MP—IgM）抗体阳性,83．64％（46／55）PeR技术检测肺炎支原体特异性DNA;④X光报告为多种形式。结论肺炎支原体（MP）感染是引起儿童慢性顽固性咳嗽的病因之一,对儿童慢性咳嗽,特别是顽固性咳嗽的诊治中应更加重视。     

Acetaminophen and acetylcysteine dose and duration: Past,present and future

Abstract

Acetylcysteine has been utilized successfully in the treatment of acetaminophen overdose since the 1970s. Although prospective trials as to efficacy and safety of acetylcysteine were conducted, there were no randomized controlled trials. This commentary addresses the reasons for this, and the background to choice of dose of acetylcysteine utilized in the oral and IV dosing regimens. Nomograms to predict possible hepatotoxicity based upon time of ingestion of acetaminophen were developed from a relatively arbitrary definition of toxicity as an aspartate aminotransferase/alanine aminotransferase (ALT/AST) greater than 1000 IU/L. While these have proved generally useful, patients still continue to develop hepatic damage after acetaminophen overdose, particularly if they present late after ingestion. The optimum management of these patients remains unclear, and one area of uncertainty is the dose and duration of acetylcysteine in various circumstances. This article discusses the issues that need to be elucidated to better target changes in acetylcysteine dose. The potential for measurements of other markers to improve treatment selection is the subject of further research.     

VEGF和NSE在良恶性嗜铬细胞瘤中的表达及意义

目的探讨肿瘤标志物血管内皮生长因子（VEGF）和神经元特异性烯醇化酶（NSE）在良、恶性嗜铬细胞瘤组织中的表达,分析其可能的临床价值及病理学意义,为临床鉴别良、恶性嗜铬细胞瘤提供辅助依据。方法应用免疫组化（SP法）检测16例恶性嗜铬细胞瘤、18例良性嗜铬细胞瘤及17例正常肾上腺髓质组织中细胞因子VEGF和NSE表达情况,显微镜下判断组织切片的染色结果。结果①恶性嗜铬细胞瘤VEGF表达明显强于正常肾上腺髓质和良性嗜铬细胞瘤（P〈0.01）。良性肿瘤和正常肾上腺髓质的VEGF表达差异无统计学意义（P〉0.05）。恶性嗜铬细胞瘤强阳性率明显高于良性嗜铬细胞瘤（P〈0.01）。②良、恶性嗜铬细胞瘤NSE表达差异有统计学意义（P〈0.05）,良性嗜铬细胞瘤NSE的表达高于正常肾上腺髓质的NSE表达（P〈0.05）。恶性嗜铬细胞瘤强阳性率高于良性嗜铬细胞瘤（P〈0.05）。③VEGF和NSE共同阳性表达在良、恶性嗜铬细胞瘤之间差异有统计学意义（P=〈0.01）。结论临床上检测VEGF和NSE可能为鉴别良、恶性嗜铬细胞瘤提供辅助依据,共同检测VEGF和NSE可能提高良、恶性嗜铬细胞瘤鉴别的敏感性。