吸入性损伤气管导管脱出原因分析及对策

目的 探讨吸入性损伤气管切开置管,导管脱出的原因及正确的护理方法,提高护士对患者的预见性护理能力.方法 对2005年1月-2011年3月收治的158例吸入性损伤气管切开患者,其中9例术后发生导管脱出的原因及护理对策进行回顾性总结.结果 9例患者发生导管脱出的主要原因有导管选用不当、剧烈咳嗽、系带过松、气囊充气不足或气囊...     

吸入性烧伤气管切开的预见性护理

[目的]探讨吸入性烧伤病人气管切开预见性护理的效果.[方法]对30例吸入性烧伤病人入院时进行评估,判断吸入性烧伤的程度,观察病人是否具有气管切开的指证,对气管切开整个过程进行预见性护理.[结果]轻度吸入性烧伤病人均未行气管切开,中度3例行气管切开,重度全部切开,经过吸氧、气道湿化、对症治疗及预见性护理,全部治愈出院.[结论]预见性护理可以为临床及时切开气管提供可靠信息,并为气管切开后提供高质量的护理,有效防止了呼吸道堵塞和减少并发症的发生.     

吸入性损伤后气道阻塞69例原因分析及护理

目的:探讨吸入性损伤后气道阻塞的原因及护理.方法:对69例吸入性损伤患者的临床资料及护理进行回顾性分析总结.结果:由于护理措施积极有效,69例患者均无因气道阻塞而发生严重并发症.结论:护理人员掌握吸入性损伤的临床特点,重视对气道阻塞早期征象的观察,预见性地实施有效的护理措施,对预防气道阻塞、挽救患者生命至关重要.     

吸入性损伤气管切开术后人工气道的护理

目的:探讨吸入性损伤气管切开术后人工气道的护理。方法:对43例吸入性损伤气管切开术后病人进行心理护理、人工气道管理、预防肺部感染等护理措施。结果:43例病人除1例发生气管套管脱落外,其余均未发生术后并发症。结论:做好吸入性损伤气管切开术后护理,对预防术后并发症的发生起着重要作用。     

颅脑损伤44例气管切开术后护理

对44例颅脑损伤气管切开术后患者行基础护理、气管套管护理、人工气道护理、心理护理、病情观察、环境护理等.结果通过以上护理措施,38例患者拔管后出院,5例死亡,1例带管出院,均未发生并发症.认为对颅脑损伤气管切开术后患者完善各种护理措施,有利于预防或减少并发症发生.     

大面积烧伤合并吸入性损伤患者气管切开后的气道湿化

目的:探讨大面积烧伤合并吸入性损伤患者气管切开后气道湿化的方法。方法:严密观察气管切开患者的病情变化,给予病房内空气湿化、套管外口敷料湿化、超声雾化吸入湿化、气道冲洗、气管内滴药及呼吸机湿化等综合气道湿化护理,观察肺部感染、气道阻塞等并发症的发生率。结果:78例患者气管切开时间为伤后2~9h,平均4.6h。拔管时间9~27d,平均13.5d。治愈73例,死亡5例,死亡原因分别为多器官功能衰竭2例,创面脓毒症2例,肺部感染1例,治愈率93.59%。没有出现气道阻塞并发症。结论:正确有效地做好大面积烧伤合并吸入性损伤患者气管切开后的气道湿化,有利于减少呼吸道并发症,是治疗吸入性损伤的有效方法。     

分阶段气道护理在重度吸入性损伤患者中的应用

总结1例重度吸入性损伤患者人工气道管理的护理经验。根据吸入性损伤病理生理改变过程行分阶段气道护理,第一阶段因烧伤后颈部水肿程度不断变化,需保证人工气道固定良好,预防气管套管非计划性拔管;第二阶段因气道黏膜坏死脱落,采用定时、带负压、分段分次吸痰,做好气道湿化,防止阻塞气管;第三阶段主要针对痰液的排出和呼吸机相关性肺炎(Ventilator-associated pneumonia VAP)的预防。     

严重烧伤合并重度吸入性损伤28例临床护理

对28例严重烧伤合并重度吸入性损伤患者给予精心护理,包括抗休克、气道管理、面、颈部护理、严格执行消毒隔离制度及心理护理.结果本组气管切开16例,应用呼吸机11例,气管切开时间12～21 d,治愈19例,死亡9例.认为对严重烧伤合并重度吸入性损伤患者给予精心护理的同时做好呼吸道管理至关重要,它可有效预防肺部并发症的发生.     

火灾中化学气体致吸入性损伤急救和护理

目的 探讨烧伤并吸入性损伤的急救和护理措施.方法 对53例火灾烧伤并吸入性损伤的急救和护理的临床资料进行回顾性分析.结果 火灾中化学气体致中、重度吸入性损伤,应常规进行支气管纤维镜检查,及时发现呼吸道吸入性损伤,尽早行气管插管或气管切开,呼吸功能不全,进行性低氧血症者(高浓度吸氧后,PaO2仍低于7.8 kPa或PaCO2大于6.5 kPa),应用呼吸器辅助呼吸,改善通气和换气功能,纠正缺氧,防止二氧化碳潴留.结果 治愈轻度吸入性损伤22例；中、重度吸入性损伤29例;死亡2例.结论 严密的病情观察,及时正确地抢救处理和有效的气道护理措施是抢救成功的重要保证.     

人工鼻在烧伤合并吸入性损伤气管切开术中的应用及护理

目的探讨人工鼻在烧伤合并吸入性损伤气管切开术中的应用效果及护理方法。方法对2012年3月-10月16例烧伤合并吸入性损伤气管切开患者,通过气管导管口接人工鼻吸氧的护理方法及应用效果进行回顾性总结。结果16例烧伤合并吸入性损伤气管切开患者,15例使用人工鼻,均无气管导管堵塞及肺部感染等并发症的发生,于伤后14～22d拔除气管导管;1例因伤后15d转入医院时已患多重细菌肺部感染,予积极控制感染、营养支持及同时使用人工鼻等治疗,于伤后38d拔除气管导管。结论人工鼻用于烧伤合并吸入性损伤气管切开术中,能使开放式的人工气道处于封闭状态,温热湿化气道,过滤空气中的灰尘,达到氧疗效果,有效预防气管导管堵塞及肺部感染,缩短带管时间,值得临床应用。     

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。