微创经皮肾镜碎石取石术中常见问题护理措施

[目的]探讨微创经皮肾镜取石术术中常见护理问题及处理措施。[方法]回顾性分析2005年1月—2006年8月间我院完成的经皮肾镜碎石取石术治疗肾结石和输尿管上段结石200例,分析围术期出现的并发症的原因,探讨护理处理措施。[结果]200例中并发出血5例,胸腔积液2例,腹腔积液1例,术后感染5例,水中毒和低钠血症2例,低体温和寒战分别为3例和10例,有39例病人在术中因体位不适出现躁动,经对症对因处理,全部治愈。[结论]微创经皮肾镜虽为微创手术,但仍存在着发生并发症的风险,加强术中护理有利于并发症的防治。     

低龄肾结石患儿行微创经皮肾镜取石术的观察与护理

[目的]总结低龄肾结石患儿行微创经皮肾镜取石术的观察与护理。[方法]对2016年3月—2017年2月收治的53例低龄肾结石患儿行微创经皮肾镜取石术,同时加强术前护理、麻醉恢复期护理、术后肾造瘘专项护理、术后并发症专项护理以及出院指导。[结果]患儿一期取石成功52例,1例行二期取石术。术后出血3例,术后膀胱痉挛5例,均经对症处理后得到控制。患儿均无术后感染。随访6个月,患儿均未发生尿性囊肿、肾周脓肿、盂管交界处狭窄等,尿常规、肾功能检查结果均正常。[结论]加强低龄肾结石患儿行微创经皮肾镜取石术的围术期护理是手术成功的保证。     

微创经皮肾镜取石术严重出血行介入治疗的护理

[目的]总结微创经皮肾镜取石术(MPCNL)严重出血行介入治疗的护理体会。[方法]回顾性分析我院21例微创经皮肾镜取石术并发严重出血行介入治疗的护理资料。[结果]MPCNL术后严密观察出血情况,及时行介入治疗,病人均停止出血并顺利康复。[结论]微创经皮肾镜取石术后出血是最严重的并发症,超选择性肾动脉造影及栓塞术是诊断和治疗微创经皮肾镜取石术并发严重出血的安全有效的方法,应有针对性、有目的性地进行MPCNL术后观察及护理,可降低术后并发症的发生。     

微创经皮肾镜碎石取石术的护理体会

[目的]探讨微创经皮肾镜碎石取石术(PCNL)的观察及护理体会。[方法]回顾分析我科98例PCNL病人围术期的护理、泌尿外科的术前一般护理、术后护理及并发症的护理。[结果]术后98例病人均顺利拔管,痊愈出院。[结论]充分的术前准备、及时合理的术后护理、准确及时的生命体征监测对微创经皮肾镜碎石取石术病人的痊愈有重要意义。可减少手术并发症的出现及提高手术效果。     

微创经皮肾镜碎石取石术的手术护理配合

[目的]探讨微创经皮肾镜碎石取石术的手术护理配合。[方法]对行微创经皮肾镜碎石取石手术病人48例,加强术前准备及术中护理配合,严密观察病情,预防并发症的发生。[结果]48例病人手术顺利,手术时间60min～240min,一期结石清除率94%(45/48),无并发症发生,无中转开放手术。[结论]微创经皮肾镜碎石取石术具有手术创伤小、恢复快、病人痛苦小的优点,充分的术前准备,密切的术中护理配合是手术成功的重要环节。     

53例肾结石或输尿管结石病人行微创经皮肾镜取石术的手术配合

[目的]总结肾结石或输尿管结石病人行微创经皮肾镜取石术的手术配合。[方法]对53例肾结石或输尿管结石病人行微创经皮肾取石术,术前做好心理护理和手术准备,术中密切配合,术后做好器械保养。[结果]53例病人均顺利完成手术,术后未发生出血及其他并发症,结石取净率91%。[结论]加强微创经皮肾镜取石术的手术配合是手术成功的保证。     

护理干预在微创经皮肾镜钬激光碎石术后出现并发症病人中的应用

[目的]观察护理干预在微创经皮肾镜钬激光碎石术后出现并发症病人中的应用效果。[方法]将38例微创经皮肾镜钬激光碎石术后出现并发症病人随机分为对照组和观察组，每组19例，对照组病人术后给予并发症常规护理，观察组病人在对照组护理的基础上给予护理干预。术后随访3个月，观察两组病人住院时间及术后并发症的复发情况。[结果]观察组病人住院时间、并发症复发率均低于对照组（P〈o．05）。[结论]对微创经皮肾镜钬激光碎石术后出现并发症病人进行护理干预，可有效缩短病人住院时间、降低术后并发症复发率。     

微创经皮肾镜取石术严重出血行介入治疗的护理

[目的]总结微创经皮肾镜取石术(MPCNL)严重出血行介入治疗的护理体会.[方法]回顾性分析我院21例微创经皮肾镜取石术并发严重出血行介入治疗的护理资料.[结果]MPCNL术后严密观察出血情况,及时行介入治疗,病人均停止出血并顺利康复.[结论]微创经皮肾镜取石术后出血是最严重的并发症,超选择性肾动脉造影及栓塞术是诊断和治疗微创经皮肾镜取石术并发严重出血的安全有效的方法,应有针对性、有目的性地进行MPCNL术后观察及护理,可降低术后并发症的发生.     

微创经皮肾镜碎石取石术的护理

总结了41例微创经皮肾镜取石术术中常见护理问题及处理措施。主要护理措施为心理护理、术后出血护理、胸腔积水腹腔积液护理、寒战及感染等护理。认为微创经皮肾镜虽为微创手术,但仍存在着发生并发症的风险,加强术中护理有利于并发症的防治。     

个性化舒适体位护理在微创经皮肾镜碎石取石术中的应用

[目的]观察微创经皮肾镜碎石取石手术病人采用个性化舒适体位护理的效果。[方法]对实施微创经皮肾镜碎石取石手术的80例病人通过术前宣教、术中针对不同个体及不同体位给予个性化舒适体位的护理,并进行术后随访。[结果]80例病人除2例因术中出血多需停止手术外,其余均顺利完成手术,无呼吸困难及循环障碍的病例,无因体位护理不当影响手术的病例,术后无胸腹部及下肢持续疼痛、麻痹病例,回访调查病人满意率为96％。[结论]微创经皮’肾镜碎石取石术时采用个性化舒适体位的护理模式是可行、有效的。     

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。