改良间歇负压封闭引流治疗严重开放性骨折22例疗效分析

目的探讨改良间歇负压封闭引流技术(vacuum sealing drainage,VSD)治疗严重开放性骨折的应用价值。方法外伤性严重开放性骨折伴皮肤软组织缺损患者57例,依据VSD方法不同分为改良间歇VSD治疗22例(A组)、普通持续VSD治疗20例(B组)和非VSD治疗15例(C组),观察各组临床疗效、相关并发症、植皮次数及创面治愈时间。结果 A,B组均未发生感染,其疗效优于C组,患者经一次植皮后治愈,其创面愈合时间均少于C组(P<0.05);A组疗效及治疗时间与B组比较差异无统计学意义(P>0.05),但堵管发生率低于B组(P<0.05)。结论 VSD是治疗严重开放性骨折伴皮肤软组织缺损的有效方法;改良间歇VSD操作方法简单,可避免或降低治疗中堵管的发生,减少VSD更换次数。     

开放性骨折合并软组织缺损的负压封闭引流治疗及护理体会

目的探讨负压封闭引流术(VSD)在开放性骨折合并软组织缺损的应用效果及手术配合的护理要点。方法将开放性骨折合并软组织缺损的69例(共78处创面)住院患者随机分为对照组与实验组。对照组按常规方法治疗。实验组分别给予武汉维斯弟成套专用敷料实施VSD治疗。结果实验组在二期缝合时间、换药次数、创面缩小程度、植皮效果等方面与对照组比较,差异均有统计学意义(P0.05)。结论VSD是治疗开放性骨折合并软组织缺损的有效方法,并能减少患者频繁换药的痛苦,减少了使用抗生素的时间和用量,减少患者住院时间及经济费用。熟练的手术配合是手术顺利进行的保证。     

负压封闭引流技术治疗下肢开放性骨折合并软组织缺损病人的疗效及护理

[目的]探讨负压封闭引流技术（VSD）治疗下肢开放性骨折合并软组织缺损的临床疗效.[方法]对24例下肢开放性骨折合并软组织缺损的病人急诊手术行清创内固定,创口及软组织缺损处应用负压封闭引流技术治疗.[结果]术后7 d～10 d拆除VSD材料,均可见创面新鲜肉芽组织生长,感染得到控制,愈合良好.[结论]持续负压封闭引流技术是治疗下肢开放性骨折合并软组织缺损的首选,可减少伤口感染几率,避免重复伤口换药,有利于肉芽组织生长,促进伤口及软组织缺损处的愈合.     

负压密闭引流治疗开放性骨折患者的护理体会

目的：探讨负压密闭引流（ VSD）治疗开放性骨折患者的护理体会。方法选取2010年3月至2014年3月收治的159例开放性骨折患者为研究对象，采用随机分层法分为对照组77例和观察组82例，对照组在在无菌骨科手术后采用传统清创处理及常规护理，观察组在无菌骨科手术彻底清创后＋VSD持续引流＋相关护理，比较两组患者创面修复疗效、骨性平均愈合时间、肉芽生长满意度、疼痛评分以及并发症发生情况。结果观察组创面修复总有效率74.39％、肉芽生长满意度60.98％、轻度疼痛79.27％，明显高于对照组；骨性平均愈合时间（6.33＆#177;0.72）个月、疼痛评分（3.86＆#177;0.67）分、并发症发生率6.1％，明显低于对照组，差异有统计学意义（ P＜0.05、P＜0.01）。结论开放性骨折术后VSD持续引流辅以相关护理干预有助于患者创面修复，促进骨性愈合，缓解疼痛程度，减少并发症的发生。     

封闭式负压引流治疗四肢创伤性软组织缺损的临床体会

目的 观察负压封闭引流（VSD）技术治疗四肢创伤软组织缺损的临床疗效.方法 72例四肢创伤性软组织缺损患者随机分为观察组和对照组各36例,两组均给予对症支持治疗,观察组给予VSD技术治疗,对照组给予常规换药处理,比较两组的疗效.结果 观察组Ⅱ期植皮的优良率为94.4%,显著高于对照组的72.2%（P〈0.05）,观察组的Ⅱ期创面植皮时间显著低于对照组,观察组的平均住院时间和总费用也显著低于对照组（P值均〈0.05）.结论 VSD技术治疗四肢创伤性软组织缺损疗效显著,可以提高Ⅱ期植皮的优良率,减少住院时间和总费用以及患者的痛苦,值得在临床推广.     

外固定支架联合VSD技术在下肢严重开放性骨折并皮肤缺损中的应用

探究外固定支架联合创面封闭式负压引流技术(VSD)技术在下肢严重开放性骨折并皮肤缺损中的应用效果。选择2016年5月~2017年1月我院骨科收治的下肢严重开放性骨折患者126例,根据随机数字表法将所有患者分为两组,每组各63例。对照组患者行外固定支架治疗,观察组行外固定支架联合VSD治疗,比较两组术后愈合、疼痛程度及并发症等情况。两组患者术后创面愈合时间、骨折愈合时间、疼痛VAS评分、换药次数及并发症发生率等指标相比,观察组均优于对照组,差异具有统计学意义(P<0.05)。外固定支架联合VSD能提高下肢严重开放性骨折并皮肤缺损的治疗效果,减少术后并发症发生率,缩短患者愈合时间,改善患者术后疼痛和生活质量。     

VSD技术联合外固定架治疗胫腓骨开放性骨折伴软组织缺损的护理

目的 探讨负压封闭引流术(VSD)联合外固定架治疗胫腓骨开放性骨折伴软组织缺损的治疗效果.方法 对20例胫腓骨开放性骨折伴软组织缺损采用VSD联合外固定架治疗.结果 20例患者骨折愈合良好,无感染发生,创面愈合良好,肢体功能良好.结论 VSD使创面引流充分,降低感染发生率,促进创面愈合,配合外固定架治疗胫腓骨开放性骨折伴软组织缺损是一种简单、有效的方法.     

负压封闭引流术治疗骨科创伤及感染创面的护理

对应用负压封闭引流术(VSD)治疗开放性骨折合并皮肤软组织缺损、皮肤套脱伤、感染性伤口的15例病人给予创面护理,保持引流通畅,加强心理护里和健康教育。结果所有病人在持续负压吸引后,均愈合良好,疗效满意。     

外固定支架术联合负压封闭引流治疗胫腓骨开放性骨折伴软组织损伤的疗效

目的探讨胫腓骨开放性骨折伴软组织损伤采用外固定支架联合负压封闭引流(VSD)治疗的临床效果。方法将60例胫腓骨开放性骨折伴软组织损伤患者按随机数字表法分为对照组和观察组,每组30例。对照组经清创、外固定支架术后进行传统换药治疗,观察组采用外固定支架术联合VSD治疗。所有患者均于创面新鲜后行植皮术。对2组患者术后组织缺损愈合时间、骨折愈合时间、踝关节功能恢复的优良率及并发症的发生情况进行比较。结果观察组缺损组织愈合时间、骨折愈合时间分别为(10.0±2.2)d、(5.5±1.3)个月;对照组缺损组织愈合时间、骨折愈合时间分别为(40.0±5.8)d、(8.0±2.5)个月,2组比较差异均有统计学意义(均P<0.05)。随访10个月,观察组踝关节功能优良率明显高于对照组(93.3%比66.7%,P<0.05)。2组均无感染、骨折移位等并发症发生。结论采用外固定支架术联合VSD治疗胫腓骨开放性骨折伴软组织损伤可充分引流,保持创面新鲜,促进创面愈合,有效地降低了感染率。     

伴软组织缺损胫骨远端粉碎性骨折封闭式负压引流疗效分析

目的:探讨封闭式负压引流(VSD)在伴软组织缺损的胫骨远端粉碎性骨折中的应用效果及其影响因素。方法:选取2013年8月～2018年1月我院创伤骨科收治的胫骨远端粉碎性骨折伴软组织损伤患者118例为研究对象。所有患者均予以封闭式负压引流治疗,根据疗效情况分为对照组(疗效差,21例)和观察组(疗效优良,97例),分析影响封闭式负压引流疗效的相关因素。结果:118例患者经治疗后,临床优良率为82.20%;单因素分析,VSD治疗效果与伴软组织缺损胫骨远端粉碎性骨折患者的年龄、创面大小、引流方式的不同、是否合并创面感染以及组织有无外露等因素有关,差异具有统计学意义(P0.05);多因素Logistic回归分析,高龄、合并创面感染、存在组织外露及间接引流是影响伴软组织缺损的胫骨远端粉碎性骨折患者VSD疗效的重要因素(P0.05)。结论:VSD在胫骨远端粉碎性骨折治疗中的应用效果较佳,但高龄、合并创面感染、存在组织和骨外露及间接引流是影响封闭式负压引流治疗疗效的危险因素。     

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。