老年痴呆患者发生院内感染因素分析及相应对策

目的对老年痴呆患者发生院内感染的危险因素进行分析,探讨相应的护理对策。方法老年痴呆患者180例,无院内感染组（58例）,院内感染组（22例）。分析患者院内感染发生情况,对两组患者临床资料进行对比。结果 180例老年痴呆住院患者院内感染发生率为12.2%;经对比,发生院内感染的患者年龄显著高于无感染患者,住院时间显著长于无院内感染患者,侵袭性操作率及抗生素不合理应用率均显著高于无院内感染患者,差异均具有统计学意义（P〈0.05）。结论老年痴呆患者发生院内感染的因素主要包括年龄、抗生素不合理应用、住院时间及侵袭性操作等,在临床中应针对院内感染发生的危险因素给予有效预防干预措施,促使老年痴呆患者院内感染发生率不断降低。     

院内感染的发生,细菌耐药性及治疗效果与医院抗生素使用规则

对９５年度１７０例院内感染病病人在感染发生前后抗生素使用情况，细菌耐药性及治疗效果进行分析，１７０全病人中，在院内感染前，因感染使用抗生素者４２．３％，预防用抗生素者１０％。院内感染发生后，使用一种抗生素控制感染６６例，其中５７例炎未使用抗生素者，从感染患者的血，尿，粪中培养细胞２４株，真菌５株，耐３种以上抗生素有１９株，对抗生素使用进行了规定，目前无耐头孢第二代，第三代以及新型喹诺酮类药物的菌株     

老年痴呆患者发生院内感染因素分析及相应对策

目的研究分析老年痴呆患者发生院内感染的因素及其相应的解决方案。方法 39例发生院内感染的老年痴呆患者作为研究组,并选择同期未发生院内感染的老年痴呆患者39例作为对照组,对比分析并观察老年痴呆患者发生院内感染的的因素,从而采取针对措施。结果两组患者年龄比较:研究组患者较之对照组年长,差异具有统计学意义(P<0.05);研究组患者中呼吸道感染所占比重最大,与其他感染部位比较差异具有统计学意义(P<0.05),其次依次为皮肤软组织感染、泌尿系统感染、胃肠道感染,其他感染。两组患者在住院时间>15 d、侵袭性操作、抗生素使用≥7 d以及抗生素联合使用≥2种,差异具有统计学意义(P<0.05)。结论老年痴呆患者发生院内感染的因素较多,其中主要为住院时间长、年龄大,侵袭性操作以及抗生素使用不合理等,因此积极有效预防老年痴呆患者院内感染。     

预防性使用抗生素对病毒性脑炎院内感染的影响

目的 :探讨病毒性脑炎患者预防性使用抗生素对院内感染的影响。方法 :对 5 3 8例病毒性脑炎患者进行了回顾性分析。结果 :入院时未合并感染的 5 19例患者中 2 82例预防性使用抗生素 (A组 ) ;2 3 7例未预防性使用抗生素 (B组 )。A组院内感染率 11 3 %明显低于B组 18 9%的院内感染率 (P <0 0 5 )。A组中发生院内感染者抗生素使用时间 ( 14 1± 8 3天 )明显长于无感染者 ( 10 4± 5 6天 ) (P <0 0 1)。预防性使用抗生素可能增加霉菌感染率 (P >0 0 5 )。结论 :预防性使用抗生素对减少院内感染有一定作用。抗生素使用应早期、短程 ,限于重症患者。     

213例儿科呼吸道感染患者抗生素使用情况分析

目的分析我院儿科呼吸道感染住院患儿抗生素使用情况,为合理应用抗生素提供参考。方法回顾性分析我院儿科2010年6月至2011年6月间收治的213例呼吸道感染患儿的病例资料,用药物利用指数(DUI)作为合理用药标准,分析其抗生素的使用情况。结果 213例呼吸道感染患儿均使用过抗生素治疗(100%),使用抗生素12种,其中3种(25%)药物使用不合理;有75例(35.2%)连用两种以上抗生素;有89例(41.8%)患儿同时使用了激素类药物;下呼吸道感染患儿药物不合理使用率及抗生素联用率分别高于上呼吸道感染者(P<0.05)。结论儿科呼吸道感染患者抗生素合理使用情况总体来满意,但仍有待改进;下呼吸道感染患儿较上呼吸道感染者更易出现抗生素使用不合理的情况,应引起临床医生的注意。     

201例2型糖尿病患者院内感染的临床分析

目的:了解2型糖尿病患者院内感染的发生情况。方法:对我院1997～2002年收治的201例2型糖尿病患者的院内感染进行回顾性分析。结果:201例2型糖尿病患者中发生院内感染36例,感染发生率17.91%,显著高于我国平均院内感染发生率(8.4%P<0.05)。感染部位以下呼吸道最常见,感染病菌主要为革兰阴性杆菌。血糖水平高低、抗生素的使用、年龄、住院时间长短是影响感染发生的因素。结论:应加强对2型糖尿病患者院内感染的预防和治疗。     

我院恶性肿瘤患者院内感染及抗菌药使用的回顾性分析

目的了解我院恶性肿瘤患者院内感染及抗菌药使用情况,以进一步合理使用抗菌药,降低院内感染的发生。方法回顾性分析我院482例住院恶性肿瘤患者院内感染的发生情况,分析发病率、发病部位、病原学检测及抗菌药使用情况。结果住院的482例患者中,发生院内感染99例,感染率为20.5%。院内感染者中上呼吸道感染最多,占26%(26/99);病原学送检率为39%(39/99),培养或(和)涂片病原学阳性率82%,其中G~-细菌占57%,G~+细菌占24%,真菌占19%;抗菌药使用率95%,其中以头孢菌素类使用率最高,占43%。联合放、化疗者院内感染的发生率高于单纯放疗或化疗者(52.9%vs.16.4%、25.1%,均P<0.05)。结论进一步加强院内感染的监测、及时进行病原学检测和药敏试验、合理使用抗菌药等措施有利于恶性肿瘤患者院内感染的防治。     

老年痴呆患者发生院内感染因素分析及相应对策

目的：对导致老年痴呆患者发生院内感染的原因进行总结,并制定相应的应对措施。方法50例老年痴呆患者作为本次研究的观察对象,对引起老年痴呆患者发生院内感染的因素进行分析总结,并制定相应的护理对策。结果本组50例观察对象的平均年龄为（75.3±2.1）岁、住院时间为（79.5±22.5）d、侵袭性操作率为54.0%、抗生素应用不合理率52.0%。结论引起老年痴呆患者发生院内感染的常见原因为患者年龄大、抗生素使用不合理、侵袭性操作、住院时间较长;而通过加强对环境管理、呼吸道管理、抗生素应用等的重视则可有效的降低感染发生率。     

老年痴呆患者发生院内感染因素分析及相应对策

目的：对老年痴呆患者发生院内感染的危险因素进行研究分析,并探讨有效的应对策略。方法分别选取本院2011年5月-2013年住院部门收治的55例发生院内感染老年痴呆患者与55例未发生院内感染的老年痴呆住院患者作为研究对象,对两组患者临床资料进行分析,总结分析观察组发生院内感染的危险因素。结果观察组平均年龄明显大于参考组（P＜0.05）;观察组住院时间〉15 d、抗生素联合使用≥2种、抗生素使用≥7 d、侵袭性操作患者明显多与参考组（P＜0.05）,观察组患者经积极对症治疗后感染均在7 d内消失,治愈率为100%,未出现死亡患者。结论高龄、住院时间过长、抗生素使用不合理及侵袭性操作等均是导致老年痴呆患者出现院内感染的危险因素,积极采取相应预防措施有助于减少院内感染的发生。     

综合性ICU院内感染因素分析与护理干预

目的:探讨综合性ICU院内感染因素和护理干预效果.方法:2008年1月～2009年12月收治782例住院病人,对其中发生89例院内感染病人进行回顾性分析,院感率11.4%.结果:感染者以老年病人居多,侵袭性操作多、抵抗力低、基础疾病重者,不合理应用抗生素以及医务人员感染控制意识不足易导致院内感染发生;感染部位以下呼吸道、泌尿道、胃肠道最常见.结论:根据科室的具体情况,指定切实可行的医院感染控制措施并不断完善,加强对医务人员、病人,探视者、物表、空气等医院感染控制各种措施落实,可有效降低ICU院内感染率.     

Quantitative in vivo and in vitro sex differences in artemisinin metabolism in rat

1. The pharmacokinetics of the antimalarial compound artemisinin were compared in the male and female Sprague-Dawley rat after single dose i.v. (20 mg.kg) or i.p. (50 mg.kg) administration of an emulsion formulation. 2. Plasma clearance of artemisinin was 12.0 (95% confidence interval: 10.4, 13.0) l.h. kg in the male rat and 10.6 (95% CI: 7.5, 15.0) l.h. kg in the female rat suggesting high hepatic extraction in combination with erythrocyte uptake or clearance. Artemisinin half-life was 0.5 h after both routes of administration in both sexes. Values for plasma clearance and half-lives did not statistically differ between the sexes. 3. After i.p. administration artemisinin AUCs were 2-fold higher in the female compared with male rat (p 0.001). Artemisinin disappearance was 3.9-fold greater in microsomes from male compared with female livers and it was inhibited in male microsomes by goat or rabbit serum containing antibodies against CYP2C11 and CYP3A2 but not CYP2B1 or CYP2E1. 4. The unbound fraction of artemisinin in plasma was lower (p 0.001) in plasma obtained from the male (8.8 2.0%) compared with the female rat (11.7 2.2%). 5. The possibility of a marked sex difference, dependent on the route of administration, has to be taken into account in the design and interpretation of toxicological studies of artemisinin in this species.     

Quantitative in vivo and in vitro sex differences in artemisinin metabolism in rat

1. The pharmacokinetics of the antimalarial compound artemisinin were compared in the male and female Sprague-Dawley rat after single dose i.v. (20 mg x kg(-1)) or i.p. (50 mg x kg(-1)) administration of an emulsion formulation. 2. Plasma clearance of artemisinin was 12.0 (95% confidence interval: 10.4, 13.0) 1 x h(-1) x kg(-1) in the male rat and 10.6 (95% CI: 7.5, 15.0) 1 x h(-1) x kg(-1) in the female rat suggesting high hepatic extraction in combination with erythrocyte uptake or clearance. Artemisinin half-life was approximately 0.5 h after both routes of administration in both sexes. Values for plasma clearance and half-lives did not statistically differ between the sexes. 3. After i.p. administration artemisinin AUCs were 2-fold higher in the female compared with male rat (p < 0.001). Artemisinin disappearance was 3.9-fold greater in microsomes from male compared with female livers and it was inhibited in male microsomes by goat or rabbit serum containing antibodies against CYP2C11 and CYP3A2 but not CYP2B1 or CYP2E1. 4. The unbound fraction of artemisinin in plasma was lower (p < 0.001) in plasma obtained from the male (8.8 +/- 2.0%) compared with the female rat (11.7 +/- 2.2%). 5. The possibility of a marked sex difference, dependent on the route of administration, has to be taken into account in the design and interpretation of toxicological studies of artemisinin in this species.     

Interindividual variability in metabolic activation in humans in vivo

In assessing interindividual variability in metabolic activation, the toxic metabolite is often too unstable for conventional analysis. Possible alternatives include a stable product of the reactive metabolite e.g. cysteinyl derivatives of N-acetyl-4-benzoquinoneimine, the toxic metabolite of paracetamol, adducts with DNA or protein, and indirect measurement of the activity of the enzyme(s) producing the active metabolite. An example of the last approach is the use of furafylline, a highly specific inhibitor of human CYP1A2, to determine the extent of the metabolic activation of the cooked food mutagens PhIP and MeIQx. The extent of inhibition, determined from levels of unchanged amine in urine, is an indirect measure of the activity of the activation pathway. Further refinement of this approach, allied to improved measures of the biological process of interest should prove of value in evaluating interindividual variability and its role in the risk assessment process.     

Theophylline kinetics in peripheral tissues in vivo in humans

Several biochemical and cellular effects have been described for methylxanthines under in vitro conditions. However, it is unknown, whether threshold concentrations required to exert these effects are attained in target tissues in vivo. We therefore employed the microdialysis technique for measuring theophylline concentrations in peripheral tissues under in vivo conditions.Following in vitro and in vivo calibration, microdialysis probes were inserted into the medial vastus muscle and into the periumbilical subcutaneous adipose layer of healthy volunteers. Following single oral dose administration of 300 mg or i.v. infusion of 240 mg theophylline, in vivo time courses of theophylline concentrations were monitored in tissues and plasma. Major pharmacokinetic parameters (c_max, t_max, AUC) were calculated for plasma and tissue time courses. The mean AUC_tissue /AUC_plasma-ratio was 0.56 (p.o.) and 0.55 (i.v.) for muscle and 0.55 (p.o.) and 0.72 (i.v.) for subcutaneous adipose tissue.We conclude that microdialysis provides important information on the distribution and the tissue pharmacokinetics of theophylline.Abbreviations FPIA Fluorescence polarisation immuno assay - AUC Area under the curve - t_max Time to peak concentration - c_max Peak concentration     

休克时血中氧自由基的变化

本实验测定10名休克患者血浆和红细胞的丙二醛(MDA)、血浆总抗的氧化活性(AOA)的含量。结果表明:休克病人红细胞膜和血浆 MDA 含量(4.298±0.722;5.348±0.834)与对照组(3.235±0.682;4.356±1.081)比较明显增高(P<0.05);血浆 AOA(39.65±7.858)与对照组(48.21±10.81)比较明显降低(P<0.01)。提示:休克时,患者机体内自由基反应增强是引起组织细胞损伤的原因之一。     

Trichinellosis in immigrants in Switzerland

We describe a case of trichinellosis diagnosed at the Division of Infectious Diseases, Hospital of Lugano, in January 2009. This case was associated with a cluster of cases and was traced to the consumption of contaminated meat after a wild boar hunt in Bosnia.     

Changes in angiopoietin expression in glomeruli involved in glomerulosclerosis in rats with daunorubicin-induced nephrosis

AIM: To study the potential pathological role of endogenous angiopoietins in daunorubicin-induced progressive glomerulosclerosis in rats. METHODS: Seventy male Wistar rats were allocated randomly into a daunorubicin group (DRB; n=40) or a control group (n=30). The rats in the DRB group were injected with DRB (15 mg/kg), in their tails. Subsequently, at intervals of 1, 2, 4, 6, 8, and 12 weeks, 5 male Wistar rats in each group were chosen randomly for 24 h urinary protein quantitative measurements (24 h UPQM), and determination of plasma tumor necrosis factor alpha (TNF-alpha), angiopoietin-1 (Ang1), and angiopoietin-2 (Ang2) levels. Kidney sections were examined by electron microscopy, Periodic Acid Schiff (PAS) staining, immunohistochemical staining and in situ hybridization histochemistry. RESULTS: As glomerulosclerosis progressed in the DRB group, expression of Ang1 mRNA and protein in glomeruli decreased and expression of TNF-alpha protein, Ang2 mRNA and protein in glomeruli increased. Expression of Ang1 mRNA and protein in glomeruli were negatively correlated with 24 h UPQM, Fn protein expression, and mean area of extracellular matrix (MAECM). In comparison, expression of Ang2 mRNA and protein in glomeruli were positively correlated with 24 h UPQM, Fn protein expression and MAECM; furthermore, there was a positive correlation between plasma Ang2 and 24 h UPQM. Plasma TNF-alpha and expression of TNF-alpha in glomeruli were positively correlated with expression of Ang2 mRNA and protein in glomeruli. There was a negative correlation between Ang1 protein expression and Ang2 protein expression in glomeruli. CONCLUSION: During DRB-induced glomerulosclerosis, podocyte injury led to a shift in the balance of Ang1 and Ang2 in glomeruli. Increased TNF-alpha in plasma and glomeruli may upregulate Ang2 expression in glomeruli. Elevated Ang2 in both plasma and glomeruli may mediate protein permeability through the glomerular filtration barrier. Moreover, local expression of Ang2 may facilitate the progress of glomerulosclerosis by upregulating a component expression of extracellular matrix.     

Hyperkalaemia in patients in hospital

A survey of all laboratory blood specimens with a plasma potassium concentration greater than or equal to 5.5 mmol/L was conducted over a three month period. Of 331 specimens with hyperkalaemia, 71 were excluded because the specimens was haemolysed, old or contaminated. The laboratory served a population of 348,561 and during this time measured the plasma potassium on 25,016 occasions. Sixty-six outpatients and 20 neonates were not evaluated. The survey was undertaken on 86 of 102 inpatients (46 males), 48 of whom were over 66 years of age. Fifty-seven patients were admitted under a medical service and 29 under a surgical service. Fifty-nine had a single episode of hyperkalaemia. Thirty-two underwent a surgical procedure. The commonest contributing factor was impaired renal function which was present in 71 (83%) patients. Although a definitive causative role for drugs could be identified in only five patients, in 52 (60%) patients drugs were a contributing factor (potassium supplements 24, ACE inhibitors 16, nonsteroidal antiinflammatory drugs 12). Thirty-five of the 86 (41%) patients died during their hospital admission. Nineteen of the 35 deaths occurred within three days of the hyperkalaemia being recorded. A normal plasma potassium was eventually documented in 50 of the 86 patients. Of the remaining 36 patients, 25 (69%) subsequently died. In general the treatment of patients with hyperkalaemia focused on identifying and treating the underlying cause. Hyperkalaemia must always be considered seriously and regard given to the overall clinical status of the patient, with particular attention to drug therapy, renal and cardiac function, acid base status and the possibility of sepsis.